Effect of long-term rhGH administration in GH-deficient adults on fat cell epinephrine response

Beauville, M; Harant, I.; Crampes, F.; Rivière, D.; Tauber, M.; Tauber, J. P.; Garrigues, M

doi:10.1152/ajpendo.1992.263.3.e467

Cited by 56 publications

(44 citation statements)

References 21 publications

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“…While the lipolytic effects of growth hormone are still debated, recent data suggest that recombinant human growth hormone administration to growth hormone de®cient adults increases the in vitro lipolytic response of isolated adipocytes to epinephrine. 26 While epinephrine and norepinephrine levels in all three groups were quantitatively similar during exercise, it is possible that because of the growth hormone response, PO women were more sensitive to the lipolytic effects of catecholamines, giving rise to high free fatty acid and a trend for elevated glycerol levels.…”

Section: Discussionmentioning

confidence: 92%

“…We did not directly measure lipolytic response of fat cells to catecholamines. Thus, we can only infer that high levels of growth hormone, as the literature suggests, 26 sensitized post-obese women to catecholamine induced lipolysis during acute exercise, and this resulted in the high level of circulating FFA. Given the preliminary nature of this observation, future Figure 5 Change in plasma free fatty acid starting at 55 min of exercise and continuing throughout 1 hr of post-exercise recovery.…”

Section: Discussionmentioning

confidence: 94%

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Substrate oxidation and availability during acute exercise in non‐obese, obese, and post‐obese sedentary females

et al. 1999

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OBJECTIVE: This study compared fat oxidation rates during an acute bout of cycle ergometry exercise (E) typical of progressive fat oxidation in healthy, but sedentary, women of different obesity histories. DESIGN: Five never-obese (NO) (mean age 25 AE 3 (s.e.)y, mean body fat 25.0 AE 2.8 (s.e.)%), ®ve obese (O) (26 AE 3 y, 44.4 AE 1.7%), and ®ve post-obese (PO) (22 AE 1 y, 32.2 AE 3.0%) women cycled for 60 min at 60 ± 65% peak VO 2 . To identify the speci®c effects of E, a control trial consisting of 60 min of seated rest (R) was also performed. E and R trials were counterbalanced one month apart in the follicular phase and conducted following a 3 d normalized, eucaloric diet. MEASUREMENTS: Dual energy X-ray absorptiometry (DEXA) was used to determine body composition, and all were weight stable for at least eight weeks prior to experimentation. During both trials breath by breath measurements of VO 2 and RER were used to determine substrate oxidation and energy expenditure. Blood samples were collected for hormone and metabolite analysis before, and every 15 min during exercise or rest. RESULTS: All three groups showed a similar and progressive shift toward fat oxidation as exercise progressed. No group differences were observed for E energy expenditure or fat oxidation. Glycerol (P`0.0001) and free fatty acids (P`0.0001) increased similarly in all three groups, but PO maintained the highest free fatty acid level during exercise (group effect; P`0.01). E and R decreased (P`0.001 for both) insulin levels across groups, with lowest levels noted in PO and highest in O. Plasma epinephrine (P`0.0001) and norepinephrine (P`0.001) increased similarly during E in all three groups. Plasma growth hormone (GH) levels rose (P`0.05) during E, with a pronounced increase observed in PO. CONCLUSION: We conclude that exercise of equal relative intensity elicited similar fat oxidation rates among NO, O, and PO women, despite group differences in free fatty acid availability. The PO women's persistently lower insulin and higher plasma GH levels may have enhanced free fatty acid availability.

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 94%

Substrate oxidation and availability during acute exercise in non‐obese, obese, and post‐obese sedentary females

et al. 1999

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“…Considering the well documented lipolytic effect of GH, 20,21 the ®nding of a preferential reduction in visceral { P`0.05 placebo group vs GH group after treatment.…”

Section: Discussionmentioning

confidence: 99%

Low-dose growth hormone treatment combined with diet restriction decreases insulin resistance by reducing visceral fat and increasing muscle mass in obese type 2 diabetic patients

Nam

Kim

et al. 2001

Int J Obes

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OBJECTIVE:To evaluate the effects of low-dose growth hormone (GH) therapy combined with diet restriction on changes in body composition and the consequent change in insulin resistance in newly-diagnosed obese type 2 diabetic patients. DESIGN: Double-blind and placebo-controlled trial of 25-kcalakg IBW diet daily with GH (n 9; rhGH, 0.15 IUakg body weightaweek) or placebo (n 9) for 12 weeks. SUBJECTS: Eighteen newly-diagnosed obese type 2 diabetic patients (age 42 ± 56 y, body mass index 28.1 AE 2.7 kgam 2 ). MEASUREMENTS: Body composition and fat distribution parameters (by bioelectrical impedance analyzer and CT scans), serum IGF-1; serum glucose, insulin and free fatty acid (FFA) during oral glucose tolerance test (OGTT); HbA 1c ; serum lipid pro®les; and glucose disposal rate (GDR) by euglycemic hyperinsulinemic clamp at baseline and after treatment. RESULTS: The fraction of body weight lost as fat lost was signi®cantly greater (0.98 AE 0.39 vs 0.52 AE 0.32 kgakg, P`0.05) and visceral fat area was decreased more in the GH-treated group compared to the placebo-treated group (27.9 vs 21.6%, P`0.05). Lean body mass and muscle area were reduced in the placebo-treated group, whereas an increase in both was observed in the GH-treated group. GDR the was signi®cantly increased in only the GH-treated group (4.67 AE 1.05 vs 6.95 AE 0.91 mgakgamin, P`0.05). The GH-induced increase in GDR was positively correlated with the decrease in the ratio of visceral fat areaamuscle area (r 0.588, P 0.001). Serum glucose levels and insulin-and FFA-area under the curve during OGTT and HbA 1c were signi®cantly decreased after GH treatment. LDL-cholesterol level was decreased in only the GH-treated group. CONCLUSION: Low-dose GH treatment combined with dietary restriction resulted not only in a decrease of visceral fat but also in an increase of muscle mass with a consequent improvement of the insulin resistance observed in obese type 2 diabetic patients.

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“…The chronic effects of GH are considered to be anti-insulin, and they include increased blood glucose concentrations, decreased peripheral insulin sensitivity despite higher levels of insulin secretion, decreased insulin-stimulated glucose uptake in muscle, increased hepatic glucose production, and stimulation of lipolysis (3). The lipolytic effects of chronic GH treatment include decreased adiposity, reduced triglyceride (TG) accumulation resulting from inhibition of lipoprotein lipase (LPL), and increased hormone-sensitive lipase (HSL) activity (4,5).…”

Section: Introductionmentioning

confidence: 99%

Inhibition of growth hormone action improves insulin sensitivity in liver IGF-1–deficient mice

et al. 2004

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Liver IGF-1-deficient (LID) mice have a 75% reduction in circulating IGF-1 levels and, as a result, a fourfold increase in growth hormone (GH) secretion. To block GH action, LID mice were crossed with GH antagonist (GHa) transgenic mice. Inactivation of GH action in the resulting LID + GHa mice led to decreased blood glucose and insulin levels and improved peripheral insulin sensitivity. Hyperinsulinemic-euglycemic clamp studies showed that LID mice exhibit severe insulin resistance. In contrast, expression of the GH antagonist transgene in LID + GHa mice led to enhanced insulin sensitivity and increased insulin-stimulated glucose uptake in muscle and white adipose tissue. Interestingly, LID + GHa mice exhibit a twofold increase in white adipose tissue mass, as well as increased levels of serumfree fatty acids and triglycerides, but no increase in the triglyceride content of liver and muscle. In conclusion, these results show that despite low levels of circulating IGF-1, insulin sensitivity in LID mice could be improved by inactivating GH action, suggesting that chronic elevation of GH levels plays a major role in insulin resistance. These results suggest that IGF-1 plays a role in maintaining a fine balance between GH and insulin to promote normal carbohydrate and lipid metabolism.

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Effect of long-term rhGH administration in GH-deficient adults on fat cell epinephrine response

Cited by 56 publications

References 21 publications

Substrate oxidation and availability during acute exercise in non‐obese, obese, and post‐obese sedentary females

Substrate oxidation and availability during acute exercise in non‐obese, obese, and post‐obese sedentary females

Low-dose growth hormone treatment combined with diet restriction decreases insulin resistance by reducing visceral fat and increasing muscle mass in obese type 2 diabetic patients

Inhibition of growth hormone action improves insulin sensitivity in liver IGF-1–deficient mice

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