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Am J Physiol Endocrinol Metab (October 14, 2003). doi:10.1152/ajpendo.00335.2003
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Submitted on July 18, 2003
Accepted on October 9, 2003

Metabolic Regulation of Growth Hormone by Free Fatty Acids, Somatostatin and Ghrelin in HIV Lipodystrophy

Polyxeni Koutkia1, Gary Meininger1, Bridget Canavan1, Jeff Breu2, and Steven Grinspoon1*

1 Neuroendocrine Unit, Massachusetts General Hospital Program in Nutritional Metabolism and Harvard Medical School, Boston, MA, USA
2 General Clinical Research Center, Massachusetts Institute of Technology, Cambridge, MA, USA

* To whom correspondence should be addressed. E-mail: sgrinspoon{at}partners.org.

HIV lipodystrophy is a syndrome characterized by changes in fat distribution and insulin resistance. Prior studies suggest markedly reduced growth hormone (GH) levels in association with excess visceral adiposity among patients with HIV lipodystrophy. We investigated mechanisms of altered GH secretion in a population of 13 male HIV-infected patients with evidence of fat redistribution, compared to 10 HIV nonlipodystrophic patients and 11 male healthy controls similar in age and BMI. Although similar in BMI, the lipodystrophic group was characterized by increase visceral adiposity, free fatty acids and insulin and reduced extremity fat. We investigated ghrelin and the effects of acute lowering of free fatty acids (FFA) by acipimox on GH responses to growth hormone releasing hormone (GHRH). We also investigated somatostatin tone comparing GH response to combined GHRH and arginine versus GHRH alone using a subtraction algorithm. Our data demonstrate an equivalent number of GH pulses (4.1±0.6, 4.7±0.8 and 4.5 ±0.3 pulses/12 hours in the HIV lipodystrophic, HIV-nonlipodystrophic and healthy control group respectively, P>0.05) but markedly reduced GH secretion pulse area (1.14± 0.27 vs. 4.67±1.24 ng/mL*min, P<0.05 HIV lipodystrophic vs. HIV nonlipodystrophic; 1.14± 0.27 vs. 3.18±0.92 ng/mL*min, P<0.05 HIV lipodystrophic vs. control), GH pulse area and GH pulse width in the HIV lipodystrophy patients compared to the control groups. Reduced ghrelin (418 ± 46 vs. 514 ± 37 pg/mL, P<0.05 HIV lipodystrophic vs. HIV nonlipodystrophic; 418 ± 46 vs. 546 ± 45 pg/mL, P<0.05 HIV lipodystrophic vs. control), impaired GH response to GHRH by excess FFA and increased somatostatin tone contribute to reduced GH secretion in patients with HIV lipodystrophy. These data provide novel insight into the metabolic regulation of GH secretion in subjects with HIV-lipodystrophy.




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