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Truncal Adiposity, Relative Growth Hormone Deficiency, and Cardiovascular Risk

Neuroendocrine Unit (K.K.M., B.M.K.B., J.G.L., A.K.), Massachusetts General Hospital, and Department of Laboratory Medicine (G.B., N.R.), Children’s Hospital, and Harvard Medical School, Boston, Massachusetts 02114

Address all correspondence and requests for reprints to: Karen K. Miller, M.D., Neuroendocrine Unit, BUL 457B, Massachusetts General Hospital, Boston, Massachusetts 02114. E-mail: KKMiller{at}Partners.org.

We hypothesized that endogenous GH would be reduced in healthy women with relative truncal adiposity despite lack of generalized obesity and that decreased GH would be associated with increased cardiovascular risk markers. Fifteen healthy female volunteers were divided into two groups, low truncal fat and high truncal fat, of comparable body mass index (BMI). Age and BMI (23.7 ± 2.1 vs. 25.8 ± 2.8 kg/m²) were similar in the two groups. Trunk fat was higher in the high-truncal-fat group, as designed. Twenty-four-hour mean GH, amplitude, and basal GH concentration were 41, 32, and 36% lower, respectively, in the high-truncal-fat group, but GH pulse frequency and IGF-I levels did not differ. In a stepwise regression model, trunk fat accounted for 38% of the variation of mean GH levels (P = 0.02), but neither total body fat nor BMI were significant determinants of mean GH in the model. There was a strong inverse association between mean 24-h GH and both truncal fat and cardiovascular risk markers, including high-sensitivity C-reactive protein. Our data suggest that visceral adiposity may be associated with reduced endogenous GH in healthy women, even in the absence of generalized obesity, and that decreased GH secretion may be associated with increased cardiovascular risk markers in this population.

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