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Prenatal environmental exposures that may influence β-cell function or insulin sensitivity in middle age

Published online by Cambridge University Press:  20 September 2010

H. S. Kahn ,
A. D. Stein  and
L. H. Lumey
H. S. Kahn*
Affiliation:
Division of Diabetes Translation, Centers for Disease Control and Prevention, Atlanta, Georgia, USA
A. D. Stein
Affiliation:
Hubert Department of Global Health, Rollins School of Public Health, Emory University, Atlanta, Georgia, USA
L. H. Lumey
Affiliation:
Department of Epidemiology, Mailman School of Public Health, Columbia University, New York, NY, USA
*
*Address for correspondence: Dr H. S. Kahn, Centers for Disease Control & Prevention – Division of Diabetes Translation, MS K-10, NCCDPHP 4770 Buford Highway, Atlanta, Georgia 30341, USA. (Email hkahn@cdc.gov)
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Abstract

The associations between fetal environment and diabetes risk are likely mediated by the offspring’s diminished pancreatic β-cell function or reduced insulin sensitivity. Our ability to distinguish between these mechanisms is impeded by the lack of markers describing an individual’s gestational environment. Fingerprints, however, are permanently fixed in the first half of gestation, and increased values of a dermatoglyphic marker that contrasts fingerprint ridge counts between the thumbs and fifth fingers (Md15) have been linked to type 2 diabetes. Among 763 adults without known diabetes from the Dutch Hunger Winter Families Study, we tested the associations of Md15 with homeostatic assessment indices of β-cell function (HOMA-b) and insulin sensitivity (QUICKI). For either outcome index, linear regression models included terms for Md15 tertiles and for maternal history of diabetes as reported by each participant. All models were corrected for sibling pairs and adjusted for age, sex and famine exposures. Increased Md15 was associated with decreased HOMA-b (P = 0.03 for Md15 tertile 3 v. 1) but not with QUICKI. In contrast, maternal history of diabetes was associated with decreased QUICKI (P < 0.001) but not with HOMA-b. Birth weight (available for 520 participants) was positively associated with increased QUICKI (P = 0.04 for birth weight tertile 3 v. 1) but not with HOMA-b. Fingerprint Md15, maternal history of diabetes and birth weight may help to identify specific defects in the control of adult glucose metabolism. Research into the environment associated with Md15 variation may suggest prenatal strategies for optimizing β-cell function in adult life.

Keywords

dermatoglyphicsfetal programminghyperglycemiainsulin sensitivitypancreatic β cells
Type
Original Articles
Information
Journal of Developmental Origins of Health and Disease , Volume 1 , Issue 5 , October 2010 , pp. 300 - 309
Copyright
Copyright © Cambridge University Press and the International Society for Developmental Origins of Health and Disease 2010 This is the work of the U.S. Government and is not subject to copyright protection in the United States

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