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Influence of maternal obesity on insulin sensitivity and secretion in offspring
Geltrude Mingrone1, Melania Manco, Maria Elena Valera Mora
1Medicine and Diabetes Center, Università Cattolica S. Cuore, Rome, Italy. gmingrone@rm.unicatt.it
Insights
Maternal obesity can lead to offspring developing obesity and insulin resistance, even with normal birth weight. This effect shows sexual dimorphism, with males exhibiting higher insulin sensitivity and secretion.
Area of Science:
- Endocrinology
- Metabolic Health
- Perinatal Medicine
Background:
- Maternal obesity is a growing concern with potential long-term health implications for offspring.
- Understanding the impact of the maternal metabolic environment on offspring's glucose homeostasis is crucial.
Purpose of the Study:
- To investigate the effects of maternal obesity on insulin sensitivity and secretion in adult offspring.
- To explore potential sex differences in these metabolic parameters.
Main Methods:
- Studied offspring from obese and normal-weight mothers, assessing body composition via dual-X-ray absorptiometry.
- Measured plasma glucose, insulin, and C-peptide during an oral glucose tolerance test (OGTT).
- Calculated insulin sensitivity, insulin secretion, and beta-cell glucose sensitivity using mathematical modeling and biochemical markers.
Main Results:
- Offspring of obese mothers (Ob group) exhibited significantly higher insulin resistance compared to controls, irrespective of offspring sex.
- Male offspring in the Ob group showed significantly higher insulin secretion post-OGTT than control males.
- Multivariate analysis indicated that maternal obesity, offspring sex, BMI, and beta-cell glucose sensitivity collectively influenced offspring's insulin sensitivity and secretion.
Conclusions:
- Maternal obesity can program offspring for later development of obesity and insulin resistance, independent of birth weight.
- A clear sexual dimorphism was observed, with male offspring demonstrating enhanced insulin sensitivity and secretion compared to females, suggesting a role for maternal genetic/epigenetic transmission.
Objective:
The purpose of this study was to clarify the effects of maternal obesity on insulin sensitivity and secretion in offspring.
Research Design And Methods:
Fifty-one offspring of both sexes of obese (Ob group) and 15 offspring of normal-weight (control group) mothers were studied. Plasma glucose, insulin, and C-peptide were measured during an oral glucose tolerance test (OGTT). Insulin sensitivity was calculated using the oral glucose insulin sensitivity index, and insulin secretion and beta-cell glucose sensitivity were computed by a mathematical model. Fasting leptin and adiponectin were also measured. Body composition was assessed by dual-X-ray absorptiometry.
Results:
No birth weight statistical difference was observed in the two groups. Of the Ob group, 69% were obese and 19% were overweight. The Ob group were more insulin resistant than the control group (398.58 +/- 79.32 vs. 513.81 +/- 70.70 ml(-1) x min(-1) x m(-2) in women, P < 0.0001; 416.42 +/- 76.17 vs. 484.242 +/- 45.76 ml(-1) x min(-1) x m(-2) in men, P < 0.05). Insulin secretion after OGTT was higher in Ob group than in control group men (63.94 +/- 21.20 vs. 35.71 +/- 10.02 nmol x m(-2), P < 0.01) but did not differ significantly in women. beta-Cell glucose sensitivity was not statistically different between groups. A multivariate analysis of variance showed that maternal obesity and offspring sex concurred together with BMI and beta-cell glucose sensitivity to determine the differences in insulin sensitivity and secretion observed in offspring.
Conclusions:
Obese mothers can give birth to normal birth weight babies who later develop obesity and insulin resistance. The maternal genetic/epigenetic transmission shows a clear sexual dimorphism, with male offspring having a higher value of insulin sensitivity (although not statistically significant) associated with significantly higher insulin secretion than female offspring.
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