MELBOURNE, AUSTRALIA – Nonalcoholic fatty liver disease is another health problem associated with the metabolic syndrome, says Professor Jacob George in his presentation at the inaugural Asia Pacific Metabolic Symposium.
His presentation, entitled “The Liver and The Metabolic Syndrome,” highlights one of the more recently linked comorbidities associated with the metabolic syndrome. He discusses why the liver develops fat and why the organ becomes damaged in the presence of a fatty environment.
Nonalcoholic fatty liver disease (NAFLD) and its subset nonalcoholic steatohepatitis (NASH) represent the liver manifestations of insulin resistance, said Prof George. Although NAFLD has not been included as a component of the metabolic syndrome, based on its definition, available data indicate that the onset of NAFLD is an early event in the development of insulin resistance and so might predict the presence or the future development of the metabolic syndrome, he explained.
Prof George added that studies have shown a positive correlation between common biomarkers of the metabolic syndrome – plasma glucose, waist circumference, triglycerides, and systolic and diastolic pressure – with increasing liver fat. Similarly, an inverse correlation has been found with serum levels of HDL cholesterol and liver fat, while other studies have associated the presence of liver fat with increased cardiovascular mortality.
Intra-hepatic fat is the best predictor of insulin action in the liver, in adipose tissue, and muscle, said Professor George, as increasing liver fat has shown reduced hepatic insulin sensitivity, decreased adipose insulin sensitivity, and decreased skeletal muscle insulin sensitivity in study participants.
Further, recent research, he said, has shown that the intra-hepatic triglyceride was responsible for between a third and 40% of the variability in insulin sensitivity – suggesting that liver fat not only controls insulin sensitivity within the liver but also within surrounding tissues.
Prof George added that other studies have provided new insight into the effect of visceral fat and hepatic fat on insulin resistance. In one related study individuals with increased hepatic fat levels were found to have the lowest insulin resistance, while individuals matched for similar hepatic fat levels, but varying visceral fat levels, showed little variance in biomarkers. This he said supports the hypothesis that it is indeed hepatic and not visceral fat that is important for measuring a person’s insulin sensitivity.
The molecular mechanisms of fatty liver includes the presence of insulin resistance, activation of endoplasmic reticulum stress, intrahepatic leptin resistance, and low adiponectin levels, all of which are meant to oxidise fat, Prof George explained.
