Published online Sep 28, 2026. doi: 10.5528/wjtm.124909
Revised: August 4, 2026
Accepted: August 17, 2026
Published online: September 28, 2026
Processing time: 69 Days and 13.5 Hours
Bariatric surgery alters adipose tissue endocrine function; however, whether Roux-en-Y gastric bypass (RYGB) and laparoscopic sleeve gastrectomy (LSG) produce different long-term adipokine profiles remains uncertain. This narrative mini-review summarizes head-to-head human evidence supported by mecha
Core Tip: Direct comparisons indicate that Roux-en-Y gastric bypass (RYGB) and laparoscopic sleeve gastrectomy produce broadly similar long-term reductions in leptin and chemerin. Adiponectin increases after both procedures; a greater post-RYGB increase has been reported in some small cohorts but is not consistent across studies. Evidence for resistin is limited. Because postoperative weight loss, baseline diabetes, supplementation, and assay differences confound comparisons, current adipokine data cannot determine the preferred operation or predict individual outcomes. Larger randomized studies with standardized measurements and > 1-year follow-up are needed.
- Citation: Salman A, Salman MA. Long-term adipocytokine changes after Roux-en-Y gastric bypass and laparoscopic sleeve gastrectomy: A comparative minireview. World J Transl Med 2026; 12(3): 124909
- URL: https://www.wjgnet.com/2220-6132/full/v12/i3/124909.htm
- DOI: https://dx.doi.org/10.5528/wjtm.124909
It has been projected that more than one billion adults will develop obesity by 2030. By 2050, overweight or obesity may affect more than 50% of adults and 30% of children[1]. Severe obesity reflects excess subcutaneous and visceral adipose tissue and has substantial physiological consequences. Bariatric surgery provides more durable weight loss and metabolic improvement than other available treatments[2]. Bariatric procedures differ in their anatomy, mechanisms, and metabolic effects. Some of these effects appear before major weight loss and may be partly weight-independent[3-5]. The manner in which each operation alters circulating adipokines over time remains unclear.
Adipokines are signaling molecules that are released by the adipose tissue. They regulate metabolism, inflammation, immune responses, cardiovascular function, and cancer biology[6]. Abnormal adipokine profiles accompany insulin resistance, type 2 diabetes mellitus, hyperlipidemia, stroke, atherosclerosis, and several cancers[7-9]. Leptin, adiponectin, and resistin are the most widely studied molecules[10]. The clinically relevant question is whether the distinct anatomies of Roux-en-Y gastric bypass (RYGB) and laparoscopic sleeve gastrectomy (LSG) produce different durable adipokine profiles. This narrative minireview evaluates the abovementioned question while separating direct comparative evidence from mechanistic inferences.
This is a narrative minireview. We searched PubMed, Scopus, Web of Science, EMBASE, and the Cochrane Library from database inception to June 2026. The database-specific strategies are listed in Table 1. The searches combined the terms for bariatric surgery, RYGB, and LSG with adipokine-related terms (adipokines, adipocytokines, leptin, adiponectin, resistin, and chemerin).
| Database | Search strategy |
| PubMed | ("bariatric surgery"[Title/Abstract] OR "Roux-en-Y gastric bypass"[Title/Abstract] OR "sleeve gastrectomy"[Title/Abstract]) AND (adipokine*[Title/Abstract] OR adipocytokine*[Title/Abstract] OR leptin[Title/Abstract] OR adiponectin[Title/Abstract] OR resistin[Title/Abstract] OR chemerin[Title/Abstract]) |
| Scopus | TITLE-ABS-KEY("bariatric surgery" OR "Roux-en-Y gastric bypass" OR "sleeve gastrectomy") AND TITLE-ABS-KEY(adipokine* OR adipocytokine* OR leptin OR adiponectin OR resistin OR chemerin) |
| Web of Science | TS=("bariatric surgery" OR "Roux-en-Y gastric bypass" OR "sleeve gastrectomy") AND TS=(adipokine* OR adipocytokine* OR leptin OR adiponectin OR resistin OR chemerin) |
| EMBASE | ('bariatric surgery':ti,ab,kw OR 'Roux-en-Y gastric bypass':ti,ab,kw OR 'sleeve gastrectomy':ti,ab,kw) AND (adipokine*:ti,ab,kw OR adipocytokine*:ti,ab,kw OR leptin:ti,ab,kw OR adiponectin:ti,ab,kw OR resistin:ti,ab,kw OR chemerin:ti,ab,kw) |
| Cochrane Library | ("bariatric surgery" OR "Roux-en-Y gastric bypass" OR "sleeve gastrectomy"):ti,ab,kw AND (adipokine* OR adipocytokine* OR leptin OR adiponectin OR resistin OR chemerin):ti,ab,kw |
We included randomized trials, prospective and retrospective cohort studies, case-control studies, systematic reviews, meta-analyses, and relevant mechanistic and animal studies. We prioritized full-text English-language human studies that reported at least one prespecified adipokine after RYGB or LSG and preferentially included direct head-to-head comparisons. We excluded reports that did not identify the operation or adipokine outcomes, or duplicated a more complete cohort. Mechanistic and animal studies have only been used to interpret biological plausibility.
This was a narrative rather than a systematic synthesis, and we did not report Preferred Reporting Items for Systematic Reviews and Meta-Analyses screening counts, prepare a flow diagram, or apply a formal study-level risk-of-bias tool. We evaluated comparative studies according to design, sample size, group comparability, follow-up, assay method, and adjustment for weight loss and baseline metabolic factors. Follow-up was classified as midterm (6-12 months) or long-term (≥ 12 months). Studies with shorter follow-up periods were used only to describe early changes.
Adipose tissue is broadly classified as white or brown[11]. White adipocytes primarily store excess energy as triglycerides and secrete numerous cytokines, including leptin, adiponectin, omentin, tumor necrosis factor-alpha (TNF-α), interleukin-6 (IL-6), monocyte chemoattractant protein-1 (MCP-1), plasminogen activator inhibitor-1, resistin, visfatin, adipsin, and retinol-binding protein 4[12]. In contrast, brown adipocytes store energy in small lipid droplets and secrete cytokines, such as fibroblast growth factor 21, bone morphogenetic protein-7, vascular endothelial growth factor-A, irisin, neuregulin 4, nesfatin-1, meteorin-like protein, chemerin, IL-6, interleukin-8, and interleukin-10; moreover, they support thermogenesis, energy expenditure, glucose homeostasis, lipid metabolism, insulin sensitivity, angiogenesis, and anti-inflammatory effects[13]. These adipokines modulate glucose homeostasis, insulin sensitivity, lipolysis, and fatty acid oxidation by acting on various tissues, including the liver, skeletal muscle, pancreas, and fat (Figure 1)[14].
Many proinflammatory adipokines are elevated in obesity and contribute to chronic low-grade inflammation[15]. TNF-α, MCP-1, and IL-6 promote pathways that are involved in obesity-related disease, whereas anti-inflammatory adipokines that are reduced in obesity may protect against metabolic comorbidity[16].
RYGB has long been the reference metabolic bariatric procedure because it results in durable weight loss and high rates of comorbidity remission[17]. It combines restriction, intestinal bypass, and neurohormonal effects. A 20-60 mL gastric pouch is anastomosed to a Roux limb, excluding the distal stomach, duodenum, and proximal jejunum. Beyond limiting the intake, RYGB lowers ghrelin levels and increases glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) levels. These hormonal changes increase satiety and may improve glycemic control before substantial weight loss[18].
LSG accounts for > 60% of all bariatric procedures worldwide. Originally used as the first stage of a more complex operation, it is now performed as a standalone procedure[19]. Approximately 80% of the stomach is removed along the greater curvature, leaving a narrow tubular remnant[20]. Smaller reservoirs limit food intake and promote early satiety. Fundus resection lowers ghrelin levels, whereas faster nutrient delivery to the distal small bowel increases levels of GLP-1 and PYY. Collectively, these changes improve postprandial satiety and glycemic control[21].
Leptin, which is encoded by the ob gene, is a 16-kDa peptide that is produced by the adipose tissue and gastric fundic chief cells. Circulating leptin informs the central nervous system regarding peripheral energy stores[22]. Adipose-derived leptin crosses the blood-brain barrier and acts on the hypothalamic arcuate nucleus. Gastric leptin is secreted into the lumen, reabsorbed in the duodenum, and may contribute to short-term satiety, whereas adipose-derived leptin mainly regulates the longer-term energy balance[23].
Leptin activates anorexigenic pro-opiomelanocortin (POMC)/cocaine- and amphetamine-regulated transcript neurons and inhibits orexigenic agouti-related peptide/neuropeptide Y (NPY) neurons, and thereby promotes satiety and energy expenditure[24]. Circulating leptin levels increase with adipose tissue mass; however, most individuals with obesity exhibit leptin resistance. The proposed mechanisms include hyperleptinemia, impaired Janus kinase 2-signal transducer and activator of transcription 3 (STAT3) signaling, defective autophagy, endoplasmic reticulum stress, inflammation, reduced leptin receptor expression, increased mammalian target of rapamycin activity, and peripheral resistance[25].
Obesity-associated hyperleptinemia contributes to leptin resistance. After bariatric surgery, the combined effects of weight loss, reduced central inflammation, and altered gut-brain signaling may improve leptin responsiveness. Rapid nutrient delivery to the distal small intestine increases the levels of GLP-1 and PYY[26], which interact with the hypothalamic pathways involved in satiety and energy expenditure[27]. Changes in the gut microbiota may also influ
After LSG, leptin concentrations generally decrease with weight and body mass index (BMI) and are associated with improved insulin sensitivity[30-32]. Temporal evidence is less uniform. A 4-month study found no significant reduction[33], whereas mid-term measurements at 6 months[34] and long-term measurements at 12 months and 18 months[35-37] showed sustained decreases. In one cohort, leptin levels remained 54% below baseline at 4 years[38]. Although Bužga et al[39] reported an approximately 50% decrease in serum leptin levels at 12 months, the change was unrelated to appetite. Another study found that LSG nearly normalized the leptin levels[40]. Across studies, leptin changes tracked weight and BMI[35,36,38]. However, these levels remained higher than those in lean controls at 12 months[35].
Mazahreh et al[41] observed post-LSG reductions in BMI, leptin-to-BMI ratio, and a proposed leptin-resistance index, which may better capture postoperative leptin signaling than leptin concentration alone; however, it has not been externally validated. A recent study reported lower gastric leptin and leptin receptor expression after LSG. Both changes were correlated with reductions in BMI and levels of glycated hemoglobin, total cholesterol, and triglycerides[42]. The resection of the gastric fundus in LSG markedly reduces ghrelin expression. Because ghrelin and leptin act in opposite directions on overlapping hypothalamic neuronal populations, lower ghrelin levels may support leptin-mediated satiety[43].
In a clinical study, leptin levels decreased within 2 months after RYGB and remained lower at 1 year. The change closely tracked BMI and occurred in patients with normal glucose tolerance, impaired glucose tolerance, and T2DM. BMI reduction explained approximately 66% of the variance[44]. A separate study detected reductions within 2 weeks before substantial weight loss[45]. The largest reported effect occurred at 6 months[46]. In obese rats, RYGB decreased leptin concentrations to those observed in lean controls and increased hypothalamic leptin-receptor, phosphorylated STAT3, and POMC expression, while reducing NPY secretion[47]. Another rat study linked leptin reduction to the loss of visceral white adipose tissue[48].
Furthermore, RYGB reduced hypothalamic inflammation and endoplasmic-reticulum stress, both of which are associated with leptin resistance. Lower Toll-like receptor 4 signaling has been linked to changes in the gut microbiota and circulating proinflammatory factors rather than weight loss alone[49].
White adipose-tissue browning contributes to energy metabolism. Adiponectin is an adipocyte-derived protein that upregulates browning genes[50] and is inversely associated with visceral adiposity[51]. Adiponectin is one of the most abundant adipokines in the human serum and has anti-steatotic, anti-inflammatory, and antifibrotic actions[52]. Furthermore, adiponectin improves insulin sensitivity by enhancing fatty acid oxidation, modulating lipoprotein metabolism, and suppressing hepatic gluconeogenesis[51].
The effects of adiponectin are mediated through adiponectin receptor 1 and adiponectin receptor 2, which activate AMP-activated protein kinase in immune cells and tissues[53]. Low blood adiponectin levels are associated with chronic inflammation in metabolic diseases, including T2DM and atherosclerosis[54]. Compared to healthy individuals, obese individuals have significantly lower serum adiponectin levels, which are associated with a risk of obesity-related diseases[55].
After LSG, adiponectin levels increase as does the adipocyte expression of browning genes[50]. These changes are accompanied by improved body composition and metabolic markers. The increase was greater in patients reporting reduced appetite and was correlated with better insulin sensitivity and lower cardiovascular risk markers[39]. Adi
In a small study of 22 patients who underwent LSG, adiponectin levels increased within 4 months[33]. Further increases were reported at the mid-term 6-month assessment and at the long-term 12-month and 18-month assessments[34-37]. At 12 months, the concentration was nearly twice that at baseline and was higher in participants with than in those without metabolic syndrome[36]. These changes were associated with improved low-density lipoprotein (LDL) cholesterol, glycated hemoglobin, and other metabolic markers; however, the study did not establish causality.
Adiponectin improves insulin sensitivity and this may partly explain the improved glycemic control after bariatric surgery[31]. A meta-analysis revealed that adiponectin levels increased after LSG[31]. However, one small study found no significant adiponectin changes 4 years after LSG[38]. However, the sample size may have been too small to detect any differences. RYGB produces a sustained increase in circulating adiponectin. In severe obesity, adiponectin secretion is suppressed. The post-RYGB increase in adiponectin has been associated with lower inflammation, better insulin sensitivity[56,57], and reduced hepatic fat[58].
The post-RYGB increase in the adiponectin/Leptin ratio correlated with a lower cardiometabolic risk[59]. The reported values may increase from < 0.5, a range associated with marked inflammation, to > 1.0[59,60]. This ratio may indicate postoperative metabolic improvement, although the clinical thresholds have not been validated.
Adiponectin levels increased within 6 months after RYGB[46,60], alongside reduced levels of leptin, resistin, and proinflammatory cytokines[56]. In one cohort, adiponectin concentrations increased by 6 weeks and continued to increase for 1 year, although they remained below the levels in normal-weight controls[61]. Both patients with and without diabetes showed increases at 12 months, and this change was related to weight and fat loss[62]. Adiponectin levels may increase within weeks after RYGB. One study found an increase at 3 weeks, without further significant change through 6 months despite continued weight loss[63]; this suggested an effect of acute negative energy balance. Another study reported a 107% increase at 6 months that was associated more strongly with reduced waist circumference than with total fat mass[64]. However, these early and mid-term findings should not be interpreted as proof of long-term durability.
Compared to gastric banding, RYGB resulted in a larger increase in adiponectin levels (approximately 70% vs 35.8%), and this increase correlated with greater weight and BMI reduction[65]. Several mechanisms may link RYGB with increased adiponectin levels. Hypertrophied adipocytes in severe obesity release TNF-α, which suppresses adiponectin expression. RYGB decreases TNF-α levels, and this suppression may enable adipose tissue to restore adiponectin production[66].
Adipose tissue remodeling after RYGB treatment reduces adipocyte size and may restore adiponectin secretion[67]. Furthermore, altered bile-acid and microbiota signaling may influence peroxisome proliferator-activated receptor-γ activity and adiponectin transcription[68]. Adiponectin supports endothelial nitric oxide production and anti-inflammatory pathways[69]; however, studies have not shown that an increase in postoperative adiponectin independently reduces the risk of myocardial infarction or stroke.
Resistin is a cysteine-rich protein that is known for its ability to induce insulin resistance in mice. In obese mice, cir
Resistin levels decreased at the midterm 6-month assessment and at the long-term 12-month and 18-month assessments after bariatric surgery[34-37]. The magnitude and clinical significance of this change remains unclear because the findings differ across cohorts and may be influenced by age, adiposity, diabetes, and vitamin D status[35,36]. A study found no relationship between changes in resistin and anthropometric or metabolic improvement[35] whereas a subsequent study linked resistin to age, weight, and BMI and found an inverse relationship between resistin, LDL cholesterol, and vitamin D levels[36]. In women with diabetes, resistin positively correlated with BMI and plasma glucose, and this constitutes a pattern that has not been observed in women without diabetes or lean controls[74].
Parreño Caparrós et al[75] found no difference in resistin levels between patients with morbid obesity and normal-weight controls or before and after weight loss. Resistin was not related to adiposity measures, such as insulin, glucose, the homeostasis model assessment index, the quantitative insulin sensitivity check index, high-sensitivity C-reactive protein, IL-6, or adiponectin.
Chemerin is a chemoattractant adipokine that is secreted by white adipose tissue and is involved in immune signaling. It regulates adipogenesis and insulin sensitivity and has been linked to body weight, hemostasis, and energy balance[76]. Serum chemerin levels are higher in obese individuals in whom adipose tissue expansion is accompanied by chronic low-grade inflammation[77]. However, evidence for the role of chemerin is limited. In a prospective comparative study, serum chemerin levels decreased 12 months after LSG and RYGB[78], and another smaller cohort study reported similar declines at 6 months and 12 months[79]. Across the available prospective cohorts, chemerin reduction at 12 months was comparable between LSG and RYGB[78,79]; however, no adequately powered randomized comparison was available.
Kalinowski et al[80] randomized 72 patients to LSG or RYGB, and 69 of these participants completed a 12-month follow-up. The baseline anthropometric and biochemical measurements were comparable, and both groups achieved similar weight loss and reductions in leptin, glucose, insulin, and insulin resistance. Randomization and balanced baseline groups strengthened the causal inference; however, the trial assessed only 1 year of follow-up and did not compare adiponectin, resistin, or chemerin levels.
In a prospective comparative cohort of 100 patients, Salman et al[78] reported similar 12-month reductions in the leptin and chemerin levels after RYGB and LSG. Likewise, Terra et al[79] found no between-procedure differences in adipokines at 6 months and 12 months, although their cohort included only 30 women. Both cohorts showed similar leptin and chemerin changes; however, neither cohort was randomized, and the follow-up ended at 12 months.
An 18-month observational study included 95 participants; however, only 12 underwent RYGB, which limits the precision of the head-to-head estimates[81]. In a 43-patient comparison, high-molecular-weight adiponectin increased similarly after LSG and RYGB, although the adiponectin level was measured in the saliva, and the sample size was small[82]. Gómez-Martin et al[83] studied 20 women each after RYGB and LSG, with 20 nonsurgical controls, and found a greater 1-year adiponectin increase after RYGB. Hosseini et al[84] reported a larger 7-month increase in adiponectin and decrease in leptin after RYGB than after LSG in an 81-patient three-procedure study. Both findings require caution because the samples were small, the treatment was not randomized, and the 7-month results were mid-term rather than long-term.
In a diet-induced mouse model exposed to a postoperative high-fat diet, RYGB produced more favorable adipose-tissue remodeling and metabolic outcomes than vertical sleeve gastrectomy[85]. Although this model helps separate anatomical effects from human behavioral factors, it cannot establish comparative clinical effectiveness or biomarker utility in patients. However, other studies have not established this comparison. A 6-month mixed-procedure cohort described early adipokine and inflammatory changes but lacked a clear head-to-head analysis[86]. A prospective gut hormone cohort found greater 1-year weight loss and different hormonal responses after RYGB without showing an independent adipokine mechanism[87]. A meta-analysis of randomized trials found higher diabetes remission rates after RYGB at 1 year; however, this difference was absent at 2-5 years[88]. The LSG-focused review did not offer long-term comparative data[89].
Leptin: A randomized trial with larger prospective cohorts showed comparable 12-month reductions after RYGB and LSG when the weight loss was similar (Table 2)[78-80]. Furthermore, a greater midterm decrease after RYGB in a nonrandomized study[84] should not override the more internally valid randomized evidence.
| Adipokine | Direct comparative findings | Design and follow-up | Interpretation and limitations |
| Leptin | Randomized and larger prospective studies show similar 12-month reductions after RYGB and LSG[78-80] | 7-18 months; one randomized trial and several small cohorts | Broadly comparable when weight loss is similar; isolated nonrandomized differences may reflect confounding[84] |
| Adiponectin | Both procedures increase adiponectin. Some cohorts favor RYGB[83,84], whereas another found comparable high-molecular-weight adiponectin[82] | 7-12 months; small nonrandomized studies | Mixed evidence; no durable procedure-specific superiority established |
| Resistin | Few direct comparisons; small observational studies report inconsistent between-procedure differences[36,86] | 6-12 months; limited observational evidence | Insufficient evidence; weight loss, diabetes, and vitamin D may confound |
| Chemerin | Two prospective cohorts report similar decreases after RYGB and LSG at 12 months[78,79] | 6 and 12 months; prospective nonrandomized cohorts | Probably comparable at 12 months, but no adequately powered randomized long-term study |
Adiponectin: Both surgeries increased adiponectin levels. Some small-cohort studies showed a greater increase after RYGB[83,84], whereas another small study found similar changes in high-molecular-weight adiponectin[82]. The evidence is mixed and does not demonstrate the superiority of either procedure.
Resistin: Direct evidence is sparse. Small observational studies suggest that resistin may decrease more after RYGB; however, sample size, baseline metabolic differences, vitamin D status, and postoperative weight loss limit interpretation[36,86].
Chemerin: The available 12-month comparative cohort reported similar reductions after RYGB and LSG[78,79]. No adequately powered randomized study has established procedure-specific long-term effects.
Lower leptin and higher adiponectin levels are correlated with weight loss, insulin sensitivity, glycemia, and inflammatory markers after bariatric surgery[31,36,39,56,59,60,64]. However, these associations do not prove that adipokine changes mediate clinical benefits. Randomized trial data showed a modest advantage for RYGB in 1-year diabetes remission but no clear difference at 2-5 years[88], and these trials did not test adipokine mediation. Post-LSG im
Leptin may decrease within weeks and thereafter track weight and fat-mass loss, whereas adiponectin usually increases over 6-12 months[44-46,61-64]. No validated postoperative trajectory or threshold predicts durable diabetes remission, liver outcomes, weight recurrence, or cardiovascular events. The leptin/ghrelin ratio and retinol-binding protein 4 have been studied as markers of improved insulin resistance after LSG[32]; however, these have not been externally validated to aid decision-making between RYGB and LSG. Before clinical use, a biomarker requires standardized assays and sampling, adjustment for weight loss and baseline disease, external validation, and evidence that improves prediction beyond routine clinical variables.
Postoperative weight loss strongly affects leptin and adiponectin levels. Differences in baseline BMI, age, sex, fat distribution, diabetes, and comorbidity may appear to be procedural effects. Comparisons of RYGB and LSG should use randomization or adjust carefully for the weight loss that is achieved.
Baseline glucose tolerance modifies adipokine responses[44], and patients with metabolic syndrome or diabetes may show greater changes than those without these conditions[36,60]. Vitamin D is associated with resistin[36]. Anti-diabetes therapy, vitamin and micronutrient supplementation, dietary intake, and physical activity have been inconsistently reported and may confound postoperative comparisons.
Most comparative studies were small, single-center, non-randomized, and followed patients for only 6-18 months. Some studies included only women or had markedly unequal procedural groups. Furthermore, assays vary by the adipokine isoform, sample matrix, and sampling time. Animal studies can test mechanisms but not clinical outcomes. These features make it difficult to separate anatomical effects from confounding.
This narrative mini-review did not use systematic review screening counts or formal risk-of-bias tools. The head-to-head literature is small and heterogeneous. Randomized evidence is largely confined to leptin at 12 months; furthermore, comparisons of adiponectin, resistin, and chemerin depended on small observational cohorts with unequal groups, different assays, and incomplete adjustments for weight loss and baseline disease. Midterm studies have focused on kinetics rather than durability. Because the review covers only four adipokines, we cannot determine whether these changes cause diabetes remission, liver improvement, cardiovascular benefits, or durable weight control. Future trials should prespecify adipokine panels and sampling times, report weight loss and supplementation, adjust for baseline metabolic phenotypes, and follow up patients beyond 3-5 years.
The next question pertains to whether early adipokine trajectories improve prediction beyond standard clinical variables and whether biomarker-guided procedure choice improves outcomes. To answer this question, externally validated models and prospective testing are required. The current evidence is insufficient for clinical selection.
Both RYGB and LSG induce sustained adipokine changes. The best comparative evidence showed similar 12-month reductions in leptin and chemerin levels. Although adiponectin levels increased after both procedures, the results of studies were inconsistent on whether the increase is greater after RYGB. However, procedure-specific evidence for resistin remains limited. These hormonal changes track weight loss and baseline metabolic status, and correlate with insulin resistance and other risk markers; however, they have not been shown to cause durable diabetes remission, liver improvement, or fewer cardiovascular events. Therefore, adipokines remain research biomarkers and should not guide the selection of the procedure.
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