On the role of vitamin D binding globulin in glucose homeostasis: Results from the San Luis Valley diabetes study

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Abstract

Several studies have reported association between noninsulin‐dependent diabetes mellitus and GC, the vitamin D binding protein of human plasma, with the GC 1 allele in significant excess among diabetics. Additionally, there is a considerable body of animal data suggesting that vitamin D has a significant impact on insulin secretion. Examination of the insulin levels in Dogrib Indians showed that the lowest levels of fasting insulin were associated with the GC 1F‐1F genotype. The present study examined levels of glucose, C‐peptide, and insulin at fasting and 1 hr and 2 hr following a 75 g oral glucose challenge, in a population of Hispanic‐Americans and Anglos in the San Luis Valley of southern Colorado. The sample comprised a total of 468 individuals with normal glucose tolerance. Of these, 289 were Anglos and 179 were Hispanic‐Americans. An analysis of covariance was performed to determine the effect of the GC genotypes on mean levels of the primary variables—glucose, C‐peptide, and insulin—and a secondary variable—insulinogenic index adjusting for the covariates age, body mass index (BMI), gender, and ethnicity. The analyses revealed that there is a significant difference in mean levels of glucose at fasting (F value = 2.46; P = 0.033) among the GC genotypes in the sample. Additionally, the differences in mean levels of 1 hr postprandial glucose among the GC genotypes although not significant at a 5% level, were significant at the 10% level. No other significant phenotypic effects were observed. These analyses, are not in concordance the results of an earlier study, where lower fasting insulin was associated with the GC 1F‐1F genotype. Copyright © 1989 Wiley‐Liss, Inc., A Wiley Company

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Iyengar, S., Hamman, R. F., Marshall, J. A., Majumder, P. P., & Ferrell, R. E. (1989). On the role of vitamin D binding globulin in glucose homeostasis: Results from the San Luis Valley diabetes study. Genetic Epidemiology, 6(6), 691–698. https://doi.org/10.1002/gepi.1370060606

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