Tissue Specific-Metabolism of Lipids for Ectopic Deposition

Tissue Specific-Metabolism of Lipids for Ectopic Deposition It is now known that triglyceride accumulates in non-adipose tissues as in liver, skeletal muscle, pancreas, and heart. Excessive accumulation of ectopic fat causes abnormal pathophysiological changes in function and mechanism within the organ. For example, excessive ectopic fat accumulation within the hepatic cells and skeletal muscle cells results in insulin resistance by inducing impairment of information transport of insulin. Ectopic fats accumulated within the cardiac epicardium and cardiac cells are associated with insulin resistance and systolic dysfunction. The ectopic fat content assessed by biopsy, echocardiograph, and proton magnetic resonance spectroscopy correlates closely with specific tissues and overall systemic insulin resistance. Ectopic fat is considered a better and a stronger predictor of insulin resistance than visceral adipose tissue. Therefore, increased triglycerides in liver, pancreas, skeletal muscle, and heart may be a part of metabolic abnormality leading to insulin resistance, and subsequent development of Type 2 diabetes mellitus. Recent studies showed that exercise, diet, and medication, decreased insulin resistance by changing the ectopic fat contents. According to these studies, the mechanisms by which exercise, diet, and medication influence lipogenic gene expressions toward intramyocellular fat contents are different, in particular, lipid metabolites including diacylglycerols and ceramides. Prevention and treatment of metabolic disease may be expected in the near future with the development of novel biochemical markers that have specific correlation to ectopic fat tissues.