scholarly journals Involvement of endogenous glucagon-like peptide-1(7–36) amide on glycaemia-lowering effect of oligofructose in streptozotocin-treated rats

2005 ◽  
Vol 185 (3) ◽  
pp. 457-465 ◽  
Author(s):  
Patrice D Cani ◽  
Catherine A Daubioul ◽  
Brigitte Reusens ◽  
Claude Remacle ◽  
Grégory Catillon ◽  
...  

We have evaluated the influence of oligofructose (OFS), a fermentable dietary fibre, on glucose homeostasis, insulin production and intestinal glucagon-like peptide-1 (GLP-1) in streptozotocin-treated diabetic rats. Male Wistar rats received either i.v. streptozotocin (STZ; 40 mg/kg) or vehicle (CT); one week later, they were fed for 6 weeks with either the standard diet (STZ-CT), or with a diet containing 10% oligofructose (STZ-OFS); both diets were available ad libitum. In a second set of experiments (duration 4 weeks), a supplemental group of food-restricted rats (STZ-Res) receiving a similar intake as CT rats, was added. OFS improved glucose tolerance and reduced food intake as compared with STZ-CT rats in both the post-prandial state and after an oral glucose tolerance test. After 6 weeks, portal and pancreatic insulin concentrations were doubled in STZ-OFS rats. Food restriction improved these parameters when compared with STZ-CT rats, but to a lesser extent than in the STZ-OFS group. We have shown that OFS treatment increased portal and colonic GLP-1(7–36) amide levels and doubled colonic proglucagon and prohormone convertase 1 mRNA levels; both OFS and food restriction lowered ileal GLP-1(7–36) amide levels as compared with levels in STZ-CT rats. We propose that OFS, through its fermentation in the colon, promotes the expression and secretion of colonic peptides, namely GLP-1(7–36) amide, with beneficial consequences on glycaemia, insulin secretion and hyperphagia in diabetic rats.






Metabolism ◽  
2014 ◽  
Vol 63 (2) ◽  
pp. 226-232 ◽  
Author(s):  
Maria A. Sleddering ◽  
Leontine E.H. Bakker ◽  
Laura G.M. Janssen ◽  
A. Edo Meinders ◽  
Ingrid M. Jazet






2018 ◽  
Vol 61 (4) ◽  
pp. 153-161 ◽  
Author(s):  
Sufang Chen ◽  
Wei Wei ◽  
Minjie Chen ◽  
Xiaobo Qin ◽  
Lianglin Qiu ◽  
...  

Numerous studies have implicated tumor necrosis factor α (TNFα) in the pathogenesis of type 2 diabetes. However, the role of its primary receptor, TNF receptor 1 (TNFR1), in homeostatic regulation of glucose metabolism is still controversial. In addition to TNFα, lymphotoxin α (LTα) binds to and activates TNFR1. Thus, TNFα and LTα together are known as TNF. To delineate the role of TNF signaling in glucose homeostasis, the present study ascertained how TNF signaling deficiency affects major regulatory components of glucose homeostasis. To this end, normal diet-fed male TNFR1-deficient mice (TNFR1−/−), TNFα/LTα/LTβ triple-deficient mice (TNF/LT∆3) and their littermate controls were subjected to intraperitoneal glucose tolerance test, insulin tolerance test and oral glucose tolerance test. The present results showed that TNFR1−/− and TNF/LT∆3 mice vs their controls had comparable body weight, tolerance to intraperitoneal glucose and sensitivity to insulin. However, their tolerance to oral glucose was significantly increased. Additionally, glucose-induced insulin secretion assessments revealed that TNFR1 or TNF/LT deficiency significantly increased oral but not intraperitoneal glucose-induced insulin secretion. Consistently, qPCR and immunohistochemistry analyses showed that TNFR1−/− and TNF/LT∆3 mice vs their controls had significantly increased ileal expression of glucagon-like peptide-1 (GLP-1), one of the primary incretins. Their oral glucose-induced secretion of GLP-1 was also significantly increased. These data collectively suggest that physiological TNF signaling regulates glucose metabolism primarily through effects on GLP-1 expression and secretion and subsequently insulin secretion.



2019 ◽  
Vol 47 (10) ◽  
pp. 4691-4700 ◽  
Author(s):  
Simona Ferjan ◽  
Mojca Jensterle ◽  
Tjasa Oblak ◽  
Irena Prodan Zitnik ◽  
Janja Marc ◽  
...  

Objective Impaired glucose homeostasis in polycystic ovary syndrome (PCOS) is associated with obesity, age, and disease phenotype. This study aimed to investigate the glucagon-like peptide-1 (GLP-1) response in patients with obesity and PCOS with normal glucose tolerance (NGT) or prediabetes. Methods Twenty-six women with obesity and PCOS were included. Thirteen women had NGT and 13 had prediabetes. Serum glucose, insulin, and GLP-1 levels were measured during an oral glucose tolerance test. Beta-cell function and insulin resistance were determined. Results Women with prediabetes had significantly lower GLP-1 levels than did those with NGT after a glucose load. GLP-1 levels <3.02 pM at 120 minutes were associated with prediabetes. Women with prediabetes had a lower oral glucose insulin sensitivity (OGIS) index and greater amount of visceral adipose tissue than did those with NGT. Plasma GLP-1 levels at 120 minutes were correlated with visceral adiposity and the OGIS index. A change in GLP-1 levels was correlated with a family history of type 2 diabetes. Conclusion The GLP-1 response is lower in patients with obesity, PCOS, and prediabetes than in those with obesity, PCOS, and NGT. Further investigation of the GLP-1 response as a potential separate risk factor for prediabetes in PCOS is required.



2017 ◽  
Vol 6 (5) ◽  
pp. 151-158 ◽  
Author(s):  
Sylwia Płaczkowska ◽  
Izabela Kokot ◽  
Lilla Pawlik-Sobecka ◽  
Agnieszka Piwowar




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