Academic Journal

Low-carbohydrate diets improved glucose homeostasis and physical performance by regulating mitochondrial function via the SIRT3/PGC1α pathway.

Λεπτομέρειες βιβλιογραφικής εγγραφής
Τίτλος: Low-carbohydrate diets improved glucose homeostasis and physical performance by regulating mitochondrial function via the SIRT3/PGC1α pathway.
Συγγραφείς: Li T; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China.; The Fourth Affiliated Hospital of Soochow University, Department of Rehabilitation Medicine, Suzhou 215000, Jiangsu, China., Wang X; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China., Lu H; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China., Chen M; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China., Zhang H; Shandong Public Health Clinical Center, Department of Rehabilitation Medicine, Jinan 250132, Shandong, China., Zhang M; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China., Sun Z; Shandong Second Medical University, School of Rehabilitation Medicine, Weifang 261053, Shandong, China.
Πηγή: Anais da Academia Brasileira de Ciencias [An Acad Bras Cienc] 2026 Oct 12; Vol. 98 (4), pp. e20251367. Date of Electronic Publication: 2026 Oct 12 (Print Publication: 2026).
Τύπος έκδοσης: Journal Article
Γλώσσα: English
Στοιχεία περιοδικού: Publisher: Academia Brasileira De Ciencias Country of Publication: Brazil NLM ID: 7503280 Publication Model: eCollection Cited Medium: Internet ISSN: 1678-2690 (Electronic) Linking ISSN: 00013765 NLM ISO Abbreviation: An Acad Bras Cienc Subsets: MEDLINE
Imprint Name(s): Original Publication: Rio De Janeiro : Academia Brasileira De Ciencias
Ιατρικοί όροι (MeSH): Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha*/metabolism , Sirtuin 3*/metabolism , Blood Glucose*/metabolism , Mitochondria*/metabolism , Mitochondria*/physiology , Glucose*/metabolism , Diet, Carbohydrate-Restricted*, Homeostasis/physiology ; Muscle, Skeletal/metabolism ; Animals ; Mice, Inbred C57BL ; Male ; Mice ; Random Allocation ; Body Weight
Περίληψη: This study aimed to analyze the effects of two low-carbohydrate diets (LCDs) on glucose homeostasis and physical performance in sedentary mice. Eighteen C57BL/6J mice were randomly divided into three groups: fed with standard chow (CON), high-fat LCD chow (HF-LCD), and high-protein LCD chow (HP-LCD). After two weeks, body weight (BW), food intake, fasting serum ketone bodies (β-OHB), blood glucose, glucose tolerance, and relative mass of skeletal muscle were measured. The physical performance was assessed using a treadmill endurance test, and the mRNA levels of mitochondrial function (SIRT3 and PGC1α) in the quadriceps were measured by qRT-PCR. Compared with the CON group, the HF-LCD group showed significantly increased fat content, β-OHB, and physical performance; the HP-LCD group showed significantly decreased calorie intake and BW. Compared with the HF-LCD group, the HP-LCD group showed significantly lower calorie intake, BW, fat content, β-OHB, skeletal muscle mass, and physical performance. Mechanistically, the mRNA levels of SIRT3-PGC1α in the HF-LCD group were higher than those in the other group. Both short-term LCDs can maintain glucose homeostasis in mice. However, only HF-LCD can increase β-OHB and physical performance without compromising skeletal muscle mass and strength. The underlying mechanism may involve transcriptional regulation of mitochondrial‑related genes via the SIRT3/PGC1α pathway.
Substance Nomenclature: 0 (Peroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alpha)
EC 3.5.1.- (Sirtuin 3)
0 (Blood Glucose)
0 (Ppargc1a protein, mouse)
0 (Sirt3 protein, mouse)
IY9XDZ35W2 (Glucose)
Entry Date(s): Date Created: 20261015 Date Completed: 20261015 Latest Revision: 20261015
Update Code: 20261016
DOI: 10.1590/0001-3765202620251367
PMID: 42879576
Βάση Δεδομένων: MEDLINE
Περιγραφή
ISSN:1678-2690
DOI:10.1590/0001-3765202620251367