Increased fat accumulation in liver may link insulin resistance with subcutaneous abdominal adipocyte enlargement, visceral adiposity, and hypoadiponectinemia in obese individuals.

Description

Several lipid partitioning abnormalities, such as increased intrahepatic lipid content, intramyocellular lipid content, and enlargement of adipocytes from subcutaneous abdominal adipose tissue, as well as metabolic complications, such as low circulating adiponectin concentrations, are associated with insulin resistance. Given the insulin-sensitizing effect of adiponectin in skeletal muscle and liver and its inverse relationship with adipocyte size, Koska et al. sought to verify in 53 obese Pima Indians the hypothesis that hypoadiponectinemia links hypertrophic obesity with insulin resistance via intramyocellular lipid content and intrahepatic lipid content. The data indicated that the enlargement of adipocytes from subcutaneous adipose tissue is not directly related to insulin action but predicts increased liver fat content among obese individuals with normal glucose tolerance. Contrary to the proposed hypothesis, no association was found between adipocyte diameter and plasma adiponectin levels. However, multivariate analyses revealed that plasma adiponectin levels, adipocyte diameter, and intra-abdominal (visceral) adipose tissue were significant predictors of increased liver fat content. These results suggest that increased lipid content in the liver may independently link hypoadiponectinemia, hypertrophic obesity, and increased intra-abdominal adiposity to peripheral and hepatic insulin resistance.