GH but not IGF-I or insulin increases lipoprotein lipase activity in muscle tissues of hypophysectomised rats

Changes in GH secretion are associated with changes in serum lipoproteins, utilisation of fuels and body composition, Since lipoprotein lipase (LPL) i s a key enzyme in the regulation of lipid and lipoprotein metabolism, chang es in LPL activity may contribute to these effects of GH. The present study was undertaken to investigate the role of GH and the GH-dependent growth f actor, IGF-I, in the regulation of LPL in heart, skeletal muscle and adipos e tissue. Female rats were hypophysectomised at 50 days of age. One week la ter, hormonal therapy was commenced. All hypophysectomised rats received L- thyroxine and cortisol. Adipose tissue, the heart, soleus and gastrocnemius muscles were excised after 1 week of hormonal therapy. The effect of insul in injections on adipose tissue and heart LPL activity was also studied. In separate experiments, LPL activity in post-heparin plasma was measured. Hy pophysectomy had no effect on adipose tissue LPL activity, whereas activity was reduced in heart, soleus and gastrocnemius muscle tissues. GH treatmen t had no significant effect on LPL activity in adipose tissue or soleus mus cle, but increased the LPL activity in heart and gastrocnemius muscle. GH t reatment increased post-heparin plasma LPL activity. Recombinant human IGF- I treatment (1.25 mg/kg per day) markedly reduced LPL activity in adipose t issue, but had no effect in muscle tissues. The effect of IGF-I treatment o n adipose tissue LPL was not reflected by a decrease in post-heparin plasma LPL activity. Daily injections of insulin for 7 days increased LPL activit y in adipose tissue but had no effect on heart LPL activity. In adipose tis sue, LPL mRNA levels tended to decrease as a result of IGF-I treatment. In the muscle tissues, no significant effects of hypophysectomy, GH or IGF-I t reatment on LPL mRNA levels were observed. It is concluded that GH increases heart and skeletal muscle tissue LPL acti vity, which probably contributes to an increased post-heparin plasma LPL ac tivity. The effect of GH on muscle LPL activity is probably not mediated by ICF-I or insulin. Insulin and IGF-I have opposite effects on LPL activity in adipose tissue.