Abstract
Beyond fat accumulation, NAFLD genetics converges on lipid droplet biology
Highlights
Nonalcoholic fatty liver disease (NAFLD) is epidemiologically associated with obesity, insulin resistance, and dyslipidemia, and is rapidly becoming the leading cause of liver disease
The impact on liver damage was independent of hepatic fat accumulation
Carriage of the rs72613567 variant exerted a more marked protection against liver damage in carriers of the PNPLA3 I148M risk variant [6]. In this issue of the Journal of Lipid Research, Pirola et al [7] confirm, in a case-control study conducted in 429 patients with histological NAFLD and 180 controls from South America, that the minor rs72613567 risk allele protects against NASH and fibrosis [7]
Summary
Nonalcoholic fatty liver disease (NAFLD) is epidemiologically associated with obesity, insulin resistance, and dyslipidemia, and is rapidly becoming the leading cause of liver disease. A splice variant (rs72613567:TA) in HSD17B13, encoding the hepatic lipid droplet protein hydroxysteroid 17-b dehydrogenase 13, has been associated through exome-wide studies with protection against progressive liver damage in both alcoholic and nonalcoholic fatty liver disease in large independent cohorts of individuals from the general population [6].
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