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

Result code in 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>

Result on the web

<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>

Result language

angličtina

Original language name

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

Original language description

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.

Czech name

—

Czech description

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Type

J_imp - Article in a specialist periodical, which is included in the Web of Science database

CEP classification

—

OECD FORD branch

30202 - Endocrinology and metabolism (including diabetes, hormones)

Project

—

Continuities

I - Institucionalni podpora na dlouhodoby koncepcni rozvoj vyzkumne organizace

Publication year

2024

Confidentiality

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

Name of the periodical

Molecular and Cellular Endocrinology

ISSN

0303-7207

e-ISSN

1872-8057

Volume of the periodical

588

Issue of the periodical within the volume

1 July

Country of publishing house

NL - THE KINGDOM OF THE NETHERLANDS

Number of pages

13

Pages from-to

112199

UT code for WoS article

001217688800001

EID of the result in the Scopus database

2-s2.0-85189553661