Insulin resistance and “Lipotoxic Liver Diseases”

This is the authors' abstract. We don't add key points for this paper.

An expanded dysfunctional adipose tissue that fails to accommodate, utilise and store as much fat as it should has emerged as the prime mover of the patho physiological sequence that leads to accumulation of fat at ectopic sites -including the liver, in metabolic syndrome and cluster of disorders that include Non alcoholic fatty Liver Disease(NAFLD). Non alcoholic steato hepatitis ( NASH) represent the aggressive subset of NAFLD that can progress to cirrhosis . Insulin is the key driver of metabolic homeostasis, particularly glucose flux across cell membrane -a phenomenon that have connotations for survival and evolution of the organism. An impaired sensitivity to insulin action at the adipocyte level is a characteristic biological event in metabolic syndrome. 6 ,7 The associations of Insulin resistance(IR) with metabolic syndrome is nearly universal -so that the two often have interchangeable pathophysiological inferences, a classical example being type 2 diabetes and the other example is NAFLD/NASH. IR through metabolic syndrome is the template that provide a point of convergence for linked clinical conditions -diabetes, obesity, dyslipidemia, hypertension and NAFLD/NASH. IR needs to be conceptualised not as a fixed cellular event -exerting an all or none effect like many biological processes, rather as a dynamic and regulated physiological response to a host of environmental factors and triggers including inflammation. IR possibly challenges energy homeostasis, nutrient availability and handling and connects metabolism with immune phenomenon. 12 There are different methods

May inform integrated cardiometabolic risk assessment; leaves open targeted interventional trials on insulin resistance.