Insulin signaling and mitochondrial phenotype of skeletal muscle are programmed in utero by maternal diabetes

Kód výsledku v IS VaVaI

<a href="https://www.isvavai.cz/riv?ss=detail&h=RIV%2F67985823%3A_____%2F24%3A00586074" target="_blank" >RIV/67985823:_____/24:00586074 - isvavai.cz</a>

Výsledek na webu

<a href="https://doi.org/10.1016/j.mce.2024.112199" target="_blank" >https://doi.org/10.1016/j.mce.2024.112199</a>

DOI - Digital Object Identifier

<a href="http://dx.doi.org/10.1016/j.mce.2024.112199" target="_blank" >10.1016/j.mce.2024.112199</a>

Jazyk výsledku

angličtina

Název v původním jazyce

Insulin signaling and mitochondrial phenotype of skeletal muscle are programmed in utero by maternal diabetes

Popis výsledku v původním jazyce

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.

Název v anglickém jazyce

Insulin signaling and mitochondrial phenotype of skeletal muscle are programmed in utero by maternal diabetes

Popis výsledku anglicky

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.

Druh

J_imp - Článek v periodiku v databázi Web of Science

CEP obor

—

OECD FORD obor

30202 - Endocrinology and metabolism (including diabetes, hormones)

Projekt

—

Návaznosti

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Rok uplatnění

2024

Kód důvěrnosti údajů

S - Úplné a pravdivé údaje o projektu nepodléhají ochraně podle zvláštních právních předpisů

Název periodika

Molecular and Cellular Endocrinology

ISSN

0303-7207

e-ISSN

1872-8057

Svazek periodika

588

Číslo periodika v rámci svazku

1 July

Stát vydavatele periodika

NL - Nizozemsko

Počet stran výsledku

13

Strana od-do

112199

Kód UT WoS článku

001217688800001

EID výsledku v databázi Scopus

2-s2.0-85189553661