• Computed tomography
• Extracellular space
• Pancreas
• Three-dimensional image
• Visceral fat

• Adolescence
• Nonalcoholic fatty pancreas disease
• Pancreatic steatosis

• Diagnosis
• metabolic syndrome
• nonalcoholic fatty pancreatic disease
• obesity
• pancreatic steatosis
• pathophysiology

• Fatty acid binding protein-1 (FABP1)
• Fatty liver
• Non-alcoholic fatty pancreas (NAFPD)

• Humans
• Male
• Female
• Adult
• Cross-Sectional Studies
• Egypt/epidemiology
• Fatty Acid-Binding Proteins/blood
• Biomarkers/blood
• Prospective Studies
• Middle Aged
• Obesity/blood
• Obesity/complications
• Pancreatic Diseases/blood
• Prevalence
• Ultrasonography

• Doppler ultrasonography
• Fetal pancreas
• Gestational diabetes
• Splenic artery

• Humans
• Female
• Pregnancy
• Diabetes, Gestational/diagnostic imaging
• Diabetes, Gestational/physiopathology
• Splenic Artery/diagnostic imaging
• Splenic Artery/physiopathology
• Case-Control Studies
• Prospective Studies
• Adult
• Pancreas/diagnostic imaging
• Pancreas/blood supply
• Ultrasonography, Prenatal/methods
• Ultrasonography, Doppler
• Blood Flow Velocity

• kidney transplantation
• non-alcoholic fatty liver
• pancreatic steatosis
• post-transplant diabetes mellitus

• Humans
• Non-alcoholic Fatty Liver Disease/etiology
• Kidney Transplantation/adverse effects
• Retrospective Studies
• Risk Factors
• Diabetes Mellitus/etiology
• Fibrosis

• Magnetic resonance imaging
• Pancreas
• Thalassemia

• Female
• Humans
• Adult
• Iron/metabolism
• beta-Thalassemia/complications
• beta-Thalassemia/diagnostic imaging
• Contrast Media/metabolism
• Liver/pathology
• Gadolinium
• Iron Overload/complications
• Iron Overload/diagnostic imaging
• Magnetic Resonance Imaging/methods
• Myocardium/pathology
• Cardiomyopathies/complications
• Glucose/metabolism
• Heart Diseases/complications
• Fibrosis
• Pancreatic Diseases/complications

• The E-MIOT project receives “no-profit support” from industrial sponsorships (Chiesi Farmaceutici S.p.A. and Bayer). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
• Università degli Studi di Padova

• fatty infiltration of the pancreas
• metabolic syndrome
• obesity
• pancreatic duct adenocarcinoma
• type 2 diabetes mellitus

• pancreatic diseases
• lipomatosis
• pancreatoduodenectomy
• pancreatopatias
• lipomatose
• duodenopancreatectomia

• Male
• Humans
• Young Adult
• Adult
• Pancreaticoduodenectomy
• Pancreas
• Abdominal Pain
• Adipose Tissue
• Pancreaticojejunostomy

Type 2 diabetes (T2D) is a multifactorial metabolic disorder affecting more than 450 million people across the globe. With the increasing prevalence of T2D and obesity, the role of fat accumulation at sites other than subcutaneous adipose tissue has received significant attention in the pathophysiology of T2D. Over the past decade and a half, a pressing concern has emerged on investigating the association of pancreatic fat accumulation or pancreatic steatosis with the development of disease. While a few reports have suggested a possible association between pancreatic fat and T2D and/or impaired glucose metabolism, a few reports suggest a lack of such association. Pancreatic fat has also been linked with genetic risk of developing T2D, prediabetes, reduced insulin secretion, and beta cell dysfunction albeit some confounding factors such as age and ethnicity may affect the outcome. With the technological advancements in clinical imaging and progress in assessment of pancreatic beta cell function, our understanding of the role of pancreatic fat in causing insulin resistance and development of various etiologies of T2D has significantly improved. This review summarizes various findings on the possible association of pancreatic fat accumulation with the pathophysiology of T2D.

• Type 2 diabetes
• Pancreatic fat
• Steatosis
• Glucose metabolism
• Beta cell function
• Non-alcoholic fatty pancreas disease
• Obesity
• Insulin resistance

• HOMA
• QUICKI
• endothelial dysfunction
• endothelial microparticles
• pancreas fat content

Nonalcoholic fatty liver disease (NAFLD) is common among patients with type 2 diabetes mellitus (T2DM) and is associated with increased risk for coronary atherosclerosis and acute cardiovascular (CV) events. We employed the validated, non-invasive Angulo NAFLD fibrosis score (FS) in an intervention study in patients with T2DM and recent acute coronary syndrome (ACS) to determine the association of FS with CV risk and treatment response to apabetalone. Apabetalone is a novel selective inhibitor of the second bromodomain of bromodomain and extra-terminal (BET) proteins, epigenetic regulators of gene expression.

The Phase 3 BETonMACE trial compared apabetalone with placebo in 2,425 patients with T2DM and recent ACS. In this post hoc analysis, we evaluated the impact of apabetalone therapy on CV risk, defined as a composite of major adverse cardiovascular events (MACE: CV death, non-fatal myocardial infarction [MI], or stroke) and hospitalization for heart failure (HHF) in two patient categories of FS that reflect the likelihood of underlying NAFLD. Patients were initially classified into three mutually exclusive categories according to a baseline Angulo FS <-1.455 (F0-F2), -1.455 to 0.675 (indeterminant), and >0.675 (F3-F4), where F0 through F4 connote fibrosis severity none, mild, moderate, severe, and cirrhosis, respectively. The composite of ischemic MACE and HHF in the placebo group was higher in indeterminant and F3-F4 categories compared to the F0-F2 category (17.2% vs 15.0% vs 9.7%). Therefore, for the present analysis, the former two categories were combined into an elevated NAFLD CVD risk group (FS+) that was compared with the F0-F2 group (lower NAFLD risk, FS_0-2).

In 73.7% of patients, FS was elevated and consistent with a moderate-to-high likelihood of advanced liver fibrosis (FS+); 26.3% of patients had a lower FS (FS_0-2). In the placebo group, FS+ patients had a higher incidence of ischemic MACE and HHF (15.4%) than FS_0-2 patients (9.7%). In FS+ patients, addition of apabetalone to standard of care treatment lowered the rate of ischemic MACE compared with placebo (HR = 0.79; 95% CI 0.60-1.05; p=0.10), HHF (HR = 0.53; 95% CI 0.33-0.86; p=0.01), and the composite of ischemic MACE and HHF (HR = 0.76; 95% CI 0.59-0.98; p=0.03). In contrast, there was no apparent benefit of apabetalone in FS_0-2 patients (HR 1.24; 95% CI 0.75-2.07; p=0.40; HR 1.12; 95% CI 0.30-4.14; p=0.87; and HR 1.13; 95% CI 0.69-1.86; p=0.62, respectively). Over a median duration of 26.5 months, FS increased from baseline in both treatment groups, but the increase was smaller in patients assigned to apabetalone than to placebo (p=0.04).

Amongst patients with T2DM, recent ACS, and a moderate-to-high likelihood of advanced liver fibrosis, apabetalone was associated with a significantly lower rate of ischemic MACE and HHF and attenuated the increase in hepatic FS over time.

Suitable animal models are essential for translational research, especially in the case of complex, multifactorial conditions, such as obesity. The non-inbred mouse (Mus musculus) line Titan, also known as DU6, is one of the world’s longest selection experiments for high body mass and was previously described as a model for metabolic healthy (benign) obesity. The present study further characterizes the geno- and phenotypes of this non-inbred mouse line and tests its suitability as an interventional obesity model. In contrast to previous findings, our data suggest that Titan mice are metabolically unhealthy obese and short-lived. Line-specific patterns of genetic invariability are in accordance with observed phenotypic traits. Titan mice also show modifications in the liver transcriptome, proteome, and epigenome linked to metabolic (dys)regulations. Importantly, dietary intervention partially reversed the metabolic phenotype in Titan mice and significantly extended their life expectancy. Therefore, the Titan mouse line is a valuable resource for translational and interventional obesity research.

This study further characterizes the non-inbred Titan (also known as DU6) mouse line, which could be a useful model for obesity research.

In traditional medicine, the maceration of seeds of Garcinia kola (GK) is used to treat various diseases including diabetes. In traditional pharmacopoeia, GK seeds are used to strengthen the immune system and as a stimulant and aphrodisiac.

This study aimed to evaluate the antidiabetic free radical scavenging effects of the hydroalcoholic extract of GK seeds (HAEGS) in a dexamethasone-induced hyperglycemic (DexIH) rat model.

This study was an interventional study.

Here using in vivo model, we assessed some pharmacological properties of HAEGS in DexIH rat. Hypoglycemia, antihyperglycemia, spasmolytic and laxative activities were also evaluated in DexIH. In vitro study assessed antiradical activity. The HAEGS was obtained by decoction introducing 250 g with water–ethanol mixture (30:70). The plant extract was administered to the animals at doses of 50 (GK50) and 100 (GK100) mg/kg body weight. All animal experiments were in accordance with ARRIVE guidelines and were performed in accordance with the scientific procedures of UK Animals. Antiradical activity of GK was assessed in vitro by inhibition of the activity of 2,2-diphenyl-1-picrylhydrazyl.

Statistical analysis was performed using GraphPad Prism 5.03 software, and P values less than 0.05 were considered statistically significant.

At doses 50 and 100 mg/kg, GK significantly (P < 0.001) regulated DexIH after two weeks of treatment compared to the normoglycemic control and hyperglycemic rats. The extract at both doses significantly (P < 0.001) inhibited the spasmolytic activity in both normoglycemic and hyperglycemic rats compared to Imodium^®. In rats DexIH rats, only dose 100 mg/kg significantly (P < 0.05) increased laxative effects when compared to the negative control. In vitro antiradical activity of GK revealed vitamin C-like antiradical activity.

This study justifies the traditional use of GK seeds as an antidiabetic.

• Magnetic resonance imaging
• Pancreas
• Pediatric obesity
• Ultrasonography

This study investigated risk factors for hyperechoic pancreas (HP) on ultrasonography (US) according to HP severity.

Between December 2008 and February 2014, 1,459 subjects who underwent abdominal US as part of health examinations were retrospectively included. Two radiologists assessed and categorized the severity of HP as normal, mild, moderate, and severe. Subjects were allocated to two groups as follows: fatty pancreas 1 (FP1; mild to severe HP) and fatty pancreas 2 (FP2; moderate to severe HP). Clinico-metabolic parameters such as the body mass index and blood test profile of subjects with normoglycemia and prediabetes/diabetes were compared (normal vs. FP1; normal or mild HP vs. FP2). Logistic regression analysis was used to evaluate the associations between HP, nonalcoholic fatty liver disease (NAFLD), and diabetes/prediabetes with adjustment for clinico-metabolic parameters.

Of the 1,459 subjects, 71.2% and 40.4% showed HP and NAFLD on US, respectively. Normoglycemia and prediabetes/diabetes were present in 74.3% and 25.7% of subjects, respectively. Univariable analysis revealed that all the clinico-metabolic parameters were significantly associated with HP (all P<0.05). In the adjusted multivariable analysis, prediabetes/diabetes, NAFLD, age, and body mass index were significantly associated with HP with the FP1 and FP2 criteria. The independent factor with the strongest association with HP was NAFLD using the FP1 criterion (odds ratio [OR], 7.93; P<0.001) and prediabetes/diabetes using the FP2 criterion (OR, 6.96; P<0.001).

NAFLD and prediabetes/diabetes were associated with US-diagnosed HP. Moderate to severe HP was a better predictor of prediabetes/diabetes, suggesting that evaluating HP severity may be useful in clinical practice.

• Diabetes
• Fatty pancreas
• Hyperechoic pancreas
• Nonalcoholic fatty liver disease
• Ultrasonography

• Gastric cancer
• Lymph node dissection
• Pancreatic steatosis
• Postoperative pancreatic fistula
• Visceral obesity

Nonalcoholic fatty pancreas disease (NAFPD) is an emerging disease that has gained an increasing amount of attention in recent years. It describes fat accumulation in the pancreas with insignificant alcohol consumption, but the pathogenesis is largely unknown. A wide range of terms have been used to describe the phenomenon of pancreatic fat accumulation, but NAFPD remains an under-recognized and non-independent disorder. Obesity, age, sex, race, and unhealthy lifestyle are established independent risk factors for NAFPD, which is strongly associated with metabolic syndrome, type 2 diabetes, pancreatitis, pancreatic fistula, pancreatic cancer, and nonalcoholic fatty liver disease. At present, imaging techniques are common diagnostic aids, but uniform criteria and consensus are lacking. Therapeutically, healthy diet, weight loss, and exercise are the mainstays to reduce pancreatic fat accumulation. It can be seen that there is a limited understanding of NAFPD at this stage and further exploration is needed. Previous studies have revealed that NAFPD may directly affect diagnosis and clinical decision-making. Therefore, exploring the pathophysiological mechanism and clinical associations of NAFPD is a major challenge for researchers and clinicians.

• Nonalcoholic fatty pancreatic disease
• Pancreatic steatosis
• Obesity
• Metabolic syndrome
• Pancreatic disease
• Pancreas

The pancreas is comprised of exocrine and endocrine compartments releasing digestive enzymes into the duodenum and regulating blood glucose levels by insulin and glucagon release. Tissue homeostasis is depending on transcription factor networks, involving Ptf1α, Ngn3, Nkx6.1, and Sox9, which are already activated during organogenesis. However, proper organ function is challenged by diets of high sugar and fat content, increasing the risk of type 2 diabetes and other disorders. A detailed understanding of processes that are important for homeostasis and are impaired during type 2 diabetes is lacking. Here, we show that Zeb1—a transcription factor known for its pivotal role in epithelial-mesenchymal transition, cell plasticity, and metastasis in cancer—is expressed at low levels in epithelial cells of the pancreas and is crucial for organogenesis and pancreas function. Loss of Zeb1 in these cells result in an increase of islet mass, impaired glucose tolerance, and sensitizes to develop liver and pancreas steatosis during diabetes and obesity. Interestingly, moderate overexpression of Zeb1 results in severe pancreas agenesis and lethality after birth, due to islet insufficiency and lack of acinar structures. We show that Zeb1 induction interferes with proper differentiation, cell survival, and proliferation during pancreas formation, due to deregulated expression of endocrine-specific transcription factors. In summary, our analysis suggests a novel role of Zeb1 for homeostasis in epithelial cells that is indispensable for pancreas morphogenesis and proper organ function involving a tight regulation of Zeb1 expression.

• atherosclerosis
• computed tomography
• diabetes mellitus
• pancreatic steatosis

• funding

• hepatic very low density lipoprotein triglyceride export
• pancreas morphology
• pathogenesis
• remission
• twin cycle hypothesis
• type 2 diabetes
• β-cell dysfunction

• fatty liver
• fatty pancreas
• metabolic syndrome
• obesity
• pancreas
• pancreatic disease

• Female obesity
• Glucose tolerance
• Insulin resistance
• Lemon balm
• Melissa officinalis
• Pancreatic dysfunction

• Adipocytes/drug effects
• Adipocytes/pathology
• Animals
• Anti-Obesity Agents/therapeutic use
• Blood Glucose/analysis
• Fatty Acids, Nonesterified/blood
• Female
• Fibrosis
• Insulin Resistance
• Melissa
• Mice, Inbred C57BL
• Obesity, Abdominal/blood
• Obesity, Abdominal/drug therapy
• Obesity, Abdominal/pathology
• Pancreas/drug effects
• Pancreas/pathology
• Plant Extracts/therapeutic use
• Triglycerides/blood

• Alcohol
• Fatty pancreas
• Metabolic syndrome
• Pancreatic cancer

CAIPIRINHA is a new technique in abdominal imaging. Pancreatic steatosis (PS) is a subject of increasing scientific interest. The aim of this study was to investigate the efficacy of the isotropic 3D-VIBE- CAIPIRINHA -DIXON technique on a new generation 3-tesla MR unit in the evaluation of PS.

In this retrospective study, the imaging findings of 49 patients with PS and 41 control subjects were examined. The pancreas-to-spleen ratio (PSR), pancreas-to-muscle ratio (PMR), and pancreatic signal intensity index (PSII) were defined as 3 new parameters and these indexes were calculated from the in-phase/out of phase 3D-VIBE- CAIPIRINHA-DIXON images.

The PSR, PMR, and PSII values were significantly different between the patient and control groups (P = 0.001, P = 0.009, P < 0.001, respectively). Statistically significant differences were observed between patient and control groups for ROI measurements of fatty areas on these sequences/images: subtraction (in-out) (P < 0.001), T2W HASTE (P < 0.001), DIXON-fat (P < 0.001), fat-suppressed T1W (P = 0.002), and subtraction (out-in) (P = 0.010).

Evaluation of PS with the 3D-VIBE-CAIPIRINHA-DIXON technique can be made rapidly and effectively.

• Pancreas
• magnetic resonance imaging
• chemical shift imaging
• MRI scans
• steatosis

• dog
• fatty infiltration
• pancreatic lipomatosis
• pancreatic lipomatous pseudohypertrophy

• Animals
• Dog Diseases/pathology
• Dogs
• Female
• Lipomatosis/veterinary
• Pancreatic Diseases/veterinary

• brain
• metabolic dysfunction
• obesity
• overweight
• weight loss

• diabetes mellitus
• obesity
• pancreas
• steatosis

• fat fraction
• liver steatosis
• magnetic resonance imaging
• metabolic syndrome
• obesity
• pancreatic steatosis

The purpose of this study was to clarify whether fatty pancreas might lead to impaired pancreatic endocrine or exocrine function.

The study involved 109 participants who had undergone the glucagon stimulation test and N-benzoyl-L-tyros-p-amino benzoic acid (BT-PABA) test to assess pancreatic function as well as unenhanced abdominal computed tomography (CT). Pancreatic endocrine impairment was defined as ΔC peptide immunoreactivity less than 2 [mmol/L] in the glucagon stimulation test, and pancreatic exocrine impairment was defined as a urinary PABA excretion rate less than 70% on the BT-PABA test. We defined as the mean CT value of pancreas / CT value of spleen (P/S ratio) as a marker to assess fatty pancreas. We analyzed the association between fatty pancreas and pancreatic impairment using the logistic regression model. The odds ratio (OR) is shown per 0.1 unit.

Pancreatic endocrine function was impaired in 33.0% of the participants, and 56.9% of those were regarded as having pancreatic exocrine impairment. The P/S ratio was significantly correlated with pancreatic endocrine impairment in univariate analysis (OR = 0.61, 95% confidence interval (CI) = 0.43–0.83, P = 0.0013) and multivariate analysis (OR = 0.38, 95% CI = 0.22–0.61, P < .0001) for all participants. Similar significant relationships were observed in both univariate (OR = 0.70, 95% CI = 0.49–0.99, P = 0.04) and multivariate (OR = 0.39, 95% CI = 0.21–0.66, P = 0.0002) analyses for the participants without diabetes (n = 93). The amount of pancreatic fat was not associated with exocrine impairment in univariate analysis (OR = 0.80, 95% CI = 0.59–1.06, P = 0.12).

Fatty pancreas was associated with pancreatic endocrine impairment but did not have a clear relationship with pancreatic exocrine impairment.

• 4-Aminobenzoic Acid/urine
• Adult
• Aged
• Aged, 80 and over
• Female
• Glucagon/administration & dosage
• Humans
• Intra-Abdominal Fat/diagnostic imaging
• Islets of Langerhans/diagnostic imaging
• Islets of Langerhans/drug effects
• Islets of Langerhans/physiopathology
• Lipomatosis/diagnostic imaging
• Lipomatosis/physiopathology
• Lipomatosis/urine
• Male
• Middle Aged
• Pancreas, Exocrine/diagnostic imaging
• Pancreas, Exocrine/drug effects
• Pancreas, Exocrine/physiopathology
• Pancreatic Diseases/diagnostic imaging
• Pancreatic Diseases/physiopathology
• Pancreatic Diseases/urine
• Spleen/diagnostic imaging
• Tomography, X-Ray Computed
• para-Aminobenzoates/administration & dosage

• Fetal development
• fetal pancreas hyperechogenicity
• fetal ultrasonography
• gestational diabetes mellitus
• oral glucose tolerance test

This study aims at determining the normal pancreatic dimensions in pediatric age groups considering demographic parameters and thus developing percentile reference curves for normal pancreatic dimensions in Indian children.

It is a cross-sectional study.

A hospital-based cross-sectional study was planned at a children hospital during July 2016–December 2017, in which the pancreatic dimensions of 1078 normal children in the age range of 1 month to 19 years were obtained through abdominal ultrasonography (USG). The demographic details like age and gender were obtained for each child.

Percentile reference curves were obtained with reference to age for each gender type independently. Generalized additive models for location, scale, and shape were used to obtain percentile plots for each pancreatic part.

The mean age of children was 6.65 ± 4.43 years and the male-to-female ratio was 1.63:1. The head, body, and tail dimensions increased with the age. For head, up to 25^th percentile, the curves were similar for both genders, while subsequent curves were higher in males as compared to females. Similar was the observation for body of pancreas. For tail, up to 75^th percentile, the curves were similar for both genders.

The normal ranges can be supportive in diagnosis of illness related to pancreas. The dimensions within 5–95^th percentile along with iso-echogenicity can be regarded as normal, while the dimensions beyond these limits along with change of echogenicity can be suspected for pancreatic disorders.

• Generalized additive models
• pancreas
• percentile curves

• Diabetes mellitus, type 2
• Diabetic retinopathy
• Fats
• Pancreas

• National Research Foundation of Korea

• Benign
• Epidermoid
• Hamartoma
• Inflammatory
• Lymphoepithelial
• Pancreatitis
• Serous
• Squamoid

• Anatomic variants
• Developmental anomalies
• Developmental variants
• Normal variants
• Pancreas

• Adipose Tissue/metabolism
• Adipose Tissue/pathology
• Adult
• Age Factors
• Aged
• Autopsy
• Biopsy, Needle
• Case-Control Studies
• Databases, Factual
• Diabetes Mellitus, Type 2/metabolism
• Diabetes Mellitus, Type 2/mortality
• Diabetes Mellitus, Type 2/pathology
• Female
• Humans
• Immunohistochemistry
• Insulin-Secreting Cells/pathology
• Japan
• Male
• Middle Aged
• Pancreas/metabolism
• Pancreas/pathology
• Reference Values
• Retrospective Studies
• Severity of Illness Index
• Sex Factors
• Survival Rate

• Ectopic fat
• Laparoscopic sleeve gastrectomy
• Pancreas volume
• Type 2 diabetes mellitus

• Adiponectin/blood
• Adult
• Blood Glucose
• Body Mass Index
• Female
• Gastrectomy/methods
• Humans
• Insulin/blood
• Insulin Resistance/physiology
• Japan
• Leptin/blood
• Lipids/blood
• Male
• Middle Aged
• Obesity, Morbid/diagnostic imaging
• Obesity, Morbid/metabolism
• Obesity, Morbid/pathology
• Obesity, Morbid/surgery
• Organ Size/physiology
• Pancreas/diagnostic imaging
• Pancreas/pathology
• Retrospective Studies
• Spleen/diagnostic imaging
• Spleen/pathology
• Tomography, X-Ray Computed
• Treatment Outcome
• Weight Loss/physiology

Arf4 is proposed to be a critical regulator of membrane protein trafficking in early secretory pathway. More recently, Arf4 was also implicated in regulating ciliary trafficking, however, this has not been comprehensively tested in vivo. To directly address Arf4’s role in ciliary transport, we deleted Arf4 specifically in either rod photoreceptor cells, kidney, or globally during the early postnatal period. Arf4 deletion in photoreceptors did not cause protein mislocalization or retinal degeneration, as expected if Arf4 played a role in protein transport to the ciliary outer segment. Likewise, Arf4 deletion in kidney did not cause cystic disease, as expected if Arf4 were involved in general ciliary trafficking. In contrast, global Arf4 deletion in the early postnatal period resulted in growth restriction, severe pancreatic degeneration and early death. These findings are consistent with Arf4 playing a critical role in endomembrane trafficking, particularly in the pancreas, but not in ciliary function.

Primary cilia are sensory organelles found on most cells and contain specific receptors that detect extracellular stimuli. Defects in trafficking receptors to cilia cause a diverse set of diseases called ciliopathies, which include polycystic kidney disease, obesity, cerebral anomalies and retinal degeneration. Based mostly on in vitro studies, the small GTPase Arf4 was thought to be critically important for localizing rhodopsin to the outer segment of photoreceptor cells and cystoproteins to kidney cilia. Here we genetically remove Arf4 from mice in either a tissue specific or time dependent manner. To our surprise, the loss of Arf4 does not cause retinal degeneration or cystic kidney disease. Since ciliary dysfunction causes retinal degeneration and cystic disease, our findings indicate that Arf4 does not play a role in ciliary function. Instead, mice have zymogen granule defects and degeneration of the exocrine pancreas supporting roles for Arf4 in regulating endomembrane trafficking in specific cells.

• ADP-Ribosylation Factors/genetics
• Animals
• Cilia/genetics
• Cilia/pathology
• Disease Models, Animal
• Humans
• Kidney/metabolism
• Kidney/pathology
• Kidney Diseases, Cystic/genetics
• Kidney Diseases, Cystic/pathology
• Mice
• Mice, Knockout
• Nucleotide Motifs/genetics
• Pancreas, Exocrine/growth & development
• Pancreas, Exocrine/pathology
• Photoreceptor Cells/metabolism
• Photoreceptor Cells/pathology
• Retinal Degeneration/genetics
• Retinal Degeneration/pathology
• Sequence Deletion

• P30 EY005722 NEI NIH HHS
• R01 DK103632 NIDDK NIH HHS
• K99 EY025732 NEI NIH HHS
• R01 GM060992 NIGMS NIH HHS
• R01 EY012859 NEI NIH HHS
• National Institute of General Medical Sciences
• National Institute of Diabetes and Digestive and Kidney Diseases
• National Eye Institute
• National Cancer Institute
• Research to Prevent Blindness
• National Institutes of Health

• Adolescent
• Adult
• Aged
• Diabetes Mellitus, Type 2/physiopathology
• Female
• Humans
• Image Processing, Computer-Assisted
• Intra-Abdominal Fat/diagnostic imaging
• Intra-Abdominal Fat/physiology
• Magnetic Resonance Imaging/methods
• Male
• Middle Aged
• Observer Variation
• Pancreas/diagnostic imaging
• Pancreas/physiology
• Parenchymal Tissue/diagnostic imaging
• Parenchymal Tissue/physiology
• Reproducibility of Results
• Young Adult

• Newcastle upon Tyne Hospitals NHS Foundation Trust

• pancreatic fat
• pediatric obesity
• beta-cell function
• metabolic syndrome
• body mass index-standard deviation score

There is an epidemic of obesity worldwide. The prevalence of obesity has doubled over the last three decades. Obesity, especially abdominal obesity is associated with insulin resistance that can lead to pancreatic steatosis and non-alcoholic fatty pancreatic disease (NAFPD). NAFPD describes a phenotype entity ranging from deposition of fat in the pancreas to pancreatic inflammation, and resultant fibrosis, which is similar to that of non-alcoholic fatty liver disease (NAFLD). NAFPD may represent a meaningful manifestation of metabolic syndrome. Pancreatic steatosis can be diagnosed on ultrasound, computed tomography (CT) scan or magnetic resonance imaging (MRI). In addition to a correlation between pancreatic steatosis and metabolic syndrome, pancreatic steatosis may lead to a worse outcome in pancreatitis and may be an etiological factor in pancreatic cancer, but we need further research to examine the associations, pathophysiology, and the impact of pancreatic steatosis and NAFPD on the human health.

• Metabolic syndrome
• Non-alcoholic fatty pancreatic disease
• Pancreatic steatosis