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Childrens Hospital of Pittsburgh, Weight Management and Wellness Center, and Division of Pediatric Endocrinology, Metabolism, and Diabetes Mellitus, Pittsburgh, Pennsylvania 15213
Address all correspondence and requests for reprints to: Silva A. Arslanian, M.D., Director, Weight Management and Wellness Center, Childrens Hospital of Pittsburgh, 3705 Fifth Avenue at DeSoto Street, Pittsburgh, Pennsylvania 15213. E-mail: silva.arslanian{at}chp.edu.
Objective: Obesity prevalence is higher in African-American (AA) vs. American white (AW) youth. Ghrelin is a "hunger" peptide that is high preprandially and decreases postprandially, and peptide YY (PYY) is a "satiety" hormone increasing after meals. Impaired regulation of ghrelin/PYY may be conducive to obesity. We hypothesized that racial differences in childhood obesity could partly be explained by differences in ghrelin/PYY dynamics.
Research Design and Methods: We investigated: 1) ghrelin suppression/PYY elevation in response to an oral glucose tolerance test (OGTT) in AA vs. AW, and 2) the relationship of ghrelin and PYY dynamics to insulin sensitivity. Thirty-three AA and 54 AW prepubertal children underwent an OGTT measuring ghrelin, PYY, glucose, and insulin. Fasting glucose to insulin ratio (GF/IF) was used to assess the relationship of insulin sensitivity to fasting and post-OGTT ghrelin and PYY levels.
Results: OGTT-induced suppression in ghrelin (
ghrelin) was lower in AA youth.
ghrelin correlated with GF/IF (r = 0.47, P < 0.001) and
insulin at 30 min (r = 0.47, P < 0.001). In multiple regression analysis, race (P = 0.013) and GF/IF (P = 0.004) contributed independently to the variance in
ghrelin (R2 = 0.28, P < 0.001). Fasting and post-OGTT PYY levels were lower in AAs and were not related to insulin sensitivity.
Conclusion: The lower suppression of ghrelin in AA, but not the lower PYY levels, correlates with insulinemia and insulin resistance. Less ghrelin suppression and PYY elevation after a meal in black youth could be a potential mechanism of race-related differences in hunger/satiety predisposing to risk of obesity.
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