The Effect of Growth Hormone upon Glucose Metabolism and Cellularity in Rat Adipose Tissue

Br, Batchelor; Js, Stern

doi:10.1055/s-0028-1093999

Cited by 10 publications

(3 citation statements)

References 3 publications

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“…These findings suggest that the effect of GH on glucose and lipid oxidation is not direct, but is mediated by its lipolytic activity. This conclusion is supported by previous in vitro studies showing that 4-to 6-h exposure to GH did not affect either glucose oxidation by adipose tissue from hypoxic rats (43) or glucose conversion to glycogen in soleus muscle in rats (44).…”

Section: Discussionsupporting

confidence: 79%

Mediation of the Hepatic Effects of Growth Hormone by Its Lipolytic Activity

Piatti

Monti

Caumo

et al. 1999

The Journal of Clinical Endocrinology & Metabolism

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The aim of the study was to investigate the acute effect of GH per se, independent from its lipolytic activity, on glucose and lipid oxidation and glucose turnover in seven healthy subjects. Five tests lasting 360 min were performed. Each test consisted of a 4-h equilibration period followed by a euglycemic hyperinsulinemic (25 mU/ kg⅐h) clamp lasting 2 h. In test 1 (control experiment) saline was infused, leaving GH and FFA at basal levels. In tests 2, 3, and 4, GH was infused (80 ng/kg⅐min) to increase GH levels. Whereas in test 2 FFA levels were free to increase due to GH lipolytic activity, in test 3 FFA elevation was prevented by using an antilipolytic compound (Acipimox) that allowed evaluation of the effect of GH at low FFA levels. In test 4 (GHϩAcipimoxϩheparin) GH infusion was associated with the administration of Acipimox and heparin to maintain FFA at the basal level to evaluate the effect of GH per se independent from GH lipolytic activity. In test 5 Acipimox and a variable heparin infusion were given to evaluate possible effects of Acipimox other than the inhibition of lipolysis.During the euglycemic hyperinsulinemic clamp in the presence of high GH and FFA levels (test 2), glucose oxidation was significantly lower and lipid oxidation was significantly higher than in tests 1, 3, 4, and 5. During the same period, hepatic glucose production was completely suppressed in the control study (test 1; 94%) and in test 5 (99.6%), whereas it was significantly less inhibited (65%, 74%, and 73%) when GH was administered in tests 2, 3, and 4.In conclusion, these results suggest that GH directly mediates the reduction of insulin's effect on the liver. In addition, the effect of GH on glucose and lipid oxidation is not direct, but is mediated by its lipolytic activity. (J Clin Endocrinol Metab 84: 1658 -1663, 1999) M ANY STUDIES have shown that GH can induce insulin resistance (1-3), although the mechanism by which an acute increase in its levels can decrease glucose uptake is still debated. In vitro studies have shown that GH decreases glucose uptake without affecting glucose oxidation in human erythrocytes (4, 5), fat tissue (6), or diaphragm cultures (7). In vivo, hepatic glucose seems to reduce forearm glucose uptake, glucose oxidation, and glycogen synthase activity and to impair insulin suppression of hepatic glucose production (8 -10) in favor of increased lipid oxidation. Recently, Neely et al. (11) have shown that after an overnight GH infusion in normal subjects, both GH and free fatty acid (FFA) levels were positively correlated with the increase in peripheral and hepatic insulin resistance. In addition, in most of the previous studies, high levels of GH were invariably associated with high circulating levels of glycerol, FFA, and ␤-hydroxybutyrate (8 -10, 12, 13). Therefore, it remains unclear whether the effect of GH on glucose metabolism is direct (10) or mediated by GH-induced lipolytic action through the well known glucose-fatty acid cycle or Randle cycle, as hypothesized by Davidson et...

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Section: Discussionsupporting

confidence: 79%

Mediation of the Hepatic Effects of Growth Hormone by Its Lipolytic Activity

Piatti

Monti

Caumo

et al. 1999

The Journal of Clinical Endocrinology & Metabolism

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“…The present results show that the impaired in¬ corporation of glucose into total lipids (almost exclusively representing the glyceride-glycerol moiety in human fat cells; Smith, in press) after long-term exposure of human adipose tissue to GH was not accompanied by an altered CO2 formation. In rat adipose tissue studied in vitro other inve¬ stigators have found an impairment in CO2 form¬ ation as well as in lipid synthesis after long-term elevation of the plasma GH levels (Âkerblom et al 1971;Batchelor & Stern 1973). Since total glucose metabolism seems to be reduced by GH the me¬ chanism responsible is likely to be the membrane transport of glucose or one of the early steps in the glycolysis.…”

Section: Discussionmentioning

confidence: 97%

“…It can be demonstrated in vivo after a lag period of about 2 h (Schalch & Kipnis 1965) and in adipose tissue in vitro after prolonged exposure of the intact animal to increased levels of GH (Âkerblom et al 1971; Batchelor & Stern 1973; Chattopadhyay et al 1969). Until recently, however, no inhibitory effect of GH added in vitro has been shown on glucose metabolism.…”

mentioning

confidence: 95%

Reduced glucose incorporation to triglycerides following chronic exposure of human fat cells to growth hormone

Nyberg

Boström

Smith

1980

Acta Endocrinologica

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Using the tissue culture technique we have recently demonstrated that long-term exposure of human adipose tissue to human growth hormone (GH) in vitro leads to an impairment in glucose incorporation into triglycerides. This effect was further studied in the present investigation. Biopsies of human adipose tissue which had been cultured for one week with or without GH were studied in subsequent short-term incubations where the conversion of glucose to CO2 and to total lipids was determined. The formation of CO2 was not changed by previous exposure of the biopsies to GH whereas the incorporation of glucose into triglycerides was reduced by about one third. Total glucose metabolism, as determined from the sum of the two pathways, was significantly reduced. The activities of three glycolytic enzymes were determined in biopsies of human adipose tissue which had been cultured with or without GH for one week. The activity of phosphofructokinase was reduced, while the hexokinase and the glucose-6-phosphate dehydrogenase activities were unchanged. The diminished activity of phosphofructokinase, the enzyme considered to be rate-limiting for glycolysis in human fat cells, may be responsible for the decreased rate of glucose metabolism found.

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The Metabolic Actions of Growth Hormone

Goodman

2001

Comprehensive Physiology

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The Effect of Growth Hormone upon Glucose Metabolism and Cellularity in Rat Adipose Tissue

Cited by 10 publications

References 3 publications

Mediation of the Hepatic Effects of Growth Hormone by Its Lipolytic Activity

Mediation of the Hepatic Effects of Growth Hormone by Its Lipolytic Activity

Reduced glucose incorporation to triglycerides following chronic exposure of human fat cells to growth hormone

The Metabolic Actions of Growth Hormone

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