Tier 3 — preclinical

SIRT6 regulates metabolic homeostasis in skeletal muscle through activation of AMPK

Xiaona Cui, Lu Yao, Xiaoying Yang, Yong Gao, Fude Fang, Jun Zhang, Qinghua Wang, Yongsheng Chang
American Journal of Physiology-Endocrinology and Metabolism 2017 313(4):E493-E505

Bibliography

PubMed
PMID 28765271
Funding
Funding indexed for this publication includes National Natural Science Foundation of China support.
Competing interests
No competing-interest statement was identified in the accessible publication record.

Study snapshot

DesignMuscle-specific SIRT6 knockout study with metabolic and exercise-performance phenotyping.
ModelGenetically modified mice and muscle-cell experiments.
SamplePreclinical experiments; endpoint-specific sample sizes reported in the paper.
InterventionMuscle-specific SIRT6 deletion with AMPK-pathway analyses.
DurationExperiment-dependent.
EndpointsGlucose homeostasis; insulin sensitivity; energy expenditure; exercise performance; AMPK activity; mitochondrial and fuel-use gene expression

What the study showed, in plain terms

Deleting SIRT6 specifically in skeletal muscle impaired glucose control, insulin sensitivity, energy expenditure and exercise performance in mice. Reduced AMPK activity helped explain the metabolic phenotype.

Key findings

SIRT6 supported skeletal-muscle metabolic homeostasis through pathways involving AMPK, fuel uptake, fatty-acid oxidation and mitochondrial oxidative phosphorylation.

What this study can and cannot tell us

This is a knockout model, not a trial of a SIRT6 activator. Results cannot be converted directly into performance claims for supplements in humans.

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