To examine how whey protein served as a premeal affects postprandial glucose excursions in women with gestational diabetes mellitus (GDM).

A placebo-controlled, single-blinded, crossover, randomized trial including women with and without GDM (20-36 weeks' gestation) was performed. Participants were studied in the laboratory and at home. In the laboratory, women were randomized to consume 20 g of whey or placebo 30 min before undergoing, 7-14 days later, a 75-g oral glucose tolerance test (OGTT). Blood was sampled consecutively 3 hours following the OGTT. The primary end point was the incremental area under the curve (iAUC) for glucose. At home, participants wore continuous glucose monitors and, on subsequent days, randomly consumed 0, 10, 15, 20, and 30 g of whey 30 min before breakfast.

Twelve women with GDM and 12 pregnant women with normal glucose tolerance (NGT) to part in the trials. Intake of premeal whey resulted in lowered peak glucose by -1.0 mmol/L (95% CI -1.6 to -0.4) in women with GDM and -0.7 mmol/L (95% CI -1.3 to -0.1) in women without GDM compared with placebo. Insulin, glucose-dependent insulinotropic polypeptide, and glucagon-like peptide-1 levels increased rapidly after whey consumption in both groups. At home, a premeal of 30 g of whey dose-dependently reduced incremental glucose peaks with a maximum of -2.0 mmol/L (95% CI -2.5 to -1.5) in women with GDM compared with placebo.

Premeal whey consumption acutely lowers postprandial blood glucose in women with GDM and those with NGT, with 15-30 g lowering the glucose iAUC of women with GDM. These findings emphasize the need for long-term studies to assess the impact of whey premeals in pregnancies affected by GDM.

Type 2 diabetes (T2D) is highly prevalent, particularly among south Asian populations, and diet is the first-line strategy to manage postprandial glucose (PG) response. Mycoprotein and guar gum reduce PG in normo-glycaemic people. This study investigates the independent and interactive effects of mycoprotein and guar gum on PG, insulin and appetite responses in white Europeans and south Asians with T2D.

In this double-blind, crossover, acute, randomised controlled trial, 18 subjects with T2D (10 white European, 8 south Asian) completed six separate visits consuming soy, chicken, and mycoprotein with and without guar gum. Incremental area under the curve (iAUC0-180 min) for PG, insulin, and appetite scores, and total AUC0-180 min glucagon-like peptide-1 (GLP-1), peptide tyrosine-tyrosine (PYY), as well as ad libitum energy intake and 48h-post-visit energy intake were measured and analysed by linear mixed models with protein, guar gum and ethnicity as fixed effects.

We found independent effects of mycoprotein, guar gum and ethnicity on PG iAUC0-180 min (mmol/L·min), where mycoprotein reduced PG vs. chicken (-129.84 [95% CI -203.16, -56.51]; p = 0.002), guar gum reduced PG vs. no guar gum (-197.35 [95% CI -254.30, -140.40; p < 0.001], and south Asian had increased PG vs. white Europeans (195.75 [95% CI 66.14, 325.35]; p = 0.005). An interaction between guar gum and ethnicity (p < 0.015) was found for insulin iAUC0-180 min (µUI/mL·min), with guar gum lowering insulin responses in south Asian participants (-1909.69 [95% CI -2834.83, -984.511]; p < 0.001). No independent or interactive effects were observed for appetite-related outcomes.

Mycoprotein and guar gum promote significant independent effects in lowering PG in both white European and south Asians with T2D.

Glucose-dependent insulinotropic polypeptide (GIP) was the first incretin identified and plays an essential role in the maintenance of glucose tolerance in healthy humans. Until recently GIP had not been developed as a therapeutic and thus has been overshadowed by the other incretin, glucagon-like peptide 1 (GLP-1), which is the basis for several successful drugs to treat diabetes and obesity. However, there has been a rekindling of interest in GIP biology in recent years, in great part due to pharmacology demonstrating that both GIPR agonism and antagonism may be beneficial in treating obesity and diabetes. This apparent paradox has reinvigorated the field, led to new lines of investigation, and deeper understanding of GIP.

In this review, we provide a detailed overview on the multifaceted nature of GIP biology and discuss the therapeutic implications of GIPR signal modification on various diseases.

Following its classification as an incretin hormone, GIP has emerged as a pleiotropic hormone with a variety of metabolic effects outside the endocrine pancreas. The numerous beneficial effects of GIPR signal modification render the peptide an interesting candidate for the development of pharmacotherapies to treat obesity, diabetes, drug-induced nausea and both bone and neurodegenerative disorders.

Previous studies have reported that the type of protein consumed as preloads significantly affects postprandial glucose and insulin excursions in healthy and type 2 diabetes. But little is known how protein synergistic preloading affects human health.

Using two typical Asian protein type (soya tofu and chicken) with carbohydrate (white rice), the aim of this study was to compare the effects of two different protein types presented synergistically as preloads on postprandial glycemia, insulinemia and incretin secretions in healthy adults.

Sixteen healthy Chinese male adults participated in a randomized, controlled, crossover meal trial. Subjects consumed, in random order, 4 experimental meals that differed in protein type and proportion. Glucose, insulin, incretins and triglyceride concentrations were measured over 3 h.

There were significant protein type preload treatment x time interaction effects on plasma glucose, insulin, glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP) and triglycerides concentrations (P < 0.001). In comparison with rice alone treatment, preloading with Soya, Chicken and Soya/Chicken (50% soya tofu combined with 50% chicken breast) prior to rice consumption all significantly attenuated postprandial glucose response. Soya + Rice treatment induced a significantly lower incremental peak and incremental area under curve (iAUC) (0-60 min) glucose level compared with Chicken + Rice. The postprandial insulin response (incremental peak, iAUC 0-180 min) was significantly lower after Soya + Rice than Chicken + Rice group. Soya/Chicken + Rice treatment did not induce any significant difference in glucose and insulin levels between Soya + Rice or Chicken + Rice group. Notably, Soya/Chicken + Rice as well as Soya + Rice induced a significantly higher GLP1 and GIP responses compared with Rice or Chicken + Rice groups. Soya + Rice and Soya/Chicken + Rice groups stimulated higher triglyceride concentration than the other two groups.

Different protein preload with rice can considerably influence its glycemic, insulinemic and incretin responses. Soya or Soya/Chicken protein synergistic preloading induced higher incretins responses to modulate glycemic response in healthy adults.

Quinine, when administered intraduodenally to activate bitter-taste receptors, in a dose of 600 mg, stimulates glucagon-like peptide-1 (GLP-1) and insulin, slows gastric emptying and lowers postprandial glucose in healthy people, with consequent implications for the management of type 2 diabetes; the effect of quinine on energy intake is uncertain. We have investigated the dose-related effects of quinine on postprandial blood glucose levels and energy intake in people with type 2 diabetes.

Male participants with type 2 diabetes (age: 68±5 years; HbA1c: 49.0±5.0 mmol/mol [6.7±0.4%], BMI: 30±1 kg/m2) received in two study parts (A and B, n=12 each), on three separate occasions each, in randomised, crossover fashion, control, or 300 mg (QHCl-300) or 600 mg (QHCl-600) quinine hydrochloride, intraduodenally 30 min before a nutrient drink (2092 kJ, 74 g carbohydrate) (part A) or a standardised buffet-lunch (part B). Both the participants and investigators performing the study procedures were blinded to the treatments. In part A, plasma glucose, GLP-1, C-peptide and glucagon were measured at baseline, for 30 min after quinine alone and for 3 h post drink. Gastric emptying of the drink was measured with a 13C-acetate breath test. In part B, energy intake from the buffet-lunch was quantified.

Quinine alone had no effect. Post drink, both quinine doses reduced peak plasma glucose markedly (QHCl-600 by 2.8±0.6 mmol/l) and slowed gastric emptying (all p<0.05; n=12, except for gastric emptying, n=11). QHCl-600, but not QHCl-300, stimulated plasma GLP-1 and C-peptide modestly (both p<0.05). Quinine did not affect energy intake.

In type 2 diabetes, acute intraduodenal administration of quinine markedly reduces the plasma glucose response to oral carbohydrate, but does not affect energy intake. These findings support the potential use of quinine to reduce postprandial blood glucose levels in type 2 diabetes.

anzctr.org.au ACTRN12620000972921/ACTRN12621000218897 FUNDING: The study was funded by a Diabetes Australia Research Project Grant.

The meal sequencing of macronutrients has been shown to ameliorate postprandial glucose excursion, but its effects in daily meals has not been investigated. We examined the impact on the glucose response to meal sequencing in healthy Japanese adults using continuous glucose monitoring (CGM) during a typical lunch meal.

The test meal was a Japanese set meal or a beef and rice bowl, the contents of which were categorized as "rice" or "non-rice". In the meal experiments, the subjects ingested the two categories of food in one of three orders: non-rice before rice, non-rice and rice together, and non-rice after rice. In the beef and rice bowl experiments, the subjects ingested either non-rice 15 min before rice or the two foods together.

The postprandial glucose level was measured over a 4 h period and the mean level of postprandial glucose was significantly lower than that when eating rice before non-rice or both together. Consuming non-rice before rice significantly reduced postprandial glycemic excursions in healthy adults in both experiments.

Meal-sequencing by "eat carbs last" is a feasible dietary strategy for the better prevention and management of diabetes.

Small nutritional preloads can reduce postprandial glucose excursions in individuals with and without metabolic syndrome or type 2 diabetes (T2D). However, most studies have focused on preloads administered before single meals and have predominantly used protein-based preloads.

To investigate the effects of sequential consumption of medium-chain triglycerides (MCT) and whey protein isolate (WPI) preloads before breakfast, lunch, and dinner on postprandial, diurnal, and 24-h glycaemia in individuals with T2D.

Participants with T2D were studied over 3 randomized 24-h periods. They consumed either water before standardized breakfast, lunch, and dinner (CONTROL), 15 g MCT before breakfast and water before lunch and dinner (MCT), or 15 g MCT before breakfast and 10 g WPI before lunch and dinner (MCT + WPI). Diurnal (08:00-23:00 h) and 24 h (08:00-08:00 h) glycaemia (incremental AUC [iAUC]) and glycaemic variability (%coefficient of variation [%CV]) were evaluated by continuous glucose monitoring. Postprandial glycaemia (PPG) after breakfast and lunch was assessed by arterialized blood glucose iAUC.

In 21 enrolled patients (8 males/13 females, mean ± standard deviation age 55.1 ± 8.5 y, body mass index 31.7 ± 4.3 kg·m-2, glycated hemoglobin 59 ± 12 mmol·mol-1) diurnal and 24-h iAUC were similar across interventions, whereas 24-h %CV was lower in MCT (16.8 ± 0.8%, P = 0.033) and MCT + WPI (16.1 ± 0.9%, P = 0.0004) than CONTROL (18.7 ± 0.9%). PPG iAUC was ∼17% lower after breakfast in MCT and MCT + WPI compared with CONTROL, but only the MCT + WPI lowered glucose by 20% (P = 0.002) over the entire day (08:30-17:30 h). Gastric inhibitory polypeptide (GIP) (P = 0.00004), peptide YY (PYY) (P = 0.01), and β-hydroxybutyrate (P = 0.0001) were higher in MCT and MCT + WPI than CONTROL. Subjective appetite ratings were lower after breakfast and lunch in MCT + WPI (P = 0.001).

Sequential consumption of MCT and WPI preloads did not affect diurnal or 24-h glycaemia but lowered PPG and 24-h glycaemic variability in individuals with T2D. These effects were associated with increased circulating β-hydroxybutyrate, PYY, and GIP, and suppression of appetite. This trial was registered at clinicaltrials.gov as NCT04905589 (https://clinicaltrials.gov/study/NCT04905589).

Purpose: Whey protein (WP) consumption prior to a meal curbs appetite and reduces postprandial glucose (PPG) through stimulating endogenous GLP-1 secretion and insulin. Methods: We assessed the metabolic effects of a concentrated WP, using a new micelle-technology (WPM), in people with type 2 diabetes (T2D) and overweight or obesity (NCT04639726). In a randomized-crossover design, participants performed two 240 min lunch meal (622 kcal) tests 7 ± 4 days apart. After an overnight fast and a standardized breakfast, 10 g (125 mL) WPM (40 kcal) or placebo (125 mL water, 0 kcal) was consumed 15 min ahead of the mixed-nutrient meal. Effects on PPG (primary endpoint), insulin, GLP-1, and branched-chain amino acids (BCAAs) were evaluated with frequent blood sampling. Changes in incremental areas under the concentration curve (iAUC) were compared using a mixed model. Results: Twenty-six individuals (14 females, mean ± SD age 62.0 ± 8.3 years, HbA1c 58 ± 12 mmol/mol/7.5 ± 1.1%, BMI 29.2 ± 4.8 kg/m2) completed both tests. WPM significantly reduced PPG iAUC0-2h by 22% (p = 0.028), and iAUC0-3h numerically by -18% (p = 0.090) vs. placebo. WPM also increased insulin iAUC0-1h by 61% (p < 0.001), and iAUC0-3h by 30% (p = 0.004), respectively. Total GLP-1 iAUC0-2h was enhanced by 66% (p < 0.001). Postprandial plasma BCAA patterns were characterized by a rapid increase and larger iAUC0-2h (all p < 0.001) after WPM. No adverse events were ascribed to consuming WPM. Conclusions: A 125 mL pre-meal drink containing just 10 g WPM before a mixed meal reduced PPG and increased insulin, GLP-1, and BCAAs. WPM may therefore serve as a metabolic modulator in people with T2D living with overweight or obesity.

This study examined the impact of live bread yeast (Saccharomyces cerevisiae) on the nutritional characteristics of Asian dried noodles. Micronutrient analysis of fermented noodles revealed a 6.9% increase in the overall amino acid content, a 37.1% increase in the vitamin B content and a 63.0% decrease in the phytic acid level. Molecular weight analysis of starch and protein contents revealed moderate decrease in the fermented noodles. The in vitro digestion of fermented noodles showed a slightly faster initial acidification, four-fold decrease in the initial shear viscosity (from 8.85 to 1.94 Pa·s). The initial large food particle count (>2 mm diameter) was 19.5% lower in the fermented noodles. The fermented noodles contained slightly higher free sugar content (73.5 mg g-1 noodle) during the gastric digestion phase. The overall nutrition and digestion results indicate nutritional improvement and digestion-easing attributes in the fermented noodles.

Dietary patterns that lower postprandial glycemia have been effective in preventing type 2 diabetes. Consuming macronutrients in a specific sequence within a meal has been considered as a novel strategy to reduce post-meal glucose spikes. Therefore, this study aimed to investigate the effect of meal sequence on postprandial glucose and insulin response among healthy adults in the United Arab Emirates.

Eighteen healthy adults participated in a cross-over randomized controlled trial. Two isocaloric meals were consumed separately in a different order: a standard mixed meal (SMM) vs vegetables and protein first followed by carbohydrates (VPF) meal. The postprandial glucose and insulin levels were determined at Fasting, 30, 60, and 120 min. Visual Analog Scale (VAS) rating was used to assess hunger at similar frequencies.

The mean glucose and insulin levels significantly reduced (p = 0.001) following VPF meal compared to SMM at 30 min. The incremental area under the curve (iAUC0-120) for glucose following the VPF meal sequence was 40.9% lower (p = 0.03) compared with the SMM (572.83; 95% CI 157.3 to 988.2) vs (968.5; 95% CI 692.4 to 1244.8 mg/dL). Furthermore, the iAUC0-120 for insulin following the VPF meal sequence was 31.7% lower than the SMM meal sequence. (2184; 95% CI 1638.30 to 2729) vs (3196.94; 95% CI 2328.19 to 4065.69) mIU/mL × 120 min, P = 0.023). The feeling of fullness measured by the hunger scale showed that the feeling of fullness was higher after 60 and 120 minutes (p = 0.05, p = 0.04) with the VPF meal sequence compared to the SMM sequence. Although, there is no significant difference in the Area under the curve (AUC) for hunger rating between the two meals.

The VPF meal sequence could significantly reduce postprandial glucose and insulin levels and sustain fullness after a meal. Meal sequencing could be an effective dietary strategy for improving the postprandial glucose and insulin response in healthy adults.

In response to nutrients, intestinal L- and K-cells naturally secrete glucagon-like peptide 1 (GLP-1). GLP-1 regulates postprandial blood glucose by increasing insulin secretion, slowing down gastric emptying and inducing satiety. A selection of specifically developed collagen hydrolysates was screened for their ability to enhance natural GLP-1 production in vitro. The best performing hydrolysate, H80 (Nextida GC), was orally administered at different doses to lean, normoglycemic mice and overweight, prediabetic mice. Lean mice were acutely challenged 45 min before an oral glucose load. While daily supplemented for 6 weeks, prediabetic mice were acutely challenged at day 21 and 34. Oral glucose tolerance, plasma insulin and GLP-1 levels were assessed, and a gastric emptying assay performed in prediabetic mice. H80 significantly lowered the blood glucose response in lean and prediabetic mice, at a 4 g/kg dose (-25% and -36%, respectively), compared to vehicle. In chronically supplemented, prediabetic mice, acute H80 administration slowed down gastric emptying (-60%) after 21 days and increased plasma insulin (+166%) after 35 days of supplementation. H80 increased plasma active GLP-1 in lean (+217%) and prediabetic (+860%) mice. Overall, the data indicate that the specific collagen hydrolysate, H80, has significant GLP-1-mediated effects on oral glucose tolerance in lean and prediabetic mice. Furthermore, effects on postprandial glucose tolerance were evaluated in a small, human, proof of concept study. H80 reduced the postprandial glucose response at a 5 g dose in healthy, normoglycemic and prediabetic participants. Oral supplementation with H80 might thus be a promising strategy to maintain normal glucose tolerance.

Glutinous rice (mochi rice), compared to non-glutinous rice (uruchi rice), exhibits a wide range of glycemic index (GI) values, from low to high. However, the underlying mechanisms behind the variation in GI values remain poorly understood. In this study, we aimed to identify rice cultivars with a low postprandial glycemic response and investigate the mechanisms, focusing on insulin and incretin hormones. We examined seven glutinous rice cultivars and three non-glutinous rice cultivars. We discovered that Anekomochi, a glutinous rice cultivar, has the lowest postprandial glycemic response. Anekomochi significantly enhanced glucagon-like peptide-1 (GLP-1) secretion while suppressing insulin secretion. These effects were completely blunted by inhibiting GLP-1 receptor signaling and denervating the common hepatic branch of vagal afferent nerves that are crucial for sensing intestinal GLP-1. Our findings demonstrate that Anekomochi markedly enhances insulin action via GLP-1 release and vagal afferent neural pathways, thereby leading to a lower postprandial glycemic response.

This review paper explores post-prandial glycemia in type 2 diabetes. Post-prandial glycemia is defined as the period of blood glucose excursion from immediately after the ingestion of food or drink to 4 to 6 hours after the end of the meal. Post-prandial hyperglycemia is an independent risk factor for cardiovascular disease with glucose "excursions" being more strongly associated with markers of oxidative stress than the fasting or pre-prandial glucose level. High blood glucose is a major promoter of enhanced free radical production and is associated with the onset and progression of type 2 diabetes. Oxidative stress impairs insulin action creating a vicious cycle where repeated post-prandial glucose spikes are key drivers in the pathogenesis of the vascular complications of type 2 diabetes, both microvascular and macrovascular. Some authors suggest post-prandial hyperglycemia is the major cause of death in type 2 diabetes. Proper management of post-prandial hyperglycemia could yield up to a 35% cut in overall cardiovascular events, and a 64% cut in myocardial infarction. The benefits of managing post-prandial hyperglycemia are similar in magnitude to those seen in type 2 diabetes patients receiving secondary prevention with statins - prevention which today is regarded as fundamental by all practitioners. Given all the evidence surrounding the impact of post-prandial glycemia on overall outcome, it is imperative that any considered strategy for the management of type 2 diabetes should include optimum dietary, pharma, and lifestyle interventions that address glucose excursion. Achieving a low post-prandial glucose response is key to prevention and progression of type 2 diabetes and cardiometabolic diseases. Further, such therapeutic interventions should be sustainable and must benefit patients in the short and long term with the minimum of intrusion and side effects. This paper reviews the current literature around dietary manipulation of post-prandial hyperglycemia, including novel approaches. A great deal of further work is required to optimize and standardize the dietary management of post-prandial glycemia in type 2 diabetes, including consideration of novel approaches that show great promise.

While clinical studies indicate that dietary protein may benefit glucose homeostasis in type 2 diabetes (T2D), the impact of dietary protein, including whether the protein is of animal or plant origin, on the risk of T2D is uncertain. We conducted a systematic review and meta-analysis to evaluate the associations of total, animal, and plant protein intakes with the risk of T2D.

A systematic search was performed using multiple data sources, including PubMed/Medline, ISI Web of Science, Scopus, and Google Scholar, with the data cut-off in May 2023. Our selection criteria focused on prospective cohort studies that reported risk estimates for the association between protein intake and T2D risk. For data synthesis, we calculated summary relative risks and 95% confidence intervals for the highest versus lowest categories of protein intake using random-effects models. Furthermore, we conducted both linear and non-linear dose-response analyses to assess the dose-response associations between protein intake and T2D risk.

Sixteen prospective cohort studies, involving 615,125 participants and 52,342 T2D cases, were identified, of which eleven studies reported data on intake of both animal and plant protein. Intakes of total (pooled effect size: 1.14, 95% CI: 1.04-1.24) and animal (pooled effect size: 1.18, 95% CI: 1.09-1.27) protein were associated with an increased risk of T2D. These effects were dose-related - each 20-g increase in total or animal protein intake increased the risk of T2D by ∼3% and ∼7%, respectively. In contrast, there was no association between intake of plant protein and T2D risk (pooled effect size: 0.98, 95% CI: 0.89-1.08), while replacing animal with plant protein intake (per each 20 g) was associated with a reduced risk of T2D (pooled effect size: 0.80, 95% CI: 0.76-0.84).

Our findings indicate that long-term consumption of animal, but not plant, protein is associated with a significant and dose-dependent increase in the risk of T2D, with the implication that replacement of animal with plant protein intake may lower the risk of T2D.

To evaluate gastric emptying (GE) and the glycaemic response to a 75-g oral glucose load in newly diagnosed, treatment-naïve Han Chinese with type 2 diabetes (T2D) before insulin pump therapy, after 4 weeks of insulin pump therapy, and 12-15 months after insulin pump therapy.

Twenty participants with T2D (baseline glycated haemoglobin [± SD] 10.7% [± 1.2%] 93 [± 10] mmol/mol) ingested a 75-g glucose drink containing 150 mg 13C-acetate, to determine the gastric half-emptying time, and underwent assessment of plasma glucose and serum insulin, C-peptide and glucagon-like peptide-1 (GLP-1) over 180 min before and after 4 weeks of insulin pump therapy (discontinued for 48 h before re-assessment). Data were compared to those in 19 healthy participants matched for sex and age. After 12-15 months, GE was re-measured in 14 of the T2D participants.

At baseline, participants with T2D exhibited substantially augmented fasting and post-glucose glycaemia, diminished insulin secretion, and more rapid GE (p < 0.05 each), but comparable GLP-1, compared to healthy participants. Following insulin pump therapy, insulin secretion increased, GLP-1 secretion was attenuated, fasting and post-glucose glycaemia were lower, and GE was slowed (p < 0.05 each). The slowing of GE in T2D participants was sustained over 12-15 months of follow-up.

In newly diagnosed Han Chinese with T2D, GE is often accelerated despite poor glycaemic control and is slowed by short-term insulin pump therapy. The effect on GE is maintained for at least 12 months.

It is well established that high-protein diets (i.e. ~25-30% of energy intake from protein) provide benefits for achieving weight loss, and subsequent weight maintenance, in individuals with obesity, and improve glycemic control in type 2 diabetes (T2D). These effects may be attributable to the superior satiating property of protein, at least in part, through stimulation of both gastrointestinal (GI) mechanisms by protein, involving GI hormone release and slowing of gastric emptying, as well as post-absorptive mechanisms facilitated by circulating amino acids. In contrast, there is evidence that the beneficial effects of greater protein intake on body weight and glycemia may only be sustained for 6-12 months. While both suboptimal dietary compliance and metabolic adaptation, as well as substantial limitations in the design of longer-term studies are all likely to contribute to this contradiction, the source of dietary protein (i.e. animal vs. plant) has received inappropriately little attention. This issue has been highlighted by outcomes of recent epidemiological studies indicating that long-term consumption of animal-based protein may have adverse effects in relation to the development of obesity and T2D, while plant-based protein showed either protective or neutral effects. This review examines information relating to the effects of dietary protein on appetite, energy intake and postprandial glycemia, and the relevant GI functions, as reported in acute, intermediate- and long-term studies in humans. We also evaluate knowledge relating to the relevance of the dietary protein source, specifically animal or plant, to the prevention, and management, of obesity and T2D.

Gestational diabetes mellitus (GDM) represents one of the most common medical complications of pregnancy and is important to the well-being of both mothers and offspring in the short and long term. Lifestyle intervention remains the mainstay for the management of GDM. The efficacy of nutritional approaches (e.g. calorie restriction and small frequent meals) to improving the maternal-neonatal outcomes of GDM was attested to by Chinese population data, discussed in two articles in recent issues of this journal. However, a specific focus on the relevance of postprandial glycaemic control was lacking. Postprandial rather than fasting hyperglycaemia often represents the predominant manifestation of disordered glucose homeostasis in Chinese women with GDM. There is now increasing appreciation that the rate of gastric emptying, which controls the delivery of nutrients for digestion and absorption in the small intestine, is a key determinant of postprandial glycaemia in both health, type 1 and 2 diabetes. It remains to be established whether gastric emptying is abnormally rapid in GDM, particularly among Chinese women, thus contributing to a predisposition to postprandial hyperglycaemia, and if so, how this influences the therapeutic response to nutritional interventions. It is essential that we understand the role of gastric emptying in the regulation of postprandial glycaemia during pregnancy and the potential for its modulation by nutritional strategies in order to improve post-prandial glycaemic control in GDM.

Metformin lowers postprandial glycaemic excursions in individuals with type 2 diabetes by modulating gastrointestinal function, including the stimulation of glucagon-like peptide-1 (GLP-1). The impact of varying the timing of metformin administration on postprandial glucose metabolism is poorly defined. We evaluated the effects of metformin, administered at different intervals before an intraduodenal glucose infusion, on the subsequent glycaemic, insulinaemic and GLP-1 responses in metformin-treated type 2 diabetes.

Sixteen participants with type 2 diabetes that was relatively well-controlled by metformin monotherapy were studied on four separate days in a crossover design. On each day, participants were randomised to receive a bolus infusion of metformin (1000 mg in 50 ml 0.9% saline) via a nasoduodenal catheter at t = -60, -30 or 0 min (and saline at the other timepoints) or saline at all timepoints (control), followed by an intraduodenal glucose infusion of 12.56 kJ/min (3 kcal/min) at t = 0-60 min. The treatments were blinded to both participants and investigators involved in the study procedures. Plasma glucose, insulin and total GLP-1 levels were measured every 30 min between t = -60 min and t = 120 min.

There was a treatment-by-time interaction for metformin in reducing plasma glucose levels and increasing plasma GLP-1 and insulin levels (p<0.05 for each). The reduction in plasma glucose levels was greater when metformin was administered at t = -60 or -30 min vs t = 0 min (p<0.05 for each), and the increases in plasma GLP-1 levels were evident only when metformin was administered at t = -60 or -30 min (p<0.05 for each). Although metformin did not influence insulin sensitivity, it enhanced glucose-induced insulin secretion (p<0.05), and the increases in plasma insulin levels were comparable on the 3 days when metformin was given.

In well-controlled metformin-treated type 2 diabetes, glucose-lowering by metformin is greater when it is given before, rather than with, enteral glucose, and this is associated with a greater GLP-1 response. These observations suggest that administration of metformin before meals may optimise its effect in improving postprandial glycaemic control.

www.anzctr.org.au ACTRN12621000878875 FUNDING: The study was not funded by a specific research grant.

The aim of the present study was to conduct a randomised, placebo-controlled, double-blind, crossover trial to determine whether pre-meal ketone monoester ingestion reduces postprandial glucose concentrations in individuals with type 2 diabetes.

In this double-blind, placebo-controlled, crossover design study, ten participants with type 2 diabetes (age 59±1.7 years, 50% female, BMI 32±1 kg/m2, HbA1c 54±2 mmol/mol [7.1±0.2%]) were randomised using computer-generated random numbers. The study took place at the Nutritional Physiology Research Unit, University of Exeter, Exeter, UK. Using a dual-glucose tracer approach, we assessed glucose kinetics after the ingestion of a 0.5 g/kg body mass ketone monoester (KME) or a taste-matched non-caloric placebo before a mixed-meal tolerance test. The primary outcome measure was endogenous glucose production. Secondary outcome measures were total glucose appearance rate and exogenous glucose appearance rate, glucose disappearance rate, blood glucose, serum insulin, β-OHB and NEFA levels, and energy expenditure.

Data for all ten participants were analysed. KME ingestion increased mean ± SEM plasma beta-hydroxybutyrate from 0.3±0.03 mmol/l to a peak of 4.3±1.2 mmol/l while reducing 2 h postprandial glucose concentrations by ~18% and 4 h postprandial glucose concentrations by ~12%, predominately as a result of a 28% decrease in the 2 h rate of glucose appearance following meal ingestion (all p<0.05). The reduction in blood glucose concentrations was associated with suppressed plasma NEFA concentrations after KME ingestion, with no difference in plasma insulin concentrations between the control and KME conditions. Postprandial endogenous glucose production was unaffected by KME ingestion (mean ± SEM 0.76±0.15 and 0.88±0.10 mg kg-1 min-1 for the control and KME, respectively). No adverse effects of KME ingestion were observed.

KME ingestion appears to delay glucose absorption in adults with type 2 diabetes, thereby reducing postprandial glucose concentrations. Future work to explore the therapeutic potential of KME supplementation in type 2 diabetes is warranted.

ClinicalTrials.gov NCT05518448.

This project was supported by a Canadian Institutes of Health Research (CIHR) Project Grant (PJT-169116) and a Natural Sciences and Engineering Research Council (NSERC) Discovery Grant (RGPIN-2019-05204) awarded to JPL and an Exeter-UBCO Sports Health Science Fund Project Grant awarded to FBS and JPL.

Metabolic syndrome (MS) is defined by the outcome of interconnected metabolic factors that directly increase the prevalence of obesity and other metabolic diseases. Currently, obesity is considered one of the most relevant topics of discussion because an epidemic heave of the incidence of obesity in both developing and underdeveloped countries has been reached. According to the World Obesity Atlas 2023 report, 38% of the world population are presently either obese or overweight. One of the causes of obesity is an imbalance of energy intake and energy expenditure, where nutritional imbalance due to consumption of high-calorie fast foods play a pivotal role. The dynamic interactions among different risk factors of obesity are highly complex; however, the underpinnings of hyperglycemia and dyslipidemia for obesity incidence are recognized. Fast foods, primarily composed of soluble carbohydrates, non-nutritive artificial sweeteners, saturated fats, and complexes of macronutrients (protein-carbohydrate, starch-lipid, starch-lipid-protein) provide high metabolic calories. Several experimental studies have pointed out that dairy proteins and peptides may modulate the activities of risk factors of obesity. To justify the results precisely, peptides from dairy milk proteins were synthesized under in vitro conditions and their contributions to biomarkers of obesity were assessed. Comprehensive information about the impact of proteins and peptides from dairy milks on fast food-induced obesity is presented in this narrative review article.

Gastric emptying (GE), with wide inter-individual but lesser intra-individual variations, is a major determinant of postprandial glycaemia in health and type 2 diabetes (T2D). However, it is uncertain whether GE of a carbohydrate-containing liquid meal is predictive of the glycaemic response to physiological meals, and whether antecedent hyperglycaemia influences GE in T2D. We evaluated the relationships of (i) the glycaemic response to both a glucose drink and mixed meals with GE of a 75 g glucose drink, and (ii) GE of a glucose drink with antecedent glycaemic control, in T2D.

Fifty-five treatment-naive Chinese adults with newly diagnosed T2D consumed standardised meals at breakfast, lunch and dinner with continuous interstitial glucose monitoring. On the subsequent day, a 75 g glucose drink containing 150 mg 13C-acetate was ingested to assess GE (breath test) and plasma glucose response. Serum fructosamine and HbA1c were also measured.

Plasma glucose incremental area under the curve (iAUC) within 2 hours after oral glucose was related inversely to the gastric half-emptying time (T50) (r = -0.34, P = 0.012). The iAUCs for interstitial glucose within 2 hours after breakfast (r = -0.34, P = 0.012) and dinner (r = -0.28, P = 0.040) were also related inversely to the T50 of oral glucose. The latter, however, was unrelated to antecedent fasting plasma glucose, 24-hour mean interstitial glucose, serum fructosamine, or HbA1c.

In newly diagnosed, treatment-naive, Chinese with T2D, GE of a 75 g glucose drink predicts the glycaemic response to both a glucose drink and mixed meals, but is not influenced by spontaneous short-, medium- or longer-term elevation in glycaemia.

Although thorough chewing lowers postprandial glucose concentrations, research on the effectiveness of chewing vegetables in different forms on postprandial glucose metabolism remains limited. This study examined the effects of vegetables consumed in solid versus puree forms on postprandial glucose metabolism. Nineteen healthy young men completed two 180-min trials on separate days in a random order: the chewing trial involved the consumption of shredded cabbage with chewing and the non-chewing trial involved the consumption of pureed cabbage without chewing. Energy jelly was consumed immediately after the consumption of shredded or puree cabbage. Blood samples were collected at 0, 30, 45, 60, 90, 120 and 180 min. Circulating concentrations of glucose, insulin, total glucagon-like peptide-1 (GLP-1) and glucose-dependent insulinotropic peptide (GIP) concentrations were measured from the plasma. Although plasma glucose concentrations did not differ between the trials, the plasma insulin and GIP incremental area under the curve values were higher in the chewing than in the non-chewing trial. Postprandial total GLP-1 concentrations were higher in the chewing than in the non-chewing trial at 45, 60 and 90 min. This study demonstrates that consuming shredded cabbage while chewing enhances postprandial incretin secretion but has no effect on postprandial glucose concentration.Trial registration: Clinical trial registration ID.: UMIN000052662, registered 31 October 2023.

The aim of the study was to explore the impact of both the macronutrient composition and snacking timing on the postprandial glycemic insulinemic responses and food intake. Seventeen healthy female volunteers completed the randomized crossover trials. The volunteers were provided a standard breakfast and lunch at 8:00 and 13:00, respectively, and an ad libitum dinner at 18:00. Provided at either 10:30 (midmorning) or 12:30 (preload), the glycemic effects of the three types of 70 kcal snacks, including chicken breast (mid-C and pre-C), apple (mid-A and pre-A), and macadamia nut (mid-M and pre-M), were compared with the non-snack control (CON), evaluated by continuous glucose monitoring (CGM). The mid-M showed increased insulin resistance after lunch compared with CON, while the pre-M did not. The pre-A stabilized the glycemic response in terms of all variability parameters after lunch, while the mid-A had no significant effect on postprandial glucose control. Both the mid-C and pre-C improved the total area under the glucose curve, all glycemic variability parameters, and the insulin resistance within 2 h after lunch compared with CON. The pre-C attained the lowest energy intake at dinner, while the mid-A and the mid-M resulted in the highest. In conclusion, the chicken breast snack effectively stabilized postprandial glycemic excursion and reduced insulin resistance while the macadamia snack did not, regardless of ingestion time. Only as a preload could the apple snack mitigate the glucose response after the subsequent meal.

Postprandial metabolic responses following dairy consumption have mostly been studied using stand-alone dairy products or milk-derived nutrients.

Assessing the impact of ingesting dairy products as part of a common breakfast on postprandial aminoacidemia, glycemic control, markers of bone metabolism, and satiety.

In this randomized, crossover study, 20 healthy young males and females consumed on 3 separate occasions an iso-energetic breakfast containing no dairy (NO-D), 1 dairy (ONE-D), or 2 dairy (TWO-D) products. Postprandial concentrations of amino acids, glucose, insulin, glucagon-like peptide-1 (GLP-1), calcium, parathyroid hormone (PTH), and markers of bone formation (P1NP) and resorption (CTX-I) were measured before and up to 300 min after initiating the breakfast, along with VAS-scales to assess satiety.

Plasma essential and branched-chained amino acids availability (expressed as total area under the curve (tAUC)) increased in a dose-dependent manner (P<0.05 for all comparisons). Plasma glucose tAUCs were lower in ONE-D and TWO-D compared with NO-D (P<0.05 for both comparisons). Plasma GLP-1 tAUC increased in a dose-dependent manner (P<0.05 for all comparisons), whereas no differences were observed in plasma insulin tAUC between conditions (P>0.05 for all comparisons). Serum calcium tAUCs were higher in ONE-D and TWO-D compared with NO-D (P<0.05 for both comparisons), along with lower PTH tAUCs in ONE-D and TWO-D compared with NO-D (P=0.001 for both comparisons). In accordance, serum CTX-I concentrations were lower in the late postprandial period in ONE-D and TWO-D compared with NO-D (P<0.01 for both comparisons). No differences were observed in P1NP tAUCs between conditions (P>0.05). The tAUC for satiety was higher in TWO-D compared with NO-D and ONE-D (P<0.05 for both comparisons).

Iso-energetic replacement of a carbohydrate-rich breakfast component with one serving of dairy improves postprandial amino acid availability, glycemic control, and bone metabolism. Adding a second serving of dairy in lieu of carbohydrates augments postprandial amino acid and GLP-1 concentrations while further promoting satiety. This study was registered at https://doi.org/10.1186/ISRCTN13531586 with Clinical Trial Registry number ISRCTN13531586.

Nutrition is one of the most influential environmental factors in both taxonomical shifts in gut microbiota as well as in the development of type 2 diabetes mellitus (T2DM). Emerging evidence has shown that the effects of nutrition on both these parameters is not mutually exclusive and that changes in gut microbiota and related metabolites such as short-chain fatty acids (SCFAs) and branched-chain amino acids (BCAAs) may influence systemic inflammation and signaling pathways that contribute to pathophysiological processes associated with T2DM. With this background, our review highlights the effects of macronutrients, carbohydrates, proteins, and lipids, as well as micronutrients, vitamins, and minerals, on T2DM, specifically through their alterations in gut microbiota and the metabolites they produce. Additionally, we describe the influences of common food groups, which incorporate varying combinations of these macronutrients and micronutrients, on both microbiota and metabolic parameters in the context of diabetes mellitus. Overall, nutrition is one of the first line modifiable therapies in the management of T2DM and a better understanding of the mechanisms by which gut microbiota influence its pathophysiology provides opportunities for optimizing dietary interventions.

We explored the association between macronutrient intake and postprandial glucose variability in a large sample of youth living with T1D and consuming free-living meals. In the Type 1 Diabetes Exercise Initiative Pediatric (T1DEXIP) Study, youth took photographs before and after their meals on 3 days during a 10 day observation period. We used the remote food photograph method to obtain the macronutrient content of youth's meals. We also collected physical activity, continuous glucose monitoring, and insulin use data. We measured glycemic variability using standard deviation (SD) and coefficient of variation (CV) of glucose for up to 3 h after meals. Our sample included 208 youth with T1D (mean age: 14 ± 2 years, mean HbA1c: 54 ± 14.2 mmol/mol [7.1 ± 1.3%]; 40% female). We observed greater postprandial glycemic variability (SD and CV) following meals with more carbohydrates. In contrast, we observed less postprandial variability following meals with more fat (SD and CV) and protein (SD only) after adjusting for carbohydrates. Insulin modality, exercise after meals, and exercise intensity did not influence associations between macronutrients and postprandial glycemic variability. To reduce postprandial glycemic variability in youth with T1D, clinicians should encourage diversified macronutrient meal content, with a goal to approximate dietary guidelines for suggested carbohydrate intake.

Insulin resistance is an important feature of metabolic syndrome and a precursor of type 2 diabetes mellitus (T2DM). Overnutrition-induced obesity is a major risk factor for the development of insulin resistance and T2DM. The intake of macronutrients plays a key role in maintaining energy balance. The components of macronutrients distinctly regulate insulin sensitivity and glucose homeostasis. Precisely adjusting the beneficial food compound intake is important for the prevention of insulin resistance and T2DM. Here, we reviewed the effects of different components of macronutrients on insulin sensitivity and their underlying mechanisms, including fructose, dietary fiber, saturated and unsaturated fatty acids, and amino acids. Understanding the diet-gene interaction will help us to better uncover the molecular mechanisms of T2DM and promote the application of precision nutrition in practice by integrating multi-omics analysis.

Aberrations in glucose, insulin, and other postprandial (PP) markers are common in obesity and cardiometabolic disorders. One potentially simple lifestyle/dietary modification to manage these issues is to change the order in which foods are consumed within meals. Carbohydrate exerts the largest effect on PP glucose, and there is some evidence that ingesting dietary fat or protein before carbohydrate delays gastric emptying of carbohydrate and reduces PP glucose. Additionally, certain dietary proteins may augment insulin release if ingested with carbohydrate, thereby improving blood glucose clearance. This review aimed to systematically evaluate evidence from acute experiments that modified the order in which foods were consumed in isocaloric meals.

Outcomes of interest were PP glucose and insulin (including area under the curve for both), C-peptide, gut hormones, and perceptual responses. Three databases were searched (PubMed, Cochrane CENTRAL, Web of Science) in February 2022. Additionally, reference lists of identified reports were searched, and an author of several studies was consulted to verify that relevant literature was included. The review included acute interventions that administered isocaloric meals of the same foods but with foods eaten in different orders. Studies were not excluded based on participant characteristics.

Eleven reports were identified. All reports that assessed glucose and insulin showed a tendency toward lower levels, at least over parts of the PP period, by consuming carbohydrates last. GLP-1 tended to be higher in carbohydrate-last conditions, though this was only measured in a few studies. Perceptual responses (hunger, fullness, etc.) were not consistently different between conditions in two studies, but the certainty of evidence was very low.

Findings indicate that, at least acutely, there may be benefits to eating carbohydrate after vegetable and/or protein-rich foods. The most consistent effect (judged as moderate certainty) is that carbohydrate-last meal orders tend to lower blood glucose and insulin excursions.

It is suggested that supplementation with milk protein (MP) has the potential to ameliorate the glycemic profile; however, the exact impact and certainty of the findings have yet to be evaluated. This systematic review and dose-response meta-analysis of randomized controlled trials (RCTs) assessed the impact of MP supplementation on the glycemic parameters in adults.

A systematic search was carried out among online databases to determine eligible RCTs published up to November 2022. A random-effects model was performed for the meta-analysis.

A total of 36 RCTs with 1851 participants were included in the pooled analysis. It was displayed that supplementation with MP effectively reduced levels of fasting blood glucose (FBG) (weighted mean difference (WMD): -1.83 mg/dL, 95% CI: -3.28, -0.38; P = 0.013), fasting insulin (WMD: -1.06 uU/mL, 95% CI: -1.76, -0.36; P = 0.003), and homeostasis model assessment of insulin resistance (HOMA-IR) (WMD: -0.27, 95% CI: -0.40, -0.14; P < 0.001) while making no remarkable changes in serum hemoglobin A1c (HbA1c) values (WMD: 0.01%, 95% CI: -0.14, 0.16; P = 0.891). However, there was a significant decline in serum levels of HbA1c among participants with normal baseline body mass index (BMI) based on sub-group analyses. In addition, HOMA-IR values were significantly lower in the MP supplement-treated group than their untreated counterparts in short- and long-term supplementation (≤ 8 and > 8 weeks) with high or moderate doses (≥ 60 or 30-60 g/d) of MP or whey protein (WP). Serum FBG levels were considerably reduced upon short-term administration of a low daily dose of WP (< 30 g). Furthermore, the levels of serum fasting insulin were remarkably decreased during long-term supplementation with high or moderate daily doses of WP.

The findings of this study suggest that supplementation with MP may improve glycemic control in adults by reducing the values of fasting insulin, FBG, and HOMA-IR. Additional trials with longer durations are required to confirm these findings.

Changes in blood glucose concentrations are underpinned by blood glucose kinetics (endogenous and exogenous glucose appearance rates and glucose disappearance rates). Exercise potently alters blood glucose kinetics and can thereby be used as a tool to control blood glucose concentration. However, most studies of exercise-induced changes in glucose kinetics are conducted in a fasted state, and therefore less is known about the effects of exercise on glucose kinetics when exercise is conducted in a postprandial state. Emerging evidence suggests that food intake prior to exercise can increase postprandial blood glucose flux compared with when meals are consumed after exercise, whereby both glucose appearance rates and disappearance rates are increased. The mechanisms underlying the mediating effect of exercise conducted in the fed versus the fasted state are yet to be fully elucidated. Current evidence demonstrates that exercise in the postprandial state increased glucose appearance rates due to both increased exogenous and endogenous appearance and may be due to changes in splanchnic blood flow, intestinal permeability, and/or hepatic glucose extraction. On the other hand, increased glucose disappearance rates after exercise in the fed state have been shown to be associated with increased intramuscular AMPK signaling via a mismatch between carbohydrate utilization and delivery. Due to differences in blood glucose kinetics and other physiological differences, studies conducted in the fasted state cannot be immediately translated to the fed state. Therefore, conducting studies in the fed state could improve the external validity of data pertaining to glucose kinetics and intramuscular signaling in response to nutrition and exercise.

Maintenance of plasma glucose (PG) homeostasis is due to a complex network system. Even a minor fall in PG activates multiple neuroendocrine actions promoting hormonal, metabolic and behavioral responses, which prevent and ultimately recover hypoglycemia, primarily neuroglycopenia. Among these responses, gastric emptying (GE) plays an important role by coordinated mechanisms which regulate transit and absorption of nutrients through the small intestine. A bidirectional relationship between GE and glycemia has been established: GE may explain the up to 30-40 % variance in glycemic response following a carbohydrate-rich meal. In addition, acute and chronic hyperglycemia induce deceleration of GE after meals. Hypoglycemia accelerates GE, but its role in counterregulation has been poorly investigated. The role of GE as a counterregulatory mechanism has been confirmed in pathophysiological conditions, such as gastroparesis or following recurrent hypoglycemia. Therefore, it could represent an "ancestral" mechanism, highly conservative and effective in all individuals, conditions and clinical contexts. Recent guidelines recommend GLP-1 receptor agonists (GLP-1RAs) either as the first injectable therapy for type 2 diabetes mellitus or in combination with insulin. Considering the potential impact on GE, it would be important to study subjects on GLP-1 RAs during hypoglycemia, to establish whether a possible deceleration of GE impairs glucose counterregulation.

Premenopausal women are at a lower risk of type 2 diabetes (T2D) compared to men, but the underlying mechanism(s) remain elusive. The secretion of the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), from the small intestine is a major determinant of glucose homeostasis and may be influenced by sex.

This study compared blood glucose and plasma insulin and incretin responses to intraduodenal glucose infusions in healthy young males and females.

In Study 1, 9 women and 20 men received an intraduodenal glucose infusion at 2 kcal/min for 60 minutes. In Study 2, 10 women and 26 men received an intraduodenal glucose at 3 kcal/min for 60 minutes. Venous blood was sampled every 15 minutes for measurements of blood glucose and plasma insulin, GLP-1 and GIP.

In response to intraduodenal glucose at 2 kcal/min, the incremental area under the curve between t = 0-60 minutes (iAUC0-60min) for blood glucose and plasma GIP did not differ between the 2 groups. However, iAUC0-60min for plasma GLP-1 (P = 0.016) and insulin (P = 0.011) were ∼2-fold higher in women than men. In response to intraduodenal glucose at 3 kcal/min, iAUC0-60min for blood glucose, plasma GIP, and insulin did not differ between women and men, but GLP-1 iAUC0-60min was 2.5-fold higher in women (P = 0.012).

Healthy young women exhibit comparable GIP but a markedly greater GLP-1 response to intraduodenal glucose than men. This disparity warrants further investigations to delineate the underlying mechanisms and may be of relevance to the reduced risk of diabetes in premenopausal women when compared to men.

Serving whey protein before a meal in order to lower postprandial blood glucose concentrations is known as a premeal. The underlying mechanisms are only partly understood but may involve stimulation of glucagon-like peptide-1 (GLP-1), glucose-dependent insulinotropic polypeptide (GIP), and insulin secretion together with a slower gastric emptying rate.

The objective of this systematic review and meta-analysis was to review all randomized clinical trials investigating premeals with whey protein in comparison with a nonactive comparator (control) that evaluated plasma glucose, GLP-1, GIP, insulin, and/or gastric emptying rate. Secondary aims included subgroup analyses on the timing and dose of the premeal together with the metabolic state of the participants [lean, obese, and type 2 diabetes mellitus (T2DM)].

We searched EMBASE, CENTRAL, PUBMED, and clinicaltrials.gov and found 16 randomized crossover trials with a total of 244 individuals. The last search was performed on 9 August, 2022.

Whey protein premeals lowered peak glucose concentration by -1.4 mmol/L [-1.9 mmol/L; -0.9 mmol/L], and the area under the curve for glucose was -0.9 standard deviation (SD) [-1.2 SD; -0.6 SD] compared with controls (high certainty). In association with these findings, whey protein premeals elevated GLP-1 (low certainty) and peak insulin (high certainty) concentrations and slowed gastric emptying rate (high certainty) compared with controls. Subgroup analyses showed a more pronounced and prolonged glucose-lowering effect in individuals with T2DM compared with participants without T2DM. The available evidence did not elucidate the role of GIP. The protein dose used varied between 4 and 55 g, and meta-regression analysis showed that the protein dose correlated with the glucose-lowering effects.

In conclusion, whey protein premeals lower postprandial blood glucose, reduce gastric emptying rate, and increase peak insulin. In addition, whey protein premeals may elevate plasma concentrations of GLP-1. Whey protein premeals may possess clinical potential, but the long-term effects await future clinical trials.

Background and Objectives: Type 2 diabetes mellitus (T2DM) is a chronic metabolic disease affecting an estimated 537 million individuals worldwide. 'Superfoods' can be integrated into the diet of T2DM patients due to their health benefits. Study Objectives: (i) To carry out a narrative review of 'superfoods' with the potential to reduce glycaemic levels in T2DM patients (2019 to 2022), (ii) to identify 'superfoods' with the potential to reduce HbA1c and (iii) to propose new guidance on the use of 'superfoods'. Materials and Methods: A narrative review was carried out using the databases PubMed, SciELO, DOAJ and Google Scholar. The keywords were ["type 2 diabetes" and ("food" or "diet" or "nutrition") and ("glycaemia" or "glycemia")]. Only review studies were included. Results: Thirty reviews were selected. The 'superfoods' identified as having a potential impact on glycaemic control were foods with polyphenols (e.g., berries), fermented dairy products, whole cereals/grains, nuts and proteins, among others. The possibility of an extensive reduction in Hb1Ac was reported for fermented dairy products, especially yoghurts enriched with vitamin D or probiotics (HbA1c reduction of around 1%) or by increasing the fibre intake by 15 g (or up to 35 g) (HbA1c reduction of around 2%). Conclusion: It is recommended that the identified 'superfoods' are included in the diet of T2DM patients, although this should not substitute an appropriate diet and exercise plan. In particular, yoghurts and an increased fibre intake (by 15 g or up to 35 g) can be used as nutraceuticals. New recommendations on the introduction of 'superfoods' in the diet of T2DM patients have been proposed.