Current evidence for a role of GLP-1 in Roux-en-Y gastric bypass-induced remission of type 2 diabetes

2011 ◽  
Vol 14 (4) ◽  
pp. 291-298 ◽  
Author(s):  
N. A. Rhee ◽  
T. Vilsbøll ◽  
F. K. Knop
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Current Evidence

scholarly journals Role of Gut-Related Peptides and Other Hormones in the Amelioration of Type 2 Diabetes after Roux-en-Y Gastric Bypass Surgery

2012 ◽  
Vol 2012 ◽  
pp. 1-13 ◽  
Author(s):  
Mirella P. Hage ◽  
Bassem Safadi ◽  
Ibrahim Salti ◽  
Mona Nasrallah
Keyword(s):  
Type 2 Diabetes ◽  
Weight Loss ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Cell Function ◽  
Gastric Bypass Surgery ◽  
Gastrointestinal Hormones ◽  
Gut Peptides

Bariatric surgery is currently the most effective and durable therapy for obesity. Roux-en-Y gastric bypass surgery, the most commonly performed procedure worldwide, causes substantial weight loss and improvement in several comorbidities associated with obesity, especially type 2 diabetes. Several mechanisms are proposed to explain the improvement in glucose metabolism after RYGB surgery: the caloric restriction and weight loss per se, the improvement in insulin resistance and beta cell function, and finally the alterations in the various gastrointestinal hormones and adipokines that have been shown to play an important role in glucose homeostasis. However, the timing, exact changes of these hormones, and the relative importance of these changes in the metabolic improvement postbariatric surgery remain to be further clarified. This paper reviews the various changes post-RYGB in adipokines and gut peptides in subjects with T2D.

The role of obestatin in Roux-en-Y gastric bypass surgery in the obese, type 2 diabetes Zucker rat

2016 ◽  
Vol 119 ◽  
pp. 57-64 ◽  
Author(s):  
Xianhui Xu ◽  
Jianli Wang ◽  
Ling Li ◽  
Chunbin Wang ◽  
Weihua Li ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Gastric Bypass ◽  
Bypass Surgery ◽  
Gastric Bypass Surgery ◽  
Zucker Rat

scholarly journals Genetic Variance inUncoupling Protein 2in Relation to Obesity, Type 2 Diabetes, and Related Metabolic Traits: Focus on the Functional −866G>A Promoter Variant (rs659366)

2011 ◽  
Vol 2011 ◽  
pp. 1-12 ◽  
Author(s):  
Louise T. Dalgaard
Keyword(s):  
Type 2 Diabetes ◽  
Candidate Gene ◽  
Transcription Initiation ◽  
Current Evidence ◽  
Inner Mitochondrial Membrane ◽  
Obesity And Diabetes ◽  
Atp Generation ◽  
Glucose Stimulated Insulin Secretion

Uncoupling proteins (UCPs) are mitochondrial proteins able to dissipate the proton gradient of the inner mitochondrial membrane when activated. This decreases ATP-generation through oxidation of fuels and may theoretically decrease energy expenditure leading to obesity. Evidence fromUcp(−/−)mice revealed a role of UCP2 in the pancreaticβ-cell, becauseβ-cells without UCP2 had increased glucose-stimulated insulin secretion. Thus, from being a candidate gene for obesity UCP2 became a valid candidate gene for type 2 diabetes mellitus. This prompted a series of studies of the human UCP2 and UCP3 genes with respect to obesity and diabetes. Of special interest was a promoter variant of UCP2 situated 866bp upstream of transcription initiation (−866G>A, rs659366). This variant changes promoter activity and has been associated with obesity and/or type 2 diabetes in several, although not all, studies. The aim of the current paper is to summarize current evidence of association of UCP2 genetic variation with obesity and type 2 diabetes, with focus on the −866G>A polymorphism.

Sign in / Sign up

Export Citation Format

Share Document