orlistat improves release of gut hormones increasing satiety in obese women

Orlistat, which reduces fat absorption by inhibiting intestinal lipase is a registered drug for obesity pharmacotherapy. Meta-analyzes indicate various positive metabolic effects of orlistat, including improvements in glucose and lipid metabolism, lowering both systolic and diastolic blood pressure. It is assumed that orlistat can reduce postprandial satiety by inhibiting the release of intestinal hormones (incretins), especially glucagon-like peptide-1 (GLP-1). Impact analysis of the secretion of incretins, with prolonged use of orlistat was conducted. The aim of the study M.Olszanecka-Glinianowicz et al. was to evaluate the effect of 8 weeks of treatment with orlistat as part of a weight loss program for preprandialnye levels of peptide YY and GLP-1.

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Inhibition of gastric emptying by acarbose is correlated with GLP-1 response and accompanied by CCK release

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.2001.281.3.g752 ◽

2001 ◽

Vol 281 (3) ◽

pp. G752-G763 ◽

Cited By ~ 68

Author(s):

Feruze Y. Enç ◽

Neşe I˙meryüz ◽

Levent Akin ◽

Turgut Turoğlu ◽

Fuat Dede ◽

...

Keyword(s):

Gastric Emptying ◽

Peptide Yy ◽

Area Under The Curve ◽

Gut Hormones ◽

Random Order ◽

Mixed Meal ◽

Carbohydrate Absorption ◽

Plasma Response ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

We investigated the effect of acarbose, an α-glucosidase and pancreatic α-amylase inhibitor, on gastric emptying of solid meals of varying nutrient composition and plasma responses of gut hormones. Gastric emptying was determined with scintigraphy in healthy subjects, and all studies were performed with and without 100 mg of acarbose, in random order, at least 1 wk apart. Acarbose did not alter the emptying of a carbohydrate-free meal, but it delayed emptying of a mixed meal and a carbohydrate-free meal given 2 h after sucrose ingestion. In meal groups with carbohydrates, acarbose attenuated responses of plasma insulin and glucose-dependent insulinotropic polypeptide (GIP) while augmenting responses of CCK, glucagon-like peptide-1 (GLP-1), and peptide YY (PYY). With mixed meal + acarbose, area under the curve (AUC) of gastric emptying was positively correlated with integrated plasma response of GLP-1 ( r = 0.68 , P < 0.02). With the carbohydrate-free meal after sucrose and acarbose ingestion, AUC of gastric emptying was negatively correlated with integrated plasma response of GIP, implying that prior alteration of carbohydrate absorption modifies gastric emptying of a meal. The results demonstrate that acarbose delays gastric emptying of solid meals and augments release of CCK, GLP-1, and PYY mainly by retarding/inhibiting carbohydrate absorption. Augmented GLP-1 release by acarbose appears to play a major role in the inhibition of gastric emptying of a mixed meal, whereas CCK and PYY may have contributory roles.

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GLP-1: A Mediator of the Beneficial Metabolic Effects of Bariatric Surgery?

Physiology ◽

10.1152/physiol.00027.2014 ◽

2015 ◽

Vol 30 (1) ◽

pp. 50-62 ◽

Cited By ~ 20

Author(s):

Sean Manning ◽

Andrea Pucci ◽

Rachel L. Batterham

Keyword(s):

Bariatric Surgery ◽

Gastric Bypass ◽

Sleeve Gastrectomy ◽

Gut Hormones ◽

Metabolic Effects ◽

Physiological Changes ◽

Gut Hormone ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

There has been increasing interest in the role that gut hormones may play in contributing to the physiological changes produced by certain bariatric procedures, such as Roux-en-Y gastric bypass and sleeve gastrectomy. Here, we review the evidence implicating one such gut hormone, glucagon-like peptide-1, as a mediator of the metabolic benefits of these two procedures.

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Eating Slowly Increases the Postprandial Response of the Anorexigenic Gut Hormones, Peptide YY And Glucagon-Like Peptide-1

Yearbook of Medicine ◽

10.1016/s0084-3873(10)79819-9 ◽

2010 ◽

Vol 2010 ◽

pp. 529-530

Author(s):

R. Ness-Abramof

Keyword(s):

Peptide Yy ◽

Gut Hormones ◽

Postprandial Response ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

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Intestinal SGLT1 in metabolic health and disease

AJP Gastrointestinal and Liver Physiology ◽

10.1152/ajpgi.00068.2016 ◽

2016 ◽

Vol 310 (11) ◽

pp. G887-G898 ◽

Cited By ~ 27

Author(s):

Anders Lehmann ◽

Pamela J. Hornby

Keyword(s):

Metabolic Diseases ◽

Apical Membrane ◽

Peptide Yy ◽

Metabolic Effects ◽

New Class ◽

Health And Disease ◽

Glucose Exposure ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1

The Na+-glucose cotransporter 1 (SGLT1/SLC5A1) is predominantly expressed in the small intestine. It transports glucose and galactose across the apical membrane in a process driven by a Na+ gradient created by Na+-K+-ATPase. SGLT2 is the major form found in the kidney, and SGLT2-selective inhibitors are a new class of treatment for type 2 diabetes mellitus (T2DM). Recent data from patients treated with dual SGLT1/2 inhibitors or SGLT2-selective drugs such as canagliflozin (SGLT1 IC50 = 663 nM) warrant evaluation of SGLT1 inhibition for T2DM. SGLT1 activity is highly dynamic, with modulation by multiple mechanisms to ensure maximal uptake of carbohydrates (CHOs). Intestinal SGLT1 inhibition lowers and delays the glucose excursion following CHO ingestion and augments glucagon-like peptide-1 (GLP-1) and peptide YY (PYY) secretion. The latter is likely due to increased glucose exposure of the colonic microbiota and formation of metabolites such as L cell secretagogues. GLP-1 and PYY secretion suppresses food intake, enhances the ileal brake, and has an incretin effect. An increase in colonic microbial production of propionate could contribute to intestinal gluconeogenesis and mediate positive metabolic effects. On the other hand, a threshold of SGLT1 inhibition that could lead to gastrointestinal intolerability is unclear. Altered Na+ homeostasis and increased colonic CHO may result in diarrhea and adverse gastrointestinal effects. This review considers the potential mechanisms contributing to positive metabolic and negative intestinal effects. Compounds that inhibit SGLT1 must balance the modulation of these mechanisms to achieve therapeutic efficacy for metabolic diseases.

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Mechanisms of oleoylethanolamide-induced changes in feeding behavior and motor activity

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00029.2005 ◽

2005 ◽

Vol 289 (3) ◽

pp. R729-R737 ◽

Cited By ~ 61

Author(s):

Karine Proulx ◽

Daniela Cota ◽

Tamara R. Castañeda ◽

Matthias H. Tschöp ◽

David A. D'Alessio ◽

...

Keyword(s):

Food Intake ◽

Motor Activity ◽

Peptide Yy ◽

Metabolic Effects ◽

Peroxisome Proliferator ◽

Peroxisome Proliferator Activated Receptor ◽

Apolipoprotein A ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Induced Changes

Oleoylethanolamide (OEA), a lipid synthesized in the intestine, reduces food intake and stimulates lipolysis through peroxisome proliferator-activated receptor-α. OEA also activates transient receptor potential vanilloid type 1 (TRPV1) in vitro. Because the anorexigenic effect of OEA is associated with delayed feeding onset and reduced locomotion, we examined whether intraperitoneal administration of OEA results in nonspecific behavioral effects that contribute to the anorexia in rats. Moreover, we determined whether circulating levels of other gut hormones are modulated by OEA and whether CCK is involved in OEA-induced anorexia. Our results indicate that OEA reduces food intake without causing a conditioned taste aversion or reducing sodium appetite. It also failed to induce a conditioned place aversion. However, OEA induced changes in posture and reduced spontaneous activity in the open field. This likely underlies the reduced heat expenditure and sodium consumption observed after OEA injection, which disappeared within 1 h. The effects of OEA on motor activity were similar to those of the TRPV1 agonist capsaicin and were also observed with the peroxisome proliferator-activated receptor-α agonist Wy-14643. Plasma levels of ghrelin, peptide YY, glucagon-like peptide 1, and apolipoprotein A-IV were not changed by OEA. Finally, antagonism of CCK-1 receptors did not affect OEA-induced anorexia. These results suggest that OEA suppresses feeding without causing visceral illness and that neither ghrelin, peptide YY, glucagon-like peptide 1, apolipoprotein A-IV, nor CCK plays a critical role in this effect. Despite that OEA-induced anorexia is unlikely to be due to impaired motor activity, our data raise a cautionary note in how specific behavioral and metabolic effects of OEA should be interpreted.

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Effects of Ramadan Intermittent Fasting on Gut Hormones and Body Composition in Males with Obesity

International Journal of Environmental Research and Public Health ◽

10.3390/ijerph17155600 ◽

2020 ◽

Vol 17 (15) ◽

pp. 5600 ◽

Cited By ~ 1

Author(s):

Hassane Zouhal ◽

Reza Bagheri ◽

Raoua Triki ◽

Ayoub Saeidi ◽

Alexei Wong ◽

...

Keyword(s):

Body Composition ◽

Peptide Yy ◽

Gut Hormones ◽

Control Group ◽

Intermittent Fasting ◽

Ramadan Fasting ◽

Blood Samples ◽

Glucagon Like Peptide ◽

Glucagon Like Peptide 1 ◽

Experimental Group

We studied the effects of Ramadan intermittent fasting (RIF) on gut hormones (leptin, glucagon-like peptide-1 (GLP-1), peptide YY (PYY), cholecystokinin (CCK), and ghrelin) in males with obesity. Thirty sedentary males were randomly allocated to either an experimental group (EG, n = 15) or a control group (CG, n = 15). The EG group completed their Ramadan fasting rituals (30 days), whereas the CG continued with their normal daily habits. Blood samples were collected at four time points: 24 h before the start of Ramadan (T0), on the 15th day of Ramadan (T1), the day after the end of Ramadan (T2) and 21 days after Ramadan (T3). There were significant pre-to-post improvements for leptin (p = 0.01, d = 1.52), GLP-1 (p = 0.022, d = 0.75), PYY (p = 0.031, d = 0.69) and CCK (p = 0.027, d = 0.81) in the EG, with no interaction effect for ghrelin (p = 0.74; d = 0.008). No significant changes (p > 0.05) occurred in plasma volume variations (ΔPV) after RIF in both EG (−0.03 ± 0.01%) and CG (0.06 ± 0.07%). RIF represents an effective strategy to modify appetite-regulating hormones, leading to improved body composition indices and reduced obesity.

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