Endocrine Abstracts

Background: The global prevalence of metabolic syndrome (MetS) characterized by type 2 Diabetes (T2D), obesity, and cardiovascular diseases, has reached alarming proportions worldwide. The prevalence is rapidly increasing among all the age groups due to calorie dense food intake and sedentary lifestyle. Beta adrenergic receptors (β ADRs), are known for its role in thermogenesis, lipolysis and glucose metabolism. Ceasrine et al., 2018, reported that pancreas-specific deletion of Adrb2 resulted in glucose intolerance and impaired insulin secretion in mice.

Objective: To develop an animal model by feeding high fat simple carbohydrate diet (HFSC) and to study the expression pattern of β2 ADRs in the pancreatic islets.

Methodology: The MetS was induced in male C57BL/6J mice (n=10) by feeding HFSC. The control animals were fed with standard diet. The MetS was confirmed by anthropometrical analysis, fasting blood glucose, total cholesterol, triglycerides, HDL and LDL. At the end of 5^thmonth of feeding, the experimental animals were sacrificed, the pancreas was isolated. The morphology of the pancreas was studied by histology and SEM. The pancreatic islets were isolated by collagenase digestion. The quality of islet was accessed by Dithiozone staining. The total islet protein was extracted by RIPA lysis method and quantified by BCA assay. The protein was separated by SDS PAGE, immune blotted and probed with β2 ADR polyclonal antibody followed by Goat anti rabbit IgH(H+L) cross adsorbed DyLight488. The blots were quantified using Biorad Geldoc XR+ with Imagelab software.

Results: The metabolic syndrome was developed in male C57BL/6J mice by feeding HFSC diet up to 5^thmonth. Blood glucose (P>0.01), triglyceride level (P>0.001), total cholesterol (P>0.01), LDL (P>0.01) of HFSC fed mice was significantly increased compared to control. The number of pancreatic islets was reduced in the HFSC fed mice compared to control. In comparison to control mice, HFSC-fed mice’s islets were depleted and had higher lymphatic infiltrates. The expression of β2 ADRs were found to be altered in the HFSC fed mice.

Conclusion: Serving as a model, HFSC fed mice more closely resembled human obesity with altered blood glucose and lipid profile. The presence of lymphatic infiltration around the islets of HFSC-fed mice indicates that the inflammatory process may also contribute to islet destruction, which could lead to T2D. Additional changes associated with the β2 ADRs and its downstream signaling will be discussed during the congress.