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Published on: June 17, 2025
Maternal obesity is necessary for programming effect of high-fat diet on offspring
Christy L White1, Megan N Purpera, Christopher D Morrison
1Pennington Biomedical Research Center, Louisiana State University System, Baton Rouge, LA 70808, USA. christy.white@pbrc.edu
Insights
Maternal obesity, not just high-fat diets, increases offspring
Area of Science:
- Reproductive biology
- Metabolic disorders
- Developmental origins of health and disease
Background:
- Maternal diet during gestation and lactation influences offspring metabolic health.
- The independent roles of maternal obesity and dietary fat intake in offspring predisposition to obesity are not fully elucidated.
Purpose of the Study:
- To investigate whether maternal high-fat (HF) diet consumption, independent of obesity, increases serum leptin in neonatal pups.
- To determine if maternal obesity predisposes offspring to adult obesity.
Main Methods:
- Female rats were fed either a high-fat (HF) diet, a low-fat (LF) diet, or an HF diet but pair-fed (PF) to match LF caloric intake.
- Offspring body weight, body fat, serum leptin, and insulin tolerance were assessed at weaning and at 18 weeks of age.
- Offspring were subsequently fed either HF or LF diets from 8 to 18 weeks of age.
Main Results:
- Offspring born to obese dams exhibited higher body fat, elevated serum leptin, and reduced insulin tolerance at weaning.
- At 18 weeks, offspring from obese dams weighed significantly more, irrespective of their own adult diet.
- Offspring consuming an HF diet weighed more than those on an LF diet, but maternal obesity had a comparable effect on offspring weight.
Conclusions:
- Maternal adiposity, rather than dietary fat per se, is a key driver of hyperleptinemia, insulin resistance, and increased adult body weight in offspring.
- Maternal obesity exerts an independent and significant influence on offspring's long-term body weight regulation.
- These findings highlight the critical role of maternal metabolic status in programming offspring for metabolic health or disease.
Abstract:
We tested the hypothesis that maternal consumption of dietary fat, independent from obesity, increases serum leptin in neonatal pups and predisposes them to adult obesity. Female rats either were fed a high-fat (HF) diet or a low-fat (LF) diet or were fed the HF diet but pair fed (PF) to the caloric intake of the LF group for 4 wk before breeding and throughout gestation and lactation. Dams consuming the HF diet had increased adiposity and were hyperphagic. At weaning, pups born to obese dams had significantly higher body fat and serum leptin levels and reduced insulin tolerance compared with offspring of LF-fed dams. Pups were weaned onto a chow diet until 8 wk of age, when they were then fed either HF or LF diet. At 18 wk of age, offspring from obese HF dams weighed more than offspring from nonobese LF or PF dams, and offspring eating HF diet weighed significantly more than those eating LF diet. Consequently, HF-fed offspring of obese HF dams weighed the most and LF-fed offspring from obese HF dams were similar in weight to HF-fed offspring from nonobese LF dams. These data suggest that maternal obesity exerts an independent effect on offspring body weight that is of similar magnitude as the effect of the offspring's adult diet. Furthermore, there was no difference in body weight between the nonobese LF and PF offspring on either diet. Together, these data suggest that maternal adiposity, and not dietary fat per se, induces hyperleptinemia and insulin resistance in offspring, as well as an increased body weight that persists into adulthood.
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