scholarly journals A Surgical Model in Male Obese Rats Uncovers Protective Effects of Bile Acids Post-Bariatric Surgery

Endocrinology ◽  
2013 ◽  
Vol 154 (7) ◽  
pp. 2341-2351 ◽  
Author(s):  
Rohit Kohli ◽  
Kenneth DR Setchell ◽  
Michelle Kirby ◽  
Andriy Myronovych ◽  
Karen K. Ryan ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Bile Acid ◽  
Glucose Tolerance ◽  
Er Stress ◽  
Bile Acids ◽  
Hepatic Steatosis ◽  
Homologous Protein ◽  
Obese Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Abstract Bariatric surgery elevates serum bile acids. Conjugated bile acid administration, such as tauroursodeoxycholic acid (TUDCA), improves insulin sensitivity, whereas short-circuiting bile acid circulation through ileal interposition surgery in rats raises TUDCA levels. We hypothesized that bariatric surgery outcomes could be recapitulated by short circuiting the normal enterohepatic bile circulation. We established a model wherein male obese rats underwent either bile diversion (BD) or Sham (SH) surgery. The BD group had a catheter inserted into the common bile duct and its distal end anchored into the middistal jejunum for 4–5 weeks. Glucose tolerance, insulin and glucagon-like peptide-1 (GLP-1) response, hepatic steatosis, and endoplasmic reticulum (ER) stress were measured. Rats post-BD lost significantly more weight than the SH rats. BD rats gained less fat mass after surgery. BD rats had improved glucose tolerance, increased higher postprandial glucagon-like peptide-1 response and serum bile acids but less liver steatosis. Serum bile acid levels including TUDCA concentrations were higher in BD compared to SH pair-fed rats. Fecal bile acid levels were not different. Liver ER stress (C/EBP homologous protein mRNA and pJNK protein) was decreased in BD rats. Bile acid gavage (TUDCA/ursodeoxycholic acid [UDCA]) in diet-induced obese rats, elevated serum TUDCA and concomitantly reduced hepatic steatosis and ER stress (C/EBP homologous protein mRNA). These data demonstrate the ability of alterations in bile acids to recapitulate important metabolic improvements seen after bariatric surgery. Further, our work establishes a model for focused study of bile acids in the context of bariatric surgery that may lead to the identification of therapeutics for metabolic disease.

Bile-induced secretion of glucagon-like peptide-1: pathophysiological implications in type 2 diabetes?

2010 ◽  
Vol 299 (1) ◽  
pp. E10-E13 ◽  
Author(s):  
Filip K. Knop
Keyword(s):  
Bile Acid ◽  
Bile Acids ◽  
Intestinal Secretion ◽  
Postprandial Glucose ◽  
Glucose Lowering ◽  
Incretin Hormone ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

During the last decades it has become clear that bile acids not only act as simple fat solubilizers, but additionally represent complex hormonal metabolic integrators. Bile acids activate both nuclear receptors (controlling transcription of genes involved in for example bile acid, cholesterol, and glucose metabolism) and the cell surface G protein-coupled receptor TGR5 (modulating energy expenditure in brown fat and muscle cells). It has been shown that TGR5 is expressed in enteroendocrine L cells, which secrete the potent glucose-lowering incretin hormone glucagon-like peptide-1 (GLP-1). Recently it was shown that bile acid-induced activation of TGR5 results in intestinal secretion of GLP-1 and that enhanced TGR5 signaling improves postprandial glucose tolerance in diet-induced obese mice. This Perspectives article presents these novel findings in the context of prior studies on nutrient-induced GLP-1 secretion and outlines the potential implications of bile acid-induced GLP-1 secretion in physiological, pathophysiological, and pharmacological perspectives.

scholarly journals Bariatric surgery induces a new gastric mucosa phenotype with increased functional glucagon-like peptide-1 expressing cells

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Lara Ribeiro-Parenti ◽  
Anne-Charlotte Jarry ◽  
Jean-Baptiste Cavin ◽  
Alexandra Willemetz ◽  
Johanne Le Beyec ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Gastric Mucosa ◽  
Human Stomach ◽  
Vertical Sleeve Gastrectomy ◽  
Dipeptidyl Peptidase 4 ◽  
Rapid Inactivation ◽  
Obese Rats ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Portal Veins

AbstractGlucagon-Like Peptide-1 (GLP-1) undergoes rapid inactivation by dipeptidyl peptidase-4 (DPP4) suggesting that target receptors may be activated by locally produced GLP-1. Here we describe GLP-1 positive cells in the rat and human stomach and found these cells co-expressing ghrelin or somatostatin and able to secrete active GLP-1 in the rats. In lean rats, a gastric load of glucose induces a rapid and parallel rise in GLP-1 levels in both the gastric and the portal veins. This rise in portal GLP-1 levels was abrogated in HFD obese rats but restored after vertical sleeve gastrectomy (VSG) surgery. Finally, obese rats and individuals operated on Roux-en-Y gastric bypass and SG display a new gastric mucosa phenotype with hyperplasia of the mucus neck cells concomitant with increased density of GLP-1 positive cells. This report brings to light the contribution of gastric GLP-1 expressing cells that undergo plasticity changes after bariatric surgeries, to circulating GLP-1 levels.

Effect of bariatric surgery on serum glucagon like peptide-1 concentration and metabolic parameters among obese type 2 diabetics

2013 ◽  
Author(s):  
Salah El Din Shelbaya ◽  
Alaa Abbas Mostafa ◽  
Salwa Seddik ◽  
Manal M. Abu Shady ◽  
Meram M. Bekhet ◽  
...  
Keyword(s):  
Bariatric Surgery ◽  
Metabolic Parameters ◽  
Type 2 Diabetics ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

scholarly journals Bile acids drive colonic secretion of glucagon-like-peptide 1 and peptide-YY in rodents

2019 ◽  
Vol 316 (5) ◽  
pp. G574-G584 ◽  
Author(s):  
Charlotte Bayer Christiansen ◽  
Samuel Addison Jack Trammell ◽  
Nicolai Jacob Wewer Albrechtsen ◽  
Kristina Schoonjans ◽  
Reidar Albrechtsen ◽  
...  
Keyword(s):  
Bile Acids ◽  
G Protein ◽  
Peptide Yy ◽  
Whole Body ◽  
Rat Colon ◽  
G Protein Coupled Receptor ◽  
L Cells ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
G Protein Coupled

A large number of glucagon-like-peptide-1 (GLP-1)- and peptide-YY (PYY)-producing L cells are located in the colon, but little is known about their contribution to whole body metabolism. Since bile acids (BAs) increase GLP-1 and PYY release, and since BAs spill over from the ileum to the colon, we decided to investigate the ability of BAs to stimulate colonic GLP-1 and PYY secretion. Using isolated perfused rat/mouse colon as well as stimulation of the rat colon in vivo, we demonstrate that BAs significantly enhance secretion of GLP-1 and PYY from the colon with average increases of 3.5- and 2.9-fold, respectively. Furthermore, we find that responses depend on BA absorption followed by basolateral activation of the BA-receptor Takeda-G protein-coupled-receptor 5. Surprisingly, the apical sodium-dependent BA transporter, which serves to absorb conjugated BAs, was not required for colonic conjugated BA absorption or conjugated BA-induced peptide secretion. In conclusion, we demonstrate that BAs represent a major physiological stimulus for colonic L-cell secretion.NEW & NOTEWORTHY By the use of isolated perfused rodent colon preparations we show that bile acids are potent and direct promoters of colonic glucagon-like-peptide 1 and peptide-YY secretion. The study provides convincing evidence that basolateral Takeda-G protein-coupled-receptor 5 activation is mediating the effects of bile acids in the colon and thus add to the existing literature described for L cells in the ileum.

scholarly journals Single-Dose Metformin Enhances Bile Acid–Induced Glucagon-Like Peptide-1 Secretion in Patients With Type 2 Diabetes

2017 ◽  
Vol 102 (11) ◽  
pp. 4153-4162 ◽  
Author(s):  
Andreas Brønden ◽  
Anders Albér ◽  
Ulrich Rohde ◽  
Jens F Rehfeld ◽  
Jens J Holst ◽  
...  
Keyword(s):  
Type 2 Diabetes ◽  
Single Dose ◽  
Bile Acid ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1

Bile acid supplementation improves established liver steatosis in obese mice independently of glucagon-like peptide-1 secretion

2014 ◽  
Vol 70 (3) ◽  
pp. 667-674 ◽  
Author(s):  
Pablo Quintero ◽  
Margarita Pizarro ◽  
Nancy Solís ◽  
Juan Pablo Arab ◽  
Oslando Padilla ◽  
...  
Keyword(s):  
Bile Acid ◽  
Liver Steatosis ◽  
Obese Mice ◽  
Acid Supplementation ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1
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