A comprehensive view of the interaction between non-alcoholic fatty liver disease and diabetes

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Lancet Diabetes Endocrinol. February 17, 2022: S2213-8587(22)00003-1. doi: 10.1016/S2213-8587(22)00003-1. Online ahead of print.


Non-alcoholic fatty liver disease (NAFLD) has become an epidemic, as have other non-communicable diseases (NCDs), such as cancer, obesity, diabetes and cardiovascular disease. The pathophysiology of NAFLD, particularly involving insulin resistance and subclinical inflammation, is not only closely linked to that of these NTMs, but also to a severe course of the communicable disease COVID-19. Genetics alone cannot explain the sharp increase in the prevalence of NAFLD over the past 2 decades and the projected increase for the next few decades. Impaired glucose and lipid metabolic pathways, which have been propelled by the global rise in the prevalence of obesity and type 2 diabetes, are most likely behind the rise in the number of people with NAFLD. As the prevalence of NAFLD varies among the subgroups of patients with diabetes and prediabetes identified by the cluster analyses, stratifying people with diabetes and prediabetes by major mechanistic disease pathways could improve the diagnosis of NAFLD and predicting its progress. In this review, we aim to understand how diabetes can affect the development of fatty liver disease and its progression to advanced liver injury. First, we highlight the extent to which NAFLD and diabetes occur together around the world. Second, we address the main mechanisms involved in the pathogenesis of NAFLD and type 2 diabetes, and discuss whether these mechanisms place NAFLD in an important position to better understand the pathogenesis of NCDs and communicable diseases. , such as COVID-19. Third, we examine whether this knowledge can be used for the personalized treatment of NAFLD in the future. Finally, we discuss current treatment strategies for people with type 2 diabetes and their effectiveness in treating the spectrum of liver disease, from simple steatosis to nonalcoholic steatohepatitis and liver fibrosis.

PMID:35183303 | DO I:10.1016/S2213-8587(22)00003-1

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