Triacylglycerols overproduction

Cause is overproduction and/or decreased removal of VLDL triacylglycerol in serum. 

Adipose-cell lipase is activated by phosphorylation. Hence, overproduction of the cAMP-activated kinase will lead to an accelerated breakdown of triacylglycerols and a depletion of fat stores. 

In the hyperlipidemias, the blood levels of cholesterol or triacylglycerols, or S both, are elevated resulting from overproduction of lipoproteins or defects in... 

Insulin normally inhibits lipolysis by decreasing the lipolytic activity of HSL in the adipocyte. Individuals such as Di Abietes, who have a deficiency of insulin, have an increase in lipolysis and a subsequent increase in the concentration of free fatty acids in the blood. The liver, in turn, uses some of these fatty acids to synthesize triacylglycerols, which then are used in the hepatic production of VLDL. VLDL is not stored in the liver but is secreted into the blood, raising its serum concentration. Di also has low levels of LPL because of decreased insulin levels. Her hypertriglyceridemia is the result, therefore, of both overproduction of VLDL by the liver and decreased breakdown of VLDL triacylglycerol for storage in adipose cells. 

Thus, the whole process of phenol formation may be considered analogous, in an overall metabolic sense, to fatty acid synthesis in well-fed animals (with the resultant formation and storage of triacylglycerol in adipose tissue) or ketogenesis in the liver of starved or diabetic animals. These situations have effectively adapted to the demands of an imbalanced overproduction of acetyl-CoA. 

The underlying causes are either the absence of a specific enzyme (e.g. lipoprotein lipase in Type I) the absence of a specific apolipoprotein (e.g. apoC2 in another form of Type I) the absence, reduction or impairment of function of specific cell surface receptors (e.g. the LDL receptor in Type Ila) the overproduction of specific apolipoproteins (e.g. apoB in Type Ilb) or the overproduction of lipids in the liver (e.g. triacylglycerols in Types IV and V). Different gene defects may produce the same lipoprotein pattern although by different mechanisms. Alternatively, factors such as body weight and dietary composition may modify the phenotypic expression of a particular genotype. 

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