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Pennington Biomedical Research Center, Louisiana State University (G.A., T.Ra., D.R.N., C.B.), Baton Rouge, Louisiana 70808; Division of Biostatistics and Departments of Genetics and Psychiatry, Washington University Medical School (T.Ri., M.A.P., D.C.R.), St. Louis, Missouri 63110; School of Kinesiology and Leisure Studies, University of Minnesota (A.S.L.), Minneapolis, Minnesota 55455; Department of Kinesiology, Indiana University (J.S.S.), Bloomington, Indiana 47405; and Department of Health and Kinesiology, Texas A&M University (J.H.W.), College Station, Texas 77843-4243
Address all correspondence and requests for reprints to: George Argyropoulos, Ph.D., Pennington Biomedical Research Center, 6400 Perkins Road, Baton Rouge, Louisiana 70808. E-mail: . argyrog{at}pbrc.edu
Abstract
The mouse agouti-related protein (AGRP) is a powerful appetite effector that results in hyperphagia and the development of obesity when administered intracerebroventricularly or when overexpressed in transgenic mice. Animal studies have also shown that exogenous administration of AGRP predisposes toward hedonic intake of high fat and high sucrose diets. The human ortholog (hAGRP) maps on chromosome 16q22 and has similar physiological properties, as tested in animal models. A polymorphism was identified in the third exon of hAGRP, c.199G
A, that resulted in a nonconservative amino acid substitution, Ala67Thr. Computational analysis of the protein showed significant differences in the coils of the two polymorphic isoforms of the protein. Human studies showed no genotype effects in individuals with a mean age of 25 yr. However, the G/G genotype was significantly associated with fatness and abdominal adiposity in the parental population with a mean age of 53 yr. The c.199GA polymorphism in hAGRP could, therefore, play a role in the development of human obesity in an age-dependent fashion.
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