Adaptive changes in pancreas post Roux‐en‐Y gastric bypass induced weight loss

Lautenbach, Anne; Wernecke, Marie; Riedel, Nina; Veigel, J; Yamamura, Jin; Keller, Sune H.; Jung, Roman; Busch, Philipp; Mann, Oliver; Knop, Filip K.; Holst, Jens J.; Meier, Juris J.; Aberle, Jens

doi:10.1002/dmrr.3025

Cited by 18 publications

(16 citation statements)

References 39 publications

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“…In our model, we did not find differences in insulin staining in b-cells in HFD rats and could not confirm the hypothesis discussed in recent mice models of diet-induced obesity 32 . However, as in the literature, we found an increase of the oral glucose tolerance test and insulin secretion after bariatric surgery 33 , 34 . Interestingly, we demonstrated that in our model, abnormal pancreatic features were detected not only in endocrine, but also in the exocrine pancreas, mainly observed beside HHF lesions, consisting in acinar-ductal metaplasia with inflammation, fibrosis, activation of stellate cells and iron deposits.…”

Section: Discussionsupporting

confidence: 84%

Obesity-induced pancreatopathy in rats is reversible after bariatric surgery

Rebours¹,

Garteiser²,

Ribeiro-Parenti³

et al. 2018

Sci Rep

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Obesity is a risk factor for pancreatic diseases. Bariatric surgery is one of the most efficient treatments of morbid obesity. The aims were to assess pancreatic endocrine and exocrine lesions in obese rats, to analyze effects of bariatric surgery. Sixty-three male Wistar rats were included in five groups: 2 fed with high fat diet (HFD) or normal diet for 3 months, 2 fed with HFD or normal diet for 6 months; 1 group fed with HFD and undergoing bariatric surgery (n = 30). Quantitative MR imaging was performed in HFD6, ND6 and HFD3-BS. Pancreas specimens were analyzed after sacrifice for adipocyte infiltration, fibrosis, acinar-ductal metaplasia, abnormality of Langerhans islets (HHF: hypertrophy, hypervascularisation, fibrosis), and hemosiderin deposits in acinar or endocrine locations. We found that HFD6 rats had more fibro-inflammatory islets (P = 0.0139) and acinar-ducal metaplasia (P = 0.0843) than HFD3 rats. Rats with HFD3+6 had more fibro-inflammatory islets (P < 0.0001), hemosiderin deposits (p < 0.0001), fat infiltration (P = 0.0008) and acinar-ductal metaplasia lesions (P = 0.0424). Weight increase was associated with glycoregulation abnormalities (r = 0.44, P = 0.08) and adipocyte infiltrations (P = 0.009). After surgery, less fibro-inflammatory islets (P = 0.0004), fat and iron infiltrates (P = 0.005 and P = 0.06), and acino-ductal metaplasia (P = 0.05) were observed compared to HFD6 rats. MR image quantifications revealed increased elasticity, fat fraction, and R2 and a decreased elasticity wave dispersion coefficient in the high fat groups that reversed after surgery. MRI parameters were in strong correlation with respective histological counterparts. In conclusion, obese rats develop pancreatic inflammatory lesions with acinar-ductal metaplasia in acinar location and the endocrine-exocrine interface. These changes can be prevented by bariatric surgery. Quantitative MR imaging is accurate in identifying early pancreatic lesions.

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Section: Discussionsupporting

confidence: 84%

Obesity-induced pancreatopathy in rats is reversible after bariatric surgery

Rebours¹,

Garteiser²,

Ribeiro-Parenti³

et al. 2018

Sci Rep

View full text Add to dashboard Cite

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“…Knockout of hsa-miR-375 in a mouse model induced a hyperglycemic phenotype with reduced beta cell mass [37]. The increased level of circulating hsa-miR-375 might therefore indicate an amelioration of beta cell function or changes in beta cell mass as indicated previously [14].…”

Section: Discussionmentioning

confidence: 53%

“…When analyzing the pancreas in obesity, pancreatic fat accumulation is thought to accompany beta cell failure at least in animal models [13]. Recent data described a normalization of pancreatic volume and steatosis in morbidly obese patients following Roux-en-Y gastric bypass (RYGB) surgery [14]. Under normal physiologic conditions, insulin biosynthesis is a multi-step process beginning with a pre-prohormone which is converted in the rough endoplasmatic reticulum to proinsulin within beta cells [15].…”

Section: Introductionmentioning

confidence: 99%

Roux-en-Y-Bariatric Surgery Reduces Markers of Metabolic Syndrome in Morbidly Obese Patients

et al. 2019

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Background Obesity is closely linked to increased markers of metabolic syndrome and development of diabetes. Roux-en-Y bariatric surgery reduces hyperinsulinemia and improves insulin sensitivity and hence benefits morbidly obese patients. Aim To determine changes in markers of metabolic syndrome, pancreatic function, and hepatic insulin sensitivity in patients before and 1 year after undergoing Roux-en-Y gastric bypass surgery. Methods We enrolled 43 consecutive patients in a single center. Markers for metabolic syndrome included proinsulin, insulin, Cpeptide, liver enzymes, and serum levels of selected microRNAs hsa-miR-122, hsa-miR-130, hsa-miR-132, and hsa-miR-375. Results After surgery, all patients showed a significant 37% drop of body mass index (p < 0.001). Furthermore, proinsulin (59% reduction, p < 0.001), insulin (76% reduction, p < 0.001), and C-peptide (56% reduction, p < 0.001) were all reduced 1 year after surgery. Using the hepatic insulin clearance score, we determined a significant increase in hepatic insulin clearance after surgery (76% increase, p < 0.001). Especially diabetic patients showed a marked 2.1-fold increase after surgery. Hepatic enzymes ALT (35% reduction, p = 0.002) and γGT (48% reduction, p < 0.001) were significantly reduced in all patients with similar improvement in diabetic and non-diabetic patients. miRNAs hsa-miR-122, hsa-miR-130, and hsa-miR-132 were all significantly reduced whereas hsa-miR-375 was increased after gastric bypass surgery (p < 0.001 for all miRNAs). Conclusion Both liver and pancreatic stress parameters were reduced significantly 1 year after Roux-en-Y gastric bypass surgery suggesting an overall amelioration of the metabolic syndrome in all patients regardless of previous health status.

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“…Similarly, the 96 . Since then, whereas one study confirmed this first finding 97 , others observed no change in pancreatic β-cell mass 98,99 post-BS. These diverging results might originate from the difficulty in directly assessing pancreatic tissue in humans.…”

Section: Changes In Hormones and Beta Cell Functionmentioning

confidence: 91%

“…These diverging results might originate from the difficulty in directly assessing pancreatic tissue in humans. Some groups have thus evaluated β-cell mass or function using tomography or magnetic resonance imaging to assess pancreatic triglyceride content 100 coupled with functional exploration (Cpeptide production and insulin sensibility) 99 . 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.…”

Section: Changes In Hormones and Beta Cell Functionmentioning

confidence: 99%

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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Adaptive changes in pancreas post Roux‐en‐Y gastric bypass induced weight loss

Cited by 18 publications

References 39 publications

Obesity-induced pancreatopathy in rats is reversible after bariatric surgery

Obesity-induced pancreatopathy in rats is reversible after bariatric surgery

Roux-en-Y-Bariatric Surgery Reduces Markers of Metabolic Syndrome in Morbidly Obese Patients

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

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