ArticleFrontiers in endocrinology2021
Offspring of Obese Dams Exhibit Sex-Differences in Pancreatic Heparan Sulfate Glycosaminoglycans and Islet Insulin Secretion.
Article in Frontiers in endocrinology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.
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Who cites it
15 citing papers in PubMed, 18 citations in OpenAlex.
- A high-fat, high-sugar diet impairs maternal metabolism throughout pregnancy and lactation in mice.The Journal of physiology · 2026Article
- Establishment of sex-specific liver transcriptomes and H3K9me3 profiles during sexual maturity: the impact of maternal obesity.Biology of sex differences · 2025Article
- Role of Maternal Obesity in Offspring Cardiovascular Development and Congenital Heart Defects.Journal of the American Heart Association · 2025Article
- Repercussions of the Maternal Obesogenic Diet on the Oxidative Balance and Pancreatic Metabolism in Male Juvenile Offspring.Nutrients · 2025Article
- The Impact of Parental Preconception Nutrition, Body Weight, and Exercise Habits on Offspring Health Outcomes: A Narrative Review.Nutrients · 2024Review
- Increased allergic inflammation and decreased lung insulin sensitivity in offspring of obese allergic mothers.Journal of leukocyte biology · 2024Article
- Glucose intolerance as a consequence of hematopoietic stem cell dysfunction in offspring of obese mice.Molecular metabolism · 2024Article
- Mechanisms of spinophilin-dependent pancreas dysregulation in obesity.American journal of physiology. Endocrinology and metabolism · 2024Article
- Vascular Heparan Sulfate and Amyloid-β in Alzheimer's Disease Patients.International journal of molecular sciences · 2024Article
- Article
- RISING STARS: Mechanistic insights into maternal-fetal cross talk and islet beta-cell development.The Journal of endocrinology · 2023Review
- Programming by maternal obesity: a pathway to poor cardiometabolic health in the offspring.The Proceedings of the Nutrition Society · 2022Review
- Diet Modification before or during Pregnancy on Maternal and Foetal Outcomes in Rodent Models of Maternal Obesity.Nutrients · 2022Review
- Maternal obesity and the impact of associated early-life inflammation on long-term health of offspring.Frontiers in cellular and infection microbiology · 2022Review
- Extracellular Matrix Deposition and Remodeling after Corneal Alkali Burn in Mice.International journal of molecular sciences · 2021Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
Abstract
Offspring of obese mothers suffer higher risks of type 2 diabetes due to increased adiposity and decreased β cell function. To date, the sex-differences in offspring islet insulin secretion during early life has not been evaluated extensively, particularly prior to weaning at postnatal day 21 (P21). To determine the role of maternal obesity on offspring islet insulin secretion, C57BL/6J female dams were fed chow or western diet from 4 weeks prior to mating to induce maternal obesity. First, offspring of chow-fed and obese dams were evaluated on postnatal day 21 (P21) prior to weaning for body composition, glucose and insulin tolerance, and islet phasic insulin-secretion. Compared to same-sex controls, both male and female P21 offspring born to obese dams (MatOb) had higher body adiposity and exhibited sex-specific differences in glucose tolerance and insulin secretion. The male MatOb offspring developed the highest extent of glucose intolerance and lowest glucose-induced insulin secretion. In contrast, P21 female offspring of obese dams had unimpaired insulin secretion. Using SAX-HPLC, we found that male MatOb had a decrease in pancreatic heparan sulfate glycosaminoglycan, which is a macromolecule critical for islet health. Notably, 8-weeks-old offspring of obese dams continued to exhibit a similar pattern of sex-differences in glucose intolerance and decreased islet insulin secretion. Overall, our study suggests that maternal obesity induces sex-specific changes to pancreatic HSG in offspring and a lasting effect on offspring insulin secretion, leading to the sex-differences in glucose intolerance.
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