Role of arsenic exposure in adipose tissue dysfunction and its possible implication in diabetes pathophysiology. (1st March 2018) - Renu, Kaviyarasi
Highlights: Arsenic mediates diabetic pathophysiology, impairment of adipose tissue metabolism. Arsenic disturbs SIRT3- FOXO3a, Ras −MAP −AP-1, PI(3)-K-Akt, ER and GPCR pathway. Arsenic inhibited adipogenesis, elevates lipolysis and disturbances of adipokines. Arsenic causes lipodystrophy and obesity depends on its valence and concentration. Targeting miRNA would act as therapeutic for arsenic mediated diabetic condition. Abstract: Exposure to arsenic in drinking water can stimulate a diverse number of diseases that originate from impaired lipid metabolism in adipose and glucose metabolism, leading to insulin resistance. Arsenic inhibits differentiation of adipocyte and mediates insulin resistance with diminutive information on arsenicosis on lipid storage and lipolysis. This review focused on different mechanisms and pathways involved in adipogenesis and lipolysis in adipose tissue during arsenic-induced diabetes. Though arsenic is known to cause type2 diabetes through different mechanisms, the role of adipose tissue in causing type2 diabetes is still unclear. With the existing literature, this review exhibits the effect of arsenic on adipose tissue and its signalling events such as SIRT3- FOXO3a signalling pathway, Ras −MAP −AP-1 cascade, PI(3)-K-Akt pathway, endoplasmic reticulum stress protein, C/EBP homologous protein (CHOP10) and GPCR pathway with role of adipokines. There is a need to elucidate the different types of adipokines which are involved in arsenic-induced diabetes. The exhibited information brings to light that arsenic has negative effects on a white adipose tissue (WAT) by decreasing adipogenesis and enhancing lipolysis. Some of the epidemiological studies show that arsenic would causes obesity. Few studies indicate that arsenic might induces lipodystrophy condition. Further research is needed to evaluate the mechanistic link between arsenic and adipose tissue dysfunction which leads to insulin resistance.