GH increases LPL activity in muscle tissue

From the journal of endocrinology...

Changes in growth hormone (GH) secretion are associated with changes in serum lipoproteins, utilisation of fuels and body composition. Since lipoprotein lipase (LPL) is a key enzyme in the regulation of lipid- and lipoprotein metabolism, changes 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 factor, insulin-like growth factor-1 (IGF-I) in the regulation of LPL in heart, skeletal muscle and adipose tissue. Female rats were hypophysectomized at 50 days of age. One week later hormonal therapy commenced. All hypophysectomized rats received L-thyroxin and cortisol. Adipose tissue, the heart, soleus and gastrocnemius muscles were excised after one week of hormonal therapy. The effect of insulin injections on adipose tissue and heart LPL activity was also studied. In separate experiments, LPL activity in post-heparin plasma was measured. Hypophysectomy had no effect on adipose tissue LPL activity, whereas activity was reduced in heart, soleus and gastrocnemius muscle tissues. GH treatment had no significant effect on LPL activity in adipose tissue or soleus muscle, but increased the LPL activity in heart and gastrocnemius muscle. GH treatment increased post-heparin plasma LPL activity. Recombinant human IGF-I treatment (1.25 mg/kg/day) markedly reduced LPL activity in adipose tissue, but had no effect in muscle tissues. The effect of IGF-I treatment on adipose tissue LPL was not reflected by a decrease in post-heparin plasma LPL activity. Daily injections of insulin for 7 days increased LPL activity in adipose tissue but had no effect on heart LPL activity. In adipose tissue, LPL mRNA levels tended to decrease as a result of IGF-I treatment. In the muscle tissues, no significant effect of hypophysectomy, GH or IGF-I treatment on LPL mRNA levels were observed.

It is concluded that GH increases heart and skeletal muscle tissue LPL activity, which probably contributes to an increased post-heparin plasma LPL activity. The effect of GH on muscle LPL activity is probably not mediated by IGF-I or insulin. Insulin and IGF-I have opposite effects on LPL activity in adipose tissue.

i'm a little confused as to what lpl does in the specific tissues? the journal claims that igf-1 decreases lpl activity in adipose (fat) tissue, so what does this mean? less fat accumulation? does lpl break down fats?

It's pretty clear that GH reduces LPL activity and increases HSL activity, but IGF-1's effects on LPL seem to be mixed, with, potentially, a reduction of LPL activity in visceral fat, but an increase in subQ fat. This doesn't correlate with real-world results of users of LR3 though, since a reduction in subQ fat is pretty clear.

J Pediatr Endocrinol Metab. 2000 Sep;13 Suppl 2:1003-9. Related Articles, Links


Effects of growth hormone on adipose tissue.

Carrel AL, Allen DB.

Department of Pediatrics, University of Wisconsin Medical School, Madison 53792, USA. [email protected]

Physiological effects of growth hormone (GH) extend beyond the stimulation of linear growth. These include important metabolic effects upon adipose tissue. GH affects both proliferation and differentiation of preadipocytes, although this varies between clonal cell lines and preadipocyte cultures. Both preadipocytes and mature adipocytes possess specific GH receptors. GH may mediate its actions via these receptors, but some effects are indirectly mediated through the GH-mediated secretion of insulin-like growth factor-I (IGF-I) within adipose tissue. GH promotes lipolysis via inhibition of lipoprotein lipase, which hydrolyzes triglycerides in the circulation to make them available for triglyceride accumulation in adipose tissue. GH also stimulates hormone sensitive lipase (HSL), the rate-limiting step for release of stored triglyceride in adipocytes (lipolysis). As GH becomes utilized for various "non-growth" concerns (see Figure 1), awareness of the metabolic effects on adipocytes is important to understand the clinical effects seen with GH therapy.








Horm Res. 2002;58(4):157-64. Related Articles, Links


The 20-kD human growth hormone reduces body fat by increasing lipolysis and decreasing lipoprotein lipase activity.

Takahashi S, Satozawa N.

Drug Discovery Institute, Nihon Schering K.K., Mobara, Japan. [email protected]

AIM: The aim of this study was to estimate the lipolytic activity of the human growth hormone variant, 20-kD human growth hormone (20K-hGH). METHODS: Obese KV-A(y) mice were given daily subcutaneous injections of 20K-hGH (0.25, 0.5, 1.0 mg/kg), 22K-hGH (0.25 mg/kg) or saline as a control for 2 weeks. Body composition (fat, water and protein), lipolysis and lipoprotein lipase (LPL) activity were measured 24 h after the final injection. RESULTS: Both growth hormone isoforms significantly reduced relative fat pad and whole body lipids. In addition, 20K-hGH produced an inhibition of LPL activity in adipose tissue and stimulated lipolysis in adipocytes. CONCLUSION: These data strongly suggest that inhibition of LPL activity in adipose tissue and stimulation of lipolysis in adipocytes by 20K-hGH treatment reduce adipose tissue mass, resulting in body fat reduction. Copyright 2002 S. Karger AG, Basel

Med Hypotheses. 2001 Aug;57(2):192-200. Related Articles, Links


Modulation of adipocyte lipoprotein lipase expression as a strategy for preventing or treating visceral obesity.

McCarty MF.

Pantox Laboratories, 4622 Santa Fe St, San Diego, CA 92109, USA.

As compared to subcutaneous adipocytes, visceral adipocytes have high basal lipolysis, are highly sensitive to catecholamines, and are poorly sensitive to insulin; these traits are amplified when visceral adipocytes hypertrophy. As a result, enlarged visceral fat stores tend to flood the portal circulation with free fatty acids at metabolically inappropriate times when fatty acids are unlikely to be oxidized, thus exposing tissues to excessive free fatty acid levels and giving rise to the insulin resistance syndrome. A logical approach to preventing or correcting visceral obesity is to down-regulate the lipoprotein lipase (LPL) activity of visceral adipocytes relative to that expressed in subcutaneous adipocytes and skeletal muscle. IGF-I activity appears to be a primary determinant of visceral LPL activity in humans; systemic IGF-I activity is decreased when diurnal insulin secretion is low, when hepatocytes detect a relative paucity of certain essential amino acids, and when estrogens are administered orally. The ability of alpha-glucosidase inhibitor therapy to selectively reduce visceral adiposity suggests that down-regulation of diurnal insulin secretion and/or IGF-I activity may indeed have a greater impact on LPL activity in visceral fat than in subcutaneous fat. Thus, low-glycemic-index, vegan, high-protein, or hypocaloric diets can be expected to decrease visceral LPL activity, as can postmenopausal estrogen therapy. Furthermore, estrogen enhances the LPL activity of non-pathogenic gluteofemoral fat cells, whereas testosterone decreases visceral LPL activity in men; this may explain why sex hormone replacement in middle-aged people of both sexes has a favorable impact on visceral fat and insulin sensitivity. Beta-adrenergic activity suppresses transcription of LPL in adipocytes; this phenomenon may contribute to the favorable impact of exercise training on visceral obesity; conceivably, preadministration of safe drugs that boost catecholamine activity (caffeine, yohimbine) could potentiate this beneficial effect of exercise. Glucocorticoids selectively increase the LPL activity of visceral adipocytes; while there is currently no convincing evidence that psychological stress is a major determinant of visceral adiposity, or that stress management techniques can help to correct visceral obesity, reports that anxiolytic therapy can improve glycemic control in type 2 diabetes should encourage further research along these lines. Copyright 2001 Harcourt Publishers Ltd.