GH has important effects on the lipoprotein metabolism. For example, hypophysec-tomy changes the lipoprotein pattern from a predominantly HDL to one with a distinct low density lipoprotein (LDL) peak in the rat (73), suggesting that the presence of GH

is essential for maintaining a normal lipoprotein pattern. Moreover, in response to GH the serum LDL-cholesterol and apolipoprotein B concentrations decrease (73), probably a result of the increased clearance of these lipoproteins through increased hepatic LDL receptor activity (74).

A common finding in both GH deficiency and Syndrome X is high levels of serum triglycerides and low HDL-cholesterol concentrations. This may be associated with their increased abdominal adiposity (75) and insulin resistance (67,68,76). However, although a dramatic reduction in visceral adipose tissue occurs in response to GH treatment, serum triglyceride concentration is not reduced (66,75,77) and the concentration of HDL-cholesterol is increased (77,78). The lipolytic action of GH treatment probably increases the flux of FFA to the liver (79) and increases the synthesis and secretion of VLDL from the liver. The LPL activity in adipose tissue is attenuated (80) and the post-heparin plasma LPL is not affected by GH treatment (81). As serum triglyceride concentrations do not increase under conditions of increased VLDL secretion the peripheral catabolism must be enhanced. Increased LPL activity in other tissues such as muscle is therefore likely (81). Furthermore, the strong association between glucose/insulin homeostasis and VLDL metabolism (56) might be reflected in the response to GH. The unaffected triglyceride levels might thus be explained by essentially unchanged insulin sensitivity (82) and glucose tolerance during more prolonged GH treatment in GH-deficient adults.

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