Insulin signaling and mitochondrial phenotype of skeletal muscle are programmed in utero by maternal diabetes
Language English Country Ireland Media print-electronic
Document type Journal Article, Research Support, Non-U.S. Gov't
PubMed
38552944
DOI
10.1016/j.mce.2024.112199
PII: S0303-7207(24)00055-8
Knihovny.cz E-resources
- Keywords
- Fetal programming, Hyperglycemia, Insulin resistance, Mitochondria, Rat, Skeletal muscle,
- MeSH
- Diabetes Mellitus, Experimental * metabolism pathology MeSH
- Phenotype * MeSH
- Diabetes, Gestational * metabolism pathology MeSH
- Insulin * metabolism blood MeSH
- Insulin Resistance * MeSH
- Muscle, Skeletal * metabolism pathology MeSH
- Blood Glucose metabolism MeSH
- Rats MeSH
- Mitochondria metabolism MeSH
- Rats, Sprague-Dawley * MeSH
- Signal Transduction * MeSH
- Pregnancy MeSH
- Prenatal Exposure Delayed Effects * metabolism MeSH
- Animals MeSH
- Check Tag
- Rats MeSH
- Pregnancy MeSH
- Female MeSH
- Animals MeSH
- Publication type
- Journal Article MeSH
- Research Support, Non-U.S. Gov't MeSH
- Names of Substances
- Insulin * MeSH
- Blood Glucose MeSH
Maternal diabetes may influence glucose metabolism in adult offspring, an area with limited research on underlying mechanisms. Our study explored the impact of maternal hyperglycemia during pregnancy on insulin resistance development. Adult female Sprague-Dawley rats from control and diabetic mothers were mated, and their female offspring were monitored for 150 days. The rats were euthanized for blood and muscle samples. Maternal diabetes led to heightened insulin levels, increased HOMA-IR, elevated triglycerides, and a raised TyG index in adult offspring. Muscle samples showed a decreased protein expression of AMPK, PI3K, MAPK, DRP1, and MFF. These changes induced intergenerational metabolic programming in female pups, resulting in insulin resistance, dyslipidemia, and glucose intolerance by day 150. Findings highlight the offspring's adaptation to maternal hyperglycemia, involving insulin resistance, metabolic alterations, the downregulation of insulin signaling sensors, and disturbed mitochondrial morphology. Maintaining maternal glycemic control emerges as crucial in mitigating diabetes-associated disorders in adult offspring.
Center for Natural and Human Sciences Santo André 09210 580 São Paulo State Brazil
Laboratory of Translational Metabolism Institute of Physiology 142 00 Prague Czech Republic
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