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From the Clinical Research Centers |
Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development (J.A.Y., S.Z.Y., A.J.B., K.N.S.); Divisions of Digestive Diseases and Nutrition (S.Z.Y., K.N.S.) and Nutrition Research Coordination (K.N.S.), National Institute of Diabetes and Digestive Disease; Clinical Neuroendocrinology Branch, National Institute of Mental Health (P.W.G.); and Nutrition Department (N.G.S.) and Rehabilitation Medicine Department (B.D.), Warren Grant Magnuson Clinical Center, National Institutes of Health, Bethesda, Maryland 20892
Address all correspondence and requests for reprints to: Jack A. Yanovski, M.D., Ph.D., Unit on Growth and Obesity, Developmental Endocrinology Branch, National Institute of Child Health and Human Development, National Institutes of Health, 10 Center Drive, MSC 1862, Building 10, Room 10N262, Bethesda, Maryland 20892-1862. E-mail: JYISi{at}NIH.Gov
African American women have a greater prevalence of obesity than Caucasian women, but the reasons for this difference are not known. We have investigated whether activity of the hypothalamic-pituitary adrenal axis plays a role in this phenomenon. Previous studies have shown that plasma ACTH immunoreactivity (ACTH-IR) of African American women, measured after ovine CRH (oCRH) stimulation, is significantly greater than ACTH-IR of Caucasian women, but is not accompanied by greater plasma cortisol concentrations. Analysis by high pressure liquid chromatography has demonstrated that after oCRH stimulation, the plasma ACTH-IR of African American women contains many nonintact ACTH fragments not found in Caucasians. To determine whether these racial differences in ACTH-IR secretion are an artifact of exogenous oCRH administration or are also found after a physiological stimulus for ACTH secretion, we measured hormones of the hypothalamic-pituitary adrenal axis before and after a standardized, maximal exercise treadmill test in 16 African American and 19 Caucasian healthy women matched for age, socioeconomic status, and body mass index.
The intensity of exercise performed was similar in the two groups, as determined by duration of exercise, perceived intensity of exertion, plasma lactate, maximal heart rate, and maximum oxygen uptake. Basal ACTH-IR measured by RIA or immunoradiometric assay and cortisol were similar in African Americans and Caucasians. Plasma ACTH-IR, measured 10 min after completion of exercise, was significantly greater in African Americans than in Caucasians [by RIA: mean ± SD ACTH-IR, 47.1 ± 30.9 vs. 25.4 ± 16.7 pmol/L (P < 0.01); by immunoradiometric assay: ACTH-IR, 45.9 ± 43.2 vs. 21.1 ± 14.6 pmol/L (P < 0.05)]. However, plasma cortisol after exercise was not different (450.2 ± 157.7 vs. 483.6 ± 180.4 nmol/L; P = 0.57).
We conclude that ACTH-IR is significantly greater in African American than in Caucasian women after intense exercise. The ACTH-IR of African Americans and Caucasians does not appear to be equipotent at adrenal melanocortin-2 receptors, because the greater ACTH-IR of African Americans does not lead to greater cortisol secretion. Whether some components of the ACTH-IR detected in African Americans affect signal transduction of the hypothalamic melanocortin-4 receptors implicated in body weight regulation and thus predispose African American women to weight gain without altering plasma cortisol remains to be determined.
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