scholarly journals Liraglutide alters DPP4 in the circumvallate papillae of type 2 diabetic rats

2016 ◽  
Vol 57 (1) ◽  
pp. 13-21 ◽  
Author(s):  
Xun Cao ◽  
Xiao Zhou ◽  
Xiao-Min Liu ◽  
Li-Hong Zhou

Liraglutide, a human glucagon-like peptide (GLP1) analog that partially inhibits dipeptidyl-peptidase 4 (DPP4), can decrease glucose levels and suppress appetite in patients with type 2 diabetes (T2DM). GLP1 and its receptor (GLP1R) also exist in the taste buds of rodents and regulate taste sensitivity. DPP4, a protease, functions in homeostasis of blood glucose, lipids, and body weight. Interactions among GLP1, GLP1R, and DPP4 likely affect taste and food-intake behavior. The aim of the present study was to investigate DPP4 expression in the taste buds of the circumvallate papillae (CV) in T2DM rats, and determine the effects of liraglutide treatment. Rats were divided into diabetic control (T2DM-C), normal control (NC), and liraglutide-treated diabetic (T2DM+LIR) groups. DPP4 localization and gene expression levels were evaluated by immunohistochemistry and quantitative reverse transcription-polymerase chain reaction (RT-qPCR), respectively. DPP4 immunoreactive cells were localized in the taste buds of the rat CV. RT-qPCR showed significantly higher expression of Dpp4 mRNA in both the taste buds and hypothalamus of T2DM-C rats compared with NC rats. However, in the T2DM+LIR group, Dpp4 expression differed between the taste buds and hypothalamus, with significantly higher and lower levels compared with the T2DM-C group, respectively. Dpp4 mRNA expression is increased in the taste buds of the CV of T2DM rats. Liraglutide simultaneously upregulated (taste buds) and downregulated (hypothalamus) Dpp4 expression in T2DM rats. Therefore, DPP4 may be closely associated with the anorexigenic signaling and weight loss induced by the treatment of liraglutide in type 2 diabetic patients.

2010 ◽  
Vol 57 (3) ◽  
pp. 237-244 ◽  
Author(s):  
Atsushi GOTO ◽  
Maki TAKAICHI ◽  
Miyako KISHIMOTO ◽  
Yoshihiko TAKAHASHI ◽  
Hiroshi KAJIO ◽  
...  

2020 ◽  
Vol 46 (2) ◽  
pp. 104-108
Author(s):  
Ashesh Kumar Chowdhury ◽  
Shahjalalur Rahman Sahi ◽  
Mohammad Moniruzzaman ◽  
Mansura Khan

Background: Immune mediated destruction of pancreatic beta cell in type-I diabetes is well established but its’ role in young type-2 diabetic patients is still not conclusive. These young diabetic patients pass through several stages where they do not need insulin but found to have serum autoantibody against islets cell and even become dependent on insulin for survival in course of time. This study aims to find the presence of islets cell auto-antibodies (ICA) and autoantibody to glutamic acid decarboxylase-65 (GAD-65) in non-insulin requiring young diabetic patients of Bangladesh. Objective: To evaluate the presence of ICA and GAD-65 between the non-insulin requiring young type-2 diabetic patients and compare with the non-diabetic control group. Method: This case control study was carried out at the Department of Immunology, BIRDEM General Hospital, Dhaka for a period of one year from July 2013, A total of 120 non-insulin requiring (≥12 months) young type-2 diabetic patients and 60 age, sex matched non-diabetic were enrolled as control subjects following inclusion and exclusion criteria. ICA and GAD-65 tests were performed by enzyme linked immune-sorbent assay (ELISA) method by using kits from DRG Inc. International, USA. Results: In this study statistically significant difference found between non insulin requiring young diabetic patients and non diabetic control in respect of positive ICA result (p=0.015). The moderately strong negative association was found between different age of onset of diabetes mellitus and value of ICA level (r=-0.45). Only 20-24 years age group showed statistically significant difference between patient and control (p=0.013). Statistically significant difference was not found in GAD-65 values of non insulin requiring young diabetic patients and non diabetic controls (p=0.441). Conclusion: This study revealed that there is significant difference present in respect of ICA among non-insulin requiring young diabetic patients and non-diabetic controls. Therefore, autoimmune pathogenesis of beta cell killing by producing ICA against islets cell take place in young type-2 diabetic patients. Bangladesh Med Res Counc Bull 2020; 46(2): 104-108


2013 ◽  
Vol 218 (3) ◽  
pp. 255-262 ◽  
Author(s):  
C Y Shan ◽  
J H Yang ◽  
Y Kong ◽  
X Y Wang ◽  
M Y Zheng ◽  
...  

For centuries, Berberine has been used in the treatment of enteritis in China, and it is also known to have anti-hyperglycemic effects in type 2 diabetic patients. However, as Berberine is insoluble and rarely absorbed in gastrointestinal tract, the mechanism by which it works is unclear. We hypothesized that it may act locally by ameliorating intestinal barrier abnormalities and endotoxemia. A high-fat diet combined with low-dose streptozotocin was used to induce type 2 diabetes in male Sprague Dawley rats. Berberine (100 mg/kg) was administered by lavage to diabetic rats for 2 weeks and saline was given to controls. Hyperinsulinemia and insulin resistance improved in the Berberine group, although there was no significant decrease in blood glucose. Berberine treatment also led to a notable restoration of intestinal villi/mucosa structure and less infiltration of inflammatory cells, along with a decrease in plasma lipopolysaccharide (LPS) level. Tight junction protein zonula occludens 1 (ZO1) was also decreased in diabetic rats but was restored by Berberine treatment. Glutamine-induced glucagon-like peptide 2 (GLP2) secretion from ileal tissue decreased dramatically in the diabetic group but was restored by Berberine treatment. Fasting insulin, insulin resistance index, plasma LPS level, and ZO1 expression were significantly correlated with GLP2 level. In type 2 diabetic rats, Berberine treatment not only augments GLP2 secretion and improves diabetes but is also effective in repairing the damaged intestinal mucosa, restoring intestinal permeability, and improving endotoxemia. Whether these effects are mechanistically related will require further studies, but they certainly support the hypothesis that Berberine acts via modulation of intestinal function.


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