scholarly journals High β-Glucan Barley Supplementation Improves Glucose Tolerance by Increasing GLP-1 Secretion in Diet-Induced Obesity Mice

Nutrients ◽  
2021 ◽  
Vol 13 (2) ◽  
pp. 527
Author(s):  
Sachina Suzuki ◽  
Seiichiro Aoe
Keyword(s):  
Glucose Tolerance ◽  
Portal Vein ◽  
Cell Function ◽  
Cell Number ◽  
Gas Chromatography Mass Spectrometry ◽  
Enzyme Linked Immunosorbent Assay ◽  
Control Group ◽  
Oral Glucose ◽  
L Cells ◽  
L Cell

The aim of this study was to investigate the underlying mechanism for the improvement of glucose tolerance following intake of high β-glucan barley (HGB) in terms of intestinal metabolism. C57BL/6J male mice were fed a fatty diet supplemented with HGB corresponding to 5% of dietary fiber for 83 days. An oral glucose tolerance test was performed at the end of the experimental period. The concentration of short-chain fatty acids (SCFAs) in the cecum was analyzed by GC–MS (gas chromatography–mass spectrometry). The mRNA expression levels related to L cell function in the ileum were measured by real-time PCR. Glucagon-like peptide-1 (GLP-1) levels in the portal vein and cecal content were assessed by enzyme-linked immunosorbent assay. GLP-1-producing L cells of the ileum were quantified by immunohistochemistry. HGB intake improved glucose tolerance and increased the cecal levels of SCFAs, acetate, and propionate. The number of GLP-1-positive L cells in the HGB group was significantly higher than in the control group. GLP-1 levels in the portal vein and cecal GLP-1 pool size in the HGB group were significantly higher than the control group. In conclusion, we report improved glucose tolerance after HGB intake induced by an increase in L cell number and subsequent rise in GLP-1 secretion.

scholarly journals The Protective Role of Hydrogen Sulfide Against Obesity-Associated Cellular Stress in Blood Glucose Regulation

Antioxidants ◽  
2020 ◽  
Vol 9 (11) ◽  
pp. 1038
Author(s):  
Ania Mezouari ◽  
Radhika Nangia ◽  
Jeffrey Gagnon
Keyword(s):  
Oxidative Stress ◽  
Hydrogen Sulfide ◽  
Blood Glucose ◽  
Cell Function ◽  
Fasting Blood Glucose ◽  
Protective Role ◽  
Oral Glucose ◽  
Chow Diet ◽  
L Cells ◽  
L Cell

Circulating palmitic acid (PA) is increased in obesity and causes metabolic stress, leading to diabetes. This includes the impairment of the glucoregulatory hormone glucagon-like peptide-1 (GLP-1) secreted from intestinal L-cells. Recently, the anti-inflammatory gasotransmitter hydrogen sulfide (H2S) has been implicated in the enhancement of GLP-1 secretion. We hypothesized that H2S can reduce the oxidative stress caused by palmitate and play a protective role in L-cell function. This study was conducted on both human and mouse L-cells and a mouse model of Western diet (WD)-induced obesity. PA-induced L-cell stress was assessed using DCF-DA. H2S was delivered using the donor GYY4137. C57BL/6 mice were fed either chow diet or PA-enriched WD for 20 weeks with ongoing measurements of glycemia and GLP-1 secretion. In both L-cell models, we demonstrated that PA caused an increase in reactive oxygen species (ROS). This ROS induction was partially blocked by the H2S administration. In mice, the WD elevated body weight in both sexes and elevated fasting blood glucose and lipid peroxidation in males. Additionally, a single GYY4137 injection improved oral glucose tolerance in WD-fed male mice and also enhanced glucose-stimulated GLP-1 release. To conclude, H2S reduces oxidative stress in GLP-1 cells and can improve glucose clearance in mice.

Glucose metabolism is altered after loss of L cells and α-cells but not influenced by loss of K cells

2013 ◽  
Vol 304 (1) ◽  
pp. E60-E73 ◽  
Author(s):  
J Pedersen ◽  
R. K. Ugleholdt ◽  
S. M. Jørgensen ◽  
J. A. Windeløv ◽  
K. V. Grunddal ◽  
...  
Keyword(s):  
Glucose Metabolism ◽  
Glucose Tolerance ◽  
Diphtheria Toxin ◽  
Cell Mass ◽  
Cell Loss ◽  
Oral Glucose ◽  
Proximal Jejunum ◽  
K Cells ◽  
L Cells ◽  
L Cell

The enteroendocrine K and L cells are responsible for secretion of glucose-dependent insulinotropic polypeptide (GIP) and glucagon like-peptide 1 (GLP-1), whereas pancreatic α-cells are responsible for secretion of glucagon. In rodents and humans, dysregulation of the secretion of GIP, GLP-1, and glucagon is associated with impaired regulation of metabolism. This study evaluates the consequences of acute removal of Gip- or Gcg-expressing cells on glucose metabolism. Generation of the two diphtheria toxin receptor cellular knockout mice, TgN(GIP.DTR) and TgN(GCG.DTR), allowed us to study effects of acute ablation of K and L cells and α-cells. Diphtheria toxin administration reduced the expression of Gip and content of GIP in the proximal jejunum in TgN(GIP.DTR) and expression of Gcg and content of proglucagon-derived peptides in both proximal jejunum and terminal ileum as well as content of glucagon in pancreas in TgN(GCG.DTR) compared with wild-type mice. GIP response to oral glucose was attenuated following K cell loss, but oral and intraperitoneal glucose tolerances were unaffected. Intraperitoneal glucose tolerance was impaired following combined L cell and α-cell loss and normal following α-cell loss. Oral glucose tolerance was improved following L cell and α-cell loss and supernormal following α-cell loss. We present two mouse models that allow studies of the effects of K cell or L cell and α-cell loss as well as isolated α-cell loss. Our findings show that intraperitoneal glucose tolerance is dependent on an intact L cell mass and underscore the diabetogenic effects of α-cell signaling. Furthermore, the results suggest that K cells are less involved in acute regulation of mouse glucose metabolism than L cells and α-cells.

Antidiabetic Effects of Ethanolic Extract of Ficus glomerata (L.) Roots

2020 ◽  
Vol 16 (1) ◽  
pp. 33-41
Author(s):  
Mohini C. Upadhye ◽  
Uday Deokate ◽  
Rohini Pujari ◽  
Vishnu Thakare
Keyword(s):  
Body Weight ◽  
Glucose Tolerance ◽  
Density Lipoprotein ◽  
Ethanolic Extract ◽  
Tolerance Test ◽  
Diabetic Rats ◽  
Antidiabetic Activity ◽  
Control Group ◽  
Oral Glucose ◽  
Ficus Glomerata

Background: Ficus glomerata (F. glomerata) Linn. Family Moraceace is a large tree found all over India including outer Himalayan ranges, Punjab, Chota Nagpur, Bihar, Orissa, West Bengal, Rajasthan, Deccan and also as a common plant in South India. It is planted around the home and temples. It is cultivated throughout the year, distributed in evergreen forests and moist localities. Objective: The Ethanolic Extract of roots of F. Glomerata (EEFG) belonging to the family Moraceace, was investigated for its antidiabetic activity using alloxan induced diabetic rats. Methods: Thirty rats were divided into 5 groups having 6 rats in each group. The alloxan was administered to the rats of all groups except normal control group through intraperitoneal route at a concentration of 140mg/kg body weight. A dose of 100mg/kg and 200 mg/kg body weight of EEFG was administered to alloxan induced diabetic rats. The administration of the extract was lasted for 11 days. Effectiveness of the extract on glucose, cholesterol, triglycerides, and high density lipoprotein and protein concentrations was analyzed. Results: Significant (p<0.05) reduction in the levels of glucose, cholesterol, triglyceride of the diabetic rats was observed after treatment with ethanolic extract. After subjecting to oral glucose tolerance test EEFG also showed significant improvement in glucose tolerance. Conclusion: F. glomerata root ethanolic extract showed that it possesses antidiabetic effect and can be found useful for the management of diabetes mellitus.

scholarly journals Fructose Consumption Contributes to Hyperinsulinemia in Adolescents With Obesity Through a GLP-1–Mediated Mechanism

2019 ◽  
Vol 104 (8) ◽  
pp. 3481-3490 ◽  
Author(s):  
Alfonso Galderisi ◽  
Cosimo Giannini ◽  
Michelle Van Name ◽  
Sonia Caprio
Keyword(s):  
Glucose Tolerance ◽  
Mixed Model ◽  
Linear Mixed Model ◽  
Cell Function ◽  
Insulin Response ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Double Blind ◽  
Obesity And Diabetes ◽  
Glucose Ingestion

Abstract Context The consumption of high-fructose beverages is associated with a higher risk for obesity and diabetes. Fructose can stimulate glucagon-like peptide 1 (GLP-1) secretion in lean adults, in the absence of any anorexic effect. Objective We hypothesized that the ingestion of glucose and fructose may differentially stimulate GLP-1 and insulin response in lean adolescents and adolescents with obesity. Design We studied 14 lean adolescents [four females; 15.9 ± 1.6 years of age; body mass index (BMI), 21.8 ± 2.2 kg/m2] and 23 adolescents with obesity (five females; 15.1 ± 1.6 years of age; BMI, 34.5 ± 4.6 kg/m2). Participants underwent a baseline oral glucose tolerance test to determine their glucose tolerance and estimate insulin sensitivity and β-cell function [oral disposition index (oDIcpep)]. Eligible subjects received, in a double-blind, crossover design, 75 g of glucose or fructose. Plasma was obtained every 10 minutes for 60 minutes for the measures of glucose, insulin, and GLP-1 (radioimmunoassay) and glucose-dependent insulinotropic polypeptide (GIP; ELISA). Incremental glucose and hormone levels were compared between lean individuals and those with obesity by a linear mixed model. The relationship between GLP-1 increment and oDIcpep was evaluated by regression analysis. Results Following the fructose challenge, plasma glucose excursions were similar in both groups, yet the adolescents with obesity exhibited a greater insulin (P &lt; 0.001) and GLP-1 (P &lt; 0.001) increase than did their lean peers. Changes in GIP were similar in both groups. After glucose ingestion, the GLP-1 response (P &lt; 0.001) was higher in the lean group. The GLP-1 increment during 60 minutes from fructose drink was correlated with a lower oDIcpep (r2 = 0.22, P = 0.009). Conclusion Fructose, but not glucose, ingestion elicits a higher GLP-1 and insulin response in adolescents with obesity than in lean adolescents. Fructose consumption may contribute to the hyperinsulinemic phenotype of adolescent obesity through a GLP-1–mediated mechanism.

scholarly journals Effects of Sucralose Ingestion versus Sucralose Taste on Metabolic Responses to an Oral Glucose Tolerance Test in Participants with Normal Weight and Obesity: A Randomized Crossover Trial

Nutrients ◽  
2019 ◽  
Vol 12 (1) ◽  
pp. 29 ◽  
Author(s):  
Alexander D. Nichol ◽  
Clara Salame ◽  
Kristina I. Rother ◽  
M. Yanina Pepino
Keyword(s):  
Glucose Tolerance ◽  
Cell Function ◽  
Normal Weight ◽  
Taste Perception ◽  
Metabolic Responses ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Β Cell ◽  
Β Cell Function ◽  
Weight Groups

Here, we tested the hypothesis that sucralose differentially affects metabolic responses to labeled oral glucose tolerance tests (OGTTs) in participants with normal weight and obesity. Participants (10 with normal weight and 11 with obesity) without diabetes underwent three dual-tracer OGTTs preceded, in a randomized order, by consuming sucralose or water, or by tasting and expectorating sucralose (e.g., sham-fed; sweetness control). Indices of β-cell function and insulin sensitivity (SI) were estimated using oral minimal models of glucose, insulin, and C-peptide kinetics. Compared with water, sucralose ingested (but not sham-fed) resulted in a 30 ± 10% increased glucose area under the curve in both weight groups. In contrast, the insulin response to sucralose ingestion differed depending on the presence of obesity: decreased within 20–40 min of the OGTT in normal-weight participants but increased within 90–120 min in participants with obesity. Sham-fed sucralose similarly decreased insulin concentrations within 60 min of the OGTT in both weight groups. Sucralose ingested (but not sham-fed) increased SI in normal-weight participants by 52 ± 20% but did not affect SI in participants with obesity. Sucralose did not affect glucose rates of appearance or β-cell function in either weight group. Our data underscore a physiological role for taste perception in postprandial glucose responses, suggesting sweeteners should be consumed in moderation.

scholarly journals Insulin secretion-independent effects of GLP-1 on canine liver glucose metabolism do not involve portal vein GLP-1 receptors

2005 ◽  
Vol 289 (5) ◽  
pp. G806-G814 ◽  
Author(s):  
Dominique Dardevet ◽  
Mary Courtney Moore ◽  
Catherine A. DiCostanzo ◽  
Ben Farmer ◽  
Doss W. Neal ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Portal Vein ◽  
Glucose Disposal ◽  
Control Group ◽  
Oral Glucose ◽  
Oral Glucose Tolerance Testing ◽  
Hyperglycemic Clamp ◽  
Independent Effects ◽  
Hepatic Portal

Whether glucagon-like peptide (GLP)-1 requires the hepatic portal vein to elicit its insulin secretion-independent effects on glucose disposal in vivo was assessed in conscious dogs using tracer and arteriovenous difference techniques. In study 1, six conscious overnight-fasted dogs underwent oral glucose tolerance testing (OGTT) to determine target GLP-1 concentrations during clamp studies. Peak arterial and portal values during OGTT ranged from 23 to 65 pM and from 46 to 113 pM, respectively. In study 2, we conducted hyperinsulinemic-hyperglycemic clamp experiments consisting of three periods (P1, P2, and P3) during which somatostatin, glucagon, insulin and glucose were infused. The control group received saline, the PePe group received GLP-1 (1 pmol·kg−1·min−1) peripherally, the PePo group received GLP-1 (1 pmol·kg−1·min−1) peripherally (P2) and then intraportally (P3), and the PeHa group received GLP-1 (1 pmol·kg−1·min−1) peripherally (P2) and then through the hepatic artery (P3) to increase the hepatic GLP-1 load to the same extent as in P3 in the PePo group ( n = 8 dogs/group). Arterial GLP-1 levels increased similarly in all groups during P2 (∼50 pM), whereas portal GLP-1 levels were significantly increased (2-fold) in the PePo vs. PePe and PeHa groups during P3. During P2, net hepatic glucose uptake (NHGU) increased slightly but not significantly (vs. P1) in all groups. During P3, GLP-1 increased NHGU in the PePo and PeHa groups more than in the control and PePe groups (change of 10.8 ± 1.3 and 10.6 ± 1.0 vs. 5.7 ± 1.0 and 5.4 ± 0.8 μmol·kg−1·min−1, respectively, P < 0.05). In conclusion, physiological GLP-1 levels increase glucose disposal in the liver, and this effect does not involve GLP-1 receptors located in the portal vein.

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