Hepatic ketogenesis is not required for exercise training to mitigate diet-induced liver steatosis in male mice
Clicks: 1
ID: 313452
2026
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.
Reader Engagement
0.0
/100
1 views
0 readers
AI Quality Assessment
Not analyzed
Readership in this journal
Ranked #51 of 53 articles by views in Food & function
Most read
Least read
Bar heights use a square-root scale.
Mint this article as an NFT
Not yet mintedCreate 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
Abstract
Accelerated hepatic fatty acid oxidation during acute exercise has been proposed as a contributor to the anti-steatotic effects of exercise training. Ketogenesis, which produces acetoacetate (AcAc) and ꞵ-hydroxybutyrate (ꞵOHB) from fatty acids, is stimulated by exercise and supports fat oxidation. This study tested the hypothesis that hepatic ketogenesis is necessary for exercise training to lower liver lipids. Liver-specific 3-hydroxymethylglutaryl-CoA synthase 2 knockout (HMGCS2 KO) mice and wild type (WT) littermates underwent sedentary, acute exercise (treadmill running), and exercise training (6-week treadmill running regime) protocols. Liver ketone bodies and lipids were determined via mass spectrometry. Stable isotope infusions in conscious, unrestrained mice defined mitochondrial oxidative fluxes during rest and treadmill running. In untrained mice, hepatic HMGCS2 deletion lowered liver AcAc and ꞵOHB and impaired their increase during acute exercise. Liver triacylglycerides (TAGs) were comparable between genotypes at rest (ad libitum fed and short-fasted conditions). In contrast, liver TAGs were higher in HMGCS2 KO compared to WT mice following acute, non-exhaustive exercise. Acute exercise stimulated TCA cycle flux in both genotypes; however, liver TCA cycle flux was higher in KO mice during rest and acute exercise. This suggests that enhanced lipid oxidation via the TCA cycle may be sufficient for TAG homeostasis in HMGCS2 KO mice at rest, but not during acute exercise. Exercise training decreased liver TAGs similarly in WT and KO mice when assessed under short-fasted conditions. In conclusion, hepatic ketogenesis supports liver lipid homeostasis during acute exercise, but is not required for exercise training to mitigate diet-induced fatty liver.
| Reference Key |
openalex_W7161164550
Use this key to autocite in the manuscript while using
SciMatic Manuscript Manager or Thesis Manager
|
|---|---|
| Authors | C Vang, Andres F. Ortega, Ruth E Pfeiffer, Jared L Hartmann, Griffin S Hampton, Hu Wang, Eric D. Queathem, Peter A. Crawford, Xianlin Han, Curtis C. Hughey |
| Journal | Food & function |
| Year | 2026 |
| DOI |
10.1152/function.008.2026
|
| URL | |
| 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.