Abstract
Over the last decade, the understanding of the association between insulin resistance (IR) and non-alcoholic fatty liver disease (NAFLD) has dramatically evolved. There is clear understanding that carriers of some common genetic variants, i.e., the patatin-like phospholipase domain-containing 3 (PNPLA3) or the transmembrane 6 superfamily member 2 (TM6SF2) are at risk of developing severe forms of NAFLD even in the presence of reduced or absent IR. In contrast, there are obese patients with “metabolic” (non-genetically driven) NAFLD who present severe IR. Owing to the epidemic obesity and the high prevalence of these genetic variants in the general population, the number of pediatric cases with combination of genetic and metabolic NAFLD is expected to be very high. Gut dysbiosis, excessive dietary intake of saturated fats/fructose-enriched foods and exposure to some chemicals contribute all to both IR and NAFLD, adding further complexity to the understanding of their relationship. Once NAFLD is established, IR can accelerate the progression to the more severe form of liver derangement that is the non-alcoholic steatohepatitis.
Highlights
Insulin resistance (IR) is one of the hallmarks of non-alcoholic fatty liver disease (NAFLD) being pivotal in the pathogenesis of the disease as associated to obesity [1]
IR is, one of the multiple hits determining the progression from NAFLD to non-alcoholic steatohepatitis (NASH) [2]
The reduced insulin sensitivity and the inappropriate hepatic glucose production (HGP) of the NAFLD patients were irrespective of their body fatness and glucose tolerance [4]
Summary
Insulin resistance (IR) is one of the hallmarks of non-alcoholic fatty liver disease (NAFLD) being pivotal in the pathogenesis of the disease as associated to obesity [1]. In children and adolescents whose visceral adipose tissue becomes insufficient to store excess fats, paper [21], in children and adolescents with “metabolic” NAFLD the assumption that the overflow the latter overflow the visceral compartment and start to of accumulate ectopically in key sensitive of lipids totothe liver is a consequence of the inadequate storage excessive fat in the subcutaneous depot remains In a most different study, patients with similar lipid increases and hepatic steatosis becomes important marker of IR,defective glucose dysregulation partitioning had impaired insulin suppression of lipolysis [22]. In obese patients with NAFLD, the impaired lipolysis causes inappropriately enhanced HGP
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