Mommy Issues: How Maternal Diet Shapes Offspring Mitochondrial Physiology

Clicks: 1
ID: 320715
2026
Free PDF
Article Quality & Performance Metrics
Overall Quality
Not rated
Combines reader engagement with the AI quality analysis. This article has not been analysed, so there is no overall score — reader engagement is measured and shown alongside.
AI Quality Assessment
Not analyzed
Readership in this journal

Ranked #218 of 221 articles by views in italian journal of animal science

Most read Least read

Bar heights use a square-root scale. Only the 120 most-read articles are drawn; the journal has 221 in total.

Mint this article as an NFT
Not yet minted

Create a permanent, verifiable on-chain record of this article on the Scimatic Network. The NFT is held in your Journament account, and you can withdraw it to your own wallet at any time.

5 SUSD one-off · no wallet required
Sign in to mint
Abstract
Exposure to early life stressors, including maternal obesity and the consumption of a calorically dense diet, during critical windows of fetal development is associated with an elevated and earlier risk of developing childhood obesity, type 2 diabetes, and other cardiometabolic diseases. As mitochondria lie at the intersection of energy metabolism and cellular stress response, alteration in their function is a likely mediator of the observed effects of maternal diet quality on offspring cardiometabolic health. This review summarizes the effect of a maternal high calorie diet on offspring mitochondrial content, architecture, and bioenergetics in skeletal and cardiac muscle, comparing these findings across various animal models used to study developmental programming. How alterations in these mitochondrial properties influence substrate dependence, oxidative capacity, and metabolic efficiency and contribute to impaired metabolic flexibility and cardiometabolic risk are highlighted. Finally, insights into potential mechanisms, such as redox imbalance, disrupted mitochondrial-nuclear communication, and epigenetic remodeling, linking maternal diet to changes in mitochondrial homeostasis are discussed. Understanding how these early alterations in mitochondrial physiology predispose offspring to increased cardiometabolic disease risk may reveal windows for therapeutic intervention.
Reference Key
openalex_W7168027604 Use this key to autocite in the manuscript while using SciMatic Manuscript Manager or Thesis Manager
Authors Avika Gomez-Sharma, Carrie E. McCurdy
Journal italian journal of animal science
Year 2026
DOI
10.1093/jas/skag208
URL
https://doi.org/10.1093/jas/skag208
Keywords Keywords not found

Citations

No citations found. To add a citation, contact the admin at info@scimatic.org

Comments

No comments yet. Be the first to comment on this article.