Comparison of the effects of growth hormone and insulin-like growth factor I on substrate oxidation and on insulin sensitivity in growth hormone-deficient humans.

Abstract

Insulin-like growth factor-I (IGF-I) is considered to be the mediator of the growth-promoting effects of growth hormone (GH). The metabolic effects of these two hormones, however, are different. Whereas GH treatment leads to elevated insulin and glucose levels, reduced insulin sensitivity, and impaired glucose tolerance, IGF-I treatment leads to reduced insulin and GH levels and enhanced insulin sensitivity. IGF-I may, therefore, not only be the mediator of the growth-promoting effects of GH but also a modulator of the effects of GH on insulin action and glucose metabolism. To study the influence of GH and IGF-I on substrate metabolism and insulin sensitivity (assessed by euglycemic, hyperinsulinemic clamping combined with indirect calorimetry and glucose tracer infusion), we have treated eight GHdeficient adults with GH (2 IU/m2 daily subcutaneously [s.c.]), IGF-I (10 jtg/kg h s.c.), or both hormones together for 7 d, respectively, and compared the effects of these treatment regimens with a control phase. Our findings suggest that (a) both GH and IGF-I promote lipolysis and lipid oxidation, albeit by different mechanisms; (b) treatment with either hormone is followed by enhanced energy expenditure and reduced protein oxidation; and (c) IGF-I reverses the insulin resistance induced by GH. (J. Clin. Invest.

IGF-I treatment in adults with type 1 diabetes: effects on glucose and protein metabolism in the fasting state and during a hyperinsulinemic-euglycemic amino acid clamp.

“…These changes included reduced circulating levels of leucine and leucine oxidation and the increased leucine MCR and net leucine balance. Similar findings have been observed after IGF-I administration in healthy subjects and GH-deficient adults (32)(33)(34)(35) and in patients with Cushing's syndrome after GH therapy (36). Evidence suggests that GH therapy results in upregulation of amino acid transporter systems (37), increasing the efficiency of cellular amino acid uptake.…”

“…It is likely that decreased GH-mediated lipolysis and simultaneously enhanced insulin sensitivity resulted in the lower circulating NEFA levels during the IGF-I administration. A study of IGF-I administration in GH-deficient adults also demonstrated reductions in NEFA levels (33), indicating that IGF-I may also regulate NEFA levels through mechanisms independent of GH.…”

Growth Hormone Administration Controls Body Composition Associated with Changes of Thermogenesis in Obese KK-Ay Mice~!2009-08-29~!2010-01-12~!2010-03-26~!

“…Each value is the mean ± standard error of the mean. GH is thought to increase the basal metabolic rate through thermogenesis [14] and the induction of catecholamine release [28], increasing the conversion of the thyroid hormone T4 to the more metabolically active T3 [29], and increasing IGF-1 secretion, which may participate in increasing resting energy expenditure [30]. Conversely, adult KK-A y mice with markedly elevated IGF-1 levels showed decreased UCP1 and UCP3 expressions.…”

Food consumed does not account for the higher prevalence of obesity among stunted adults in a very-low-income population in the Northeast of Brazil (Maceió, Alagoas)

“…The mean energy intake of the individuals in our study (E6213 kJ) was below that reported in a population-based study comprising the whole Brazilian population (EN-DEF ¼ National Study of Family Expenditure), a study carried out in 1974/1975, and in which the mean energy consumption was 8493 kJ (Fundação IBGE, 1977). More recently, another population-based study (Hussain et al, 1994) found even higher numbers (10 878 kJ). Obesity, stunting and food pattern T T Florêncio et al…”

“…For instance, the lower concentration of the insulin-like growth factor I (IGF-I) is accompanied by a lower sensitivity of the hormone sensitive lipase to the lipolytic hormones. For this reason, any reduction in IGF-I may result in lower fat oxidation (Hussain et al, 1994).…”