September 8, 2009 | Elisa Fabbriña, Faidon Magkos, B. Selma Mohammed, Terri Pietka, Nada A. Abumrad, Bruce W. Patterson, Adewole Okunade, and Samuel Klein
The study by Fabbriini et al. investigates the relationship between intrahepatic triglyceride (IHTG) content and metabolic complications associated with obesity, contrasting it with visceral adipose tissue (VAT). The authors found that IHTG content, not VAT volume, is a better marker of metabolic dysfunction. They demonstrated that subjects with higher IHTG content had impaired insulin sensitivity in the liver, skeletal muscle, and adipose tissue, while VAT volume did not show significant differences in these measures. Additionally, subjects with higher IHTG content had increased hepatic very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rates, which were primarily due to the contribution of non-systemic fatty acids derived from lipolysis of IHTG. The study also revealed that alterations in CD36 expression and content in adipose tissue and skeletal muscle may play a role in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. These findings challenge the prevailing notion that VAT is solely responsible for metabolic abnormalities and suggest that IHTG content is a more critical factor.The study by Fabbriini et al. investigates the relationship between intrahepatic triglyceride (IHTG) content and metabolic complications associated with obesity, contrasting it with visceral adipose tissue (VAT). The authors found that IHTG content, not VAT volume, is a better marker of metabolic dysfunction. They demonstrated that subjects with higher IHTG content had impaired insulin sensitivity in the liver, skeletal muscle, and adipose tissue, while VAT volume did not show significant differences in these measures. Additionally, subjects with higher IHTG content had increased hepatic very-low-density lipoprotein-triglyceride (VLDL-TG) secretion rates, which were primarily due to the contribution of non-systemic fatty acids derived from lipolysis of IHTG. The study also revealed that alterations in CD36 expression and content in adipose tissue and skeletal muscle may play a role in the pathogenesis of ectopic triglyceride accumulation and metabolic disease. These findings challenge the prevailing notion that VAT is solely responsible for metabolic abnormalities and suggest that IHTG content is a more critical factor.