High-fat-diet induced obesity and diabetes mellitus in Th1 and Th2 biased mice strains: A brief overview and hypothesis
- VernacularTitle:High-fat-diet induced obesity and diabetes mellitus in Th1 and Th2 biased mice strains: A brief overview and hypothesis
- Author:
Sankaran Prakash SOMI
1
Author Information
- Publication Type:Journal Article
- Keywords: Balbc mice; C57bl/6 mice; diabetes mellitus; immunometabolism; obesity; Th1/Th2 bias
- From: Chronic Diseases and Translational Medicine 2023;09(1):14-19
- CountryChina
- Language:English
- Abstract: Obesity and diabetes mellitus are common metabolic diseases prevalent worldwide. Mice are commonly used to study the pathogenesis of these two conditions. Obesity and diabetes mellitus are induced by administering a high-fat diet in many studies although other diet-induced models are also used. Several factors may influence the outcome of the studies done to study diet-induced obesity in mice. The immune system plays a crucial role in the susceptibility of mice to develop obesity and metabolic disease. In this article, the reasons for differences in susceptibility to develop obesity and diabetes mellitus in mice in response to high-fat-diet feeding and the influence of immunological bias of the mice strain used in studies are evaluated. Mice strains that induce proinflammatory and Th1-type immune responses are found to be susceptible to high-fat-diet-induced obesity. A few studies which directly compared the effect of a high-fat diet on obesity and diabetic phenotype in Th1- and Th2-biased mice strains were briefly analyzed. Based on the observations, it is proposed that the liver and adipose tissue may respond differently to high-fat-diet feeding regimens in Th1- and Th2-biased mice strains. For instance, in Th1-biased mice, adipose tissue fat content was high both in the baseline as well as in response to a high-fat diet whereas in the liver, it was found to be less. It can be inferred that the immune responses to diet-induced models may provide insights into the pathogenesis of obesity and diabetes mellitus.
