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Prenatal environmental exposures that may influence β-cell function or insulin sensitivity in middle age
H S Kahn1, A D Stein2, L H Lumey3
11Division of Diabetes Translation, Centers for Disease Control and Prevention, Atlanta, Georgia, USA.
Journal of Developmental Origins of Health and Disease
|August 22, 2014
Summary
Fingerprint patterns (Md15) may indicate fetal environment effects on diabetes risk. Increased Md15 is linked to reduced pancreatic beta-cell function, suggesting prenatal strategies for diabetes prevention.
Area of Science:
- Endocrinology
- Developmental Biology
- Genetics
Background:
- Fetal environment impacts offspring diabetes risk via beta-cell function or insulin sensitivity.
- Lack of markers for gestational environment hinders understanding of diabetes mechanisms.
- Fingerprints, fixed early in gestation, offer a potential marker.
Purpose of the Study:
- To investigate the association between a dermatoglyphic marker (Md15) and markers of beta-cell function (HOMA-b) and insulin sensitivity (QUICKI).
- To explore if fingerprint patterns can identify specific defects in glucose metabolism control.
Main Methods:
- Utilized data from 763 adults in the Dutch Hunger Winter Families Study.
- Employed linear regression to assess Md15, maternal diabetes history, and birth weight against HOMA-b and QUICKI.
- Adjusted for sibling pairs, age, sex, and famine exposure.
Main Results:
- Increased Md15 was significantly associated with decreased HOMA-b (beta-cell function), but not QUICKI (insulin sensitivity).
- Maternal history of diabetes correlated with decreased QUICKI, while birth weight positively associated with QUICKI.
- Md15 appears to reflect distinct prenatal influences on glucose metabolism compared to maternal history or birth weight.
Conclusions:
- Fingerprint marker Md15 may identify individuals with reduced pancreatic beta-cell function due to early-life environmental exposures.
- Maternal diabetes history and birth weight are associated with insulin sensitivity.
- These markers could aid in identifying specific metabolic defects and developing prenatal strategies for diabetes prevention.
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