Roux-en-Y gastric bypass (RYGB) results in rapid weight loss, reduced adiposity, and improved glucose metabolism. These effects are not simply attributable to decreased caloric intake or absorption, but the mechanisms linking rearrangement of the gastrointestinal tract to these metabolic outcomes are largely unknown. Studies in humans and rats have shown that RYGB restructures the gut microbiota, prompting the hypothesis that some of the effects of RYGB are caused by altered host-microbial interactions. To test this hypothesis, we used a mouse model of RYGB that recapitulates many of the metabolic outcomes in humans. 16S ribosomal RNA gene sequencing of murine fecal samples collected after RYGB surgery, sham surgery, or sham surgery coupled to caloric restriction revealed that alterations to the gut microbiota after RYGB are conserved among humans, rats, and mice, resulting in a rapid and sustained increase in the relative abundance of Gammaproteobacteria (Escherichia) and Verrucomicrobia (Akkermansia). These changes were independent of weight change and caloric restriction, were detectable throughout the length of the gastrointestinal tract, and were most evident in the distal gut, downstream of the surgical manipulation site. Transfer of the gut microbiota from RYGB-treated mice to nonoperated, germ-free mice resulted in weight loss and decreased fat mass in the recipient animals relative to recipients of microbiota induced by sham surgery, potentially due to altered microbial production of short-chain fatty acids. These findings provide the first empirical support for the claim that changes in the gut microbiota contribute to reduced host weight and adiposity after RYGB surgery.

/pdf/conserved-shifts-in-the-gut-microbiota-due-to-gastric-bypass-32i3genqkl.pdf

Conserved Shifts in the Gut Microbiota Due to Gastric Bypass Reduce Host Weight and Adiposity

Mechanisms of early improvement / resolution of type 2 diabetes after bariatric surgery

In this “clinical” contribution to the Bench to Clinic Symposia, we will show data to support the hypothesis that fasting hyperinsulinemia is the initial underlying cause of type 2 diabetes mellitus (T2DM) and that the remission of the disease following bariatric surgery may be due to the correction of hyperinsulinemia. The intent of this article is to elicit critical thinking about the pathophysiology of T2DM in view of the effects of surgery and to open debate. If our hypothesis is correct, then more research resources should be focused on the cause(s) of fasting hyperinsulinemia and the therapies that may correct it.

The study of diabetes has always focused on glucose. Whether the diagnosis was made by the attraction of flies to urine as described in ancient India in 1552 BC (1), the sweet taste of the urine noted by Shushruta in 400 BC (2), or our current dependence on fasting blood glucose levels, HbA1c, and glucose tolerance curves, the severity of the disease is still measured by the level of hyperglycemia.

Similarly, our therapeutic directions also aim, almost exclusively, to reverse the hyperglycemia. In 1921 when Banting and Best reported that a pancreatic extract reversed the soaring glucose levels following a pancreatectomy in a dog, the use of insulin spread rapidly to children and adults alike. By the time Sir Harold Percival Himsworth noted, in 1936, that there were at least two types of diabetes (3), the objectives of T2DM treatment were already set; goals that still continue today. Even though type 1 diabetes mellitus (T1DM) and T2DM are virtually two opposite diseases, i.e., a total lack of insulin production versus abnormally high levels, the therapeutic goals for both entities continue to be the same: lower glucose levels by 1 ) giving insulin, 2 ) increasing insulin production, and/or 3 …

https://care.diabetesjournals.org/content/diacare/35/12/2438.full.pdf

Diabetes: Have We Got It All Wrong? Hyperinsulinism as the culprit: surgery provides the evidence

Osteoarthritis (OA) has become a major public health problem not only because of its increasing prevalence worldwide but also because of its frequent association with cardiovascular disease, the leading cause of death in industrialized countries. There is growing evidence that OA is not simply a disease related to aging or mechanical stress of joints but rather a "metabolic disorder" in which various interrelated lipid, metabolic, and humoral mediators contribute to the initiation and progression of the disease process. Indeed, OA has been linked not only to obesity but also to other cardiovascular risk factors, namely, diabetes, dyslipidemia, hypertension, and insulin resistance.

Osteoarthritis: Another Component of Metabolic Syndrome?

BACKGROUND. Roux-en-Y gastric bypass (RYGB) surgery causes profound weight loss and improves insulin sensitivity (SI) in obese patients. Regular exercise can also improve SI in obese individuals; however, it is unknown whether exercise and RYGB surgery–induced weight loss would additively improve SI and other cardiometabolic factors.

METHODS. We conducted a single-blind, prospective, randomized trial with 128 men and women who recently underwent RYGB surgery (within 1–3 months). Participants were randomized to either a 6-month semi-supervised moderate exercise protocol (EX, n = 66) or a health education control (CON; n = 62) intervention. Main outcomes measured included SI and glucose effectiveness (SG), which were determined from an intravenous glucose tolerance test and minimal modeling. Secondary outcomes measured were cardiorespiratory fitness (VO2 peak) and body composition. Data were analyzed using an intention-to-treat (ITT) and per-protocol (PP) approach to assess the efficacy of the exercise intervention (>120 min of exercise/week).

RESULTS. 119 (93%) participants completed the interventions, 95% for CON and 91% for EX. There was a significant decrease in body weight and fat mass for both groups (P < 0.001 for time effect). SI improved in both groups following the intervention (ITT: CON vs. EX; +1.64 vs. +2.24 min–1/μU/ml, P = 0.18 for Δ, P < 0.001 for time effect). A PP analysis revealed that exercise produced an additive SI improvement (PP: CON vs. EX; +1.57 vs. +2.69 min–1/μU/ml, P = 0.019) above that of surgery. Exercise also improved SG (ITT: CON vs. EX; +0.0023 vs. +0.0063 min–1, P = 0.009) compared with the CON group. Exercise improved cardiorespiratory fitness (VO2 peak) compared with the CON group.

CONCLUSION. Moderate exercise following RYGB surgery provides additional improvements in SI, SG, and cardiorespiratory fitness compared with a sedentary lifestyle during similar weight loss.

TRIAL REGISTRATION. clinicaltrials.gov identifier: {"type":"clinical-trial","attrs":{"text":"NCT00692367","term_id":"NCT00692367"}}NCT00692367.

FUNDING. This study was funded by the NIH/National Institute of Diabetes and Digestive and Kidney Diseases (R01 DK078192) and an NIH/National Center for Research Resources/Clinical and Translational Science Award (UL1 RR024153).

/pdf/clinical-trial-demonstrates-exercise-following-bariatric-4fra0rla83.pdf

Clinical trial demonstrates exercise following bariatric surgery improves insulin sensitivity

Department of Endocrinology-Metabolism, School of Medicine, Catholic University, Daegu, Korea Address correspondence to: G. Lynis Dohm, Ph.D. Department of Physiology Brody School of Medicine East Carolina University 6N98 600 Moye Blvd Greenville, NC 27834 Tel: (252) 744-2682 Fax: (252) 744-3460 E-mail: dohmg@ecu.edu Disclosure Statement: The authors have nothing to disclose. Keywords: Gastric Bypass, Insulin Sensitivity, Glucose Transport, BMI, IKKβSupport: This work was supported by NIH grant R01 DK046121 (to G.L.D.). Word count (text): 3,742 Word count (abstract): 236 Tables: 1 Figures: 9

MECHANISM FOR IMPROVED INSULIN SENSITIVITY AFTER GASTRIC BYPASS SURGERY Short Title: Gastric Bypass and Insulin Sensitivity

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MECHANISM FOR IMPROVED INSULIN SENSITIVITY AFTER GASTRIC BYPASS SURGERY Short Title: Gastric Bypass and Insulin Sensitivity