Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Zhou, Xinrong; Qian, Bangguo; Ji, Ning; Lui, Conghui; Liu, Zhiyuan; Li, Bing; Zhou, Huarong; Yan, Caifeng

doi:10.1530/joe-14-0701

Cited by 17 publications

(13 citation statements)

References 42 publications

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“…Rather than increase observed previously, a decrease in pancreatic β-cell mass was shown due to the reduction in pancreatic steatosis and decreased pancreatic insulin content, a phenomenon suggested to be linked to pancreas adaptation following weight loss. Similarly to heterogeneous findings in humans, animal model studies report either enhanced 101,102 or decreased 95,103,104…”

Section: Changes In Hormones and Beta Cell Functionmentioning

confidence: 72%

Impact of bariatric surgery on type 2 diabetes: contribution of inflammation and gut microbiome?

et al. 2019

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Obesity is a chronic low-grade inflammatory disease (both at the systemic and adipose tissue level) that continues to rise worldwide. It is associated with an abundance of comorbidities, including type 2 diabetes (T2D). Bariatric surgery, which induces modifications of the intestinal tract, is to date the most successful treatment for obesity. Its use has dramatically increased in number as it enables both weight reduction and metabolic improvements, with 60% of patients even achieving diabetes remission. Several mechanisms are actually demonstrated to be involved in those clinical improvements. Importantly, both obesity and T2D share many phenotypic characteristics, including increased systemic and adipose tissue inflammation, as well as gut microbiota dysbiosis. These characteristics are deeply modulated after bariatric surgery. This review will specifically focus on the host metabolic changes induced by bariatric surgery in regards of the induced gut architectural changes, as well as on the modifications in the inflammatory tone and gut microbiota observed subsequently to bariatric surgery induced weight loss.

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Section: Changes In Hormones and Beta Cell Functionmentioning

confidence: 72%

Impact of bariatric surgery on type 2 diabetes: contribution of inflammation and gut microbiome?

et al. 2019

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“…13 On the other hand, in diabetic GK rats, multiple and bigger effects on islet architecture have been reported, including pancreatic hyperplasia, enlarged beta cell-mass, and increased ratio of beta cells to non-beta endocrine cells. 14 Similar surgery-mediated changes were also described in diet-induced obese (DIO) mice in association with increased islet numbers, 15 implying a direct influence of bariatric surgery on pancreatic cellular turnover and islet structure. Although several factors are likely to cause this, it is now clear that alteration in enterohormone release is one of the major effector.…”

Section: Improvement In Islet Function Is Crucial For Diabetes Remissmentioning

confidence: 75%

PYY, a Therapeutic Option for Type 2 Diabetes?

Guida

Ramracheya

2020

Clin Med Insights Endocrinol Diabetes

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Metabolic surgery leads to rapid and effective diabetes reversal in humans, by weight-independent mechanisms. The crucial improvement in pancreatic islet function observed after surgery is induced by alteration in several factors, including gut hormones. In addition to glucagon-like peptide 1 (GLP-1), increasing lines of evidence show that peptide tyrosine tyrosine (PYY) plays a key role in the metabolic benefits associated with the surgery, ranging from appetite regulation to amelioration of islet secretory properties and survival. Here, we summarize the current knowledge and the latest advancements in the field, which pitch a strong case for the development of novel PYY-based therapy for the treatment of diabetes.

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“…Few studies have reported beta-cell morphology, and in all of these, including the present study, only larger beta-cell mass and/or stronger insulin staining were detected in RYGB, SG, DJB or IT animals compared with their diabetic control. It is regrettable that no comparison was performed between pre- and postoperative rats[35-37]. Therefore, there has been no evidence supporting islets hyperplasia or beta-cell turnover after bariatric surgeries until now.…”

Section: Discussionmentioning

confidence: 99%

Diabetes recurrence after metabolic surgeries correlates with re-impaired insulin sensitivity rather than beta-cell function

Zhong

Liu

et al. 2017

WJG

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AIMTo investigate factors causing diabetes recurrence after sleeve gastrectomy (SG) and duodenal-jejunal bypass (DJB).METHODSSG and DJB were performed on rats with diabetes induced by high-fat diet (HFD) and streptozotocin (STZ). HFD was used to induce diabetes recurrence at 4 wk postoperatively. Body weight, oral glucose tolerance test, homeostatic model assessment of insulin resistance (HOMA-IR), insulin signaling [IR, insulin receptor substrate (IRS)1, IRS2, phosphatidylinositol 3-kinase and AKT in liver and skeletal muscle], oral glucose stimulated insulin secretion, beta-cell morphology (mass, apoptosis and insulin secretion), glucagon-like peptide (GLP)-1, PYY and ghrelin were compared among SG rats with common low-fat diet (SG-LFD), SG with HFD (SG-HFD), DJB rats with LFD (DJB-LFD), DJB with HFD (DJB-HFD) and sham-operation with LFD (Sham) at targeted postoperative times.RESULTSSG and DJB resulted in significant improvement in glucose tolerance, lower HOMA-IR, up-regulated hepatic and muscular insulin signaling, higher levels of oral glucose-stimulated insulin secretion, bigger beta-cell mass, higher immunofluorescence intensity of insulin, fewer transferase-mediated dUTP-biotin 3’ nick end-labeling (TUNEL)-positive beta cells and higher postprandial GLP-1 and PYY levels than in the Sham group. The improvement in glucose tolerance was reversed at 12 wk postoperatively. Compared with the SG-LFD and DJB-LFD groups, the SG-HFD and DJB-HFD groups showed higher HOMA-IR, down-regulated hepatic and muscular insulin signaling, and more TUNEL-positive beta cells. No significant difference was detected between HFD and LFD groups for body weight, glucose-stimulated insulin secretion, beta-cell mass, immunofluorescence intensity of insulin, and postprandial GLP-1 and PYY levels. Fasting serum ghrelin decreased in SG groups, and there was no difference between HFD-SG and LFD-SG groups.CONCLUSIONHFD reverses the improvement in glucose homeostasis after SG and DJB. Diabetes recurrence may correlate with re-impaired insulin sensitivity, but not with alterations of beta-cell function and body weight.

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Pancreatic hyperplasia after gastric bypass surgery in a GK rat model of non-obese type 2 diabetes

Cited by 17 publications

References 42 publications

Impact of bariatric surgery on type 2 diabetes: contribution of inflammation and gut microbiome?

Impact of bariatric surgery on type 2 diabetes: contribution of inflammation and gut microbiome?

PYY, a Therapeutic Option for Type 2 Diabetes?

Diabetes recurrence after metabolic surgeries correlates with re-impaired insulin sensitivity rather than beta-cell function

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