Nonalcoholic Fatty Liver Disease: Lipids and Insulin Resistance

Clin Liver Dis. 2016 May;20(2):245-62. doi: 10.1016/j.cld.2015.10.007. Epub 2016 Feb 18.

Abstract

Obesity and its major comorbidities, including type 2 diabetes mellitus, nonalcoholic fatty liver disease (NAFLD), obesity cardiomyopathy, and certain cancers, have caused life expectancy in the United States to decline in recent years. Obesity is the increased accumulation of triglycerides (TG), which are synthesized from glycerol and long-chain fatty acids (LCFA) throughout the body. LCFA enter adipocytes, hepatocytes, and cardiomyocytes via specific, facilitated transport processes. Metabolism of increased cellular TG content in obesity may lead to comorbidities such as NAFLD and cardiomyopathy. Better understanding of LCFA transport processes may lead to successful treatment of obesity and NAFLD.

Keywords: Facilitated transport; Leptin; Lipotoxicity; Spexin; Weight regain.

Publication types

  • Research Support, N.I.H., Extramural
  • Review

MeSH terms

  • Animals
  • Disease Models, Animal
  • Fatty Acids / metabolism*
  • Humans
  • Insulin Resistance*
  • Leptin / metabolism
  • Non-alcoholic Fatty Liver Disease / genetics
  • Non-alcoholic Fatty Liver Disease / metabolism*
  • Obesity / metabolism
  • Peptide Hormones / metabolism
  • Triglycerides / metabolism*

Substances

  • Fatty Acids
  • Leptin
  • Peptide Hormones
  • SPX protein, human
  • Triglycerides