Insulin signaling and mitochondrial phenotype of skeletal muscle are programmed in utero by maternal diabetes
Jazyk angličtina Země Irsko Médium print-electronic
Typ dokumentu časopisecké články, práce podpořená grantem
PubMed
38552944
DOI
10.1016/j.mce.2024.112199
PII: S0303-7207(24)00055-8
Knihovny.cz E-zdroje
- Klíčová slova
- Fetal programming, Hyperglycemia, Insulin resistance, Mitochondria, Rat, Skeletal muscle,
- MeSH
- experimentální diabetes mellitus * metabolismus patologie MeSH
- fenotyp * MeSH
- gestační diabetes * metabolismus patologie MeSH
- inzulin * metabolismus krev MeSH
- inzulinová rezistence * MeSH
- kosterní svaly * metabolismus patologie MeSH
- krevní glukóza metabolismus MeSH
- krysa rodu Rattus MeSH
- mitochondrie metabolismus MeSH
- potkani Sprague-Dawley * MeSH
- signální transdukce * MeSH
- těhotenství MeSH
- zpožděný efekt prenatální expozice * metabolismus MeSH
- zvířata MeSH
- Check Tag
- krysa rodu Rattus MeSH
- těhotenství MeSH
- ženské pohlaví MeSH
- zvířata MeSH
- Publikační typ
- časopisecké články MeSH
- práce podpořená grantem MeSH
- Názvy látek
- inzulin * MeSH
- krevní glukóza 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
Citace poskytuje Crossref.org
