Comparing the behaviour of human and rodent beta cell lines for in vitro diabetes mellitus study

For the past 30 years, considerable effort has been made to generate useful rodent and human insulin-secreting cell lines to understand the complexity and functionality of the pancreatic beta cells. Since then, numerous types of research have been carried out using these cell lines to assess the pathology of diabetes mellitus. Among them, the cell lines INS-1, MIN6, 1.1B4 and EndoC-βH1 are the most widely used due to their stability and appropriate response to glucose stimulation. With multiple choices of cell lines available, there is a question of which cell line can be the best cell model for in vitro pancreatic beta cell study. The characterisation of each of these cell lines has already been vigorously studied, but there is still the need to understand how rodent and human cell lines differ from each other in order to choose the most appropriate cell model for a specific study. In this review, we explore the differences between human and rodent insulin-secreting cell lines in terms of their culturing condition, glucose-stimulated insulin secretion and reaction toward oxidative stress. Together, it is hoped that these comparisons could provide new perspectives for researchers in dealing with the available insulin-secreting cell lines for their in vitro diabetic studies

Short-chain fatty acids: possible regulators of insulin secretion

The benefits of gut microbiota-derived short-chain fatty acids (SCFAs) towards health and metabolism have been emerging since the past decade. Extensive studies have been carried out to understand the mechanisms responsible in initiating the functionalities of these SCFAs towards body tissues, which greatly involves the SCFA-specific receptors free fatty acid receptor 2 (FFAR2) and free fatty acid receptor 3 (FFAR3). This review intends to discuss the potential of SCFAs particularly in regulating insulin secretion in pancreatic β-cells, by explaining the production of SCFAs in the gut, the fate of each SCFAs after their production, involvement of FFAR2 and FFAR3 signalling mechanisms and their impacts on insulin secretion. Increased secretion of insulin after SCFAs treatments were reported in many studies, but contradicting evidence also exist in several other studies. Hence, no clear consensus was achieved in determining the true potential of SCFA in regulating insulin secretion. In this review, we explore how such differences were possible and hopefully be able to shed some perspectives in understanding SCFAs-signalling behaviour and preferences