Research

Hormonal

Genetic disruption of AMPK-glycogen binding in skeletal muscle (via AMPK beta2 subunit mutation) leads to increased adiposity and impaired glucose handling, whereas disruption in liver (via AMPK beta1 subunit mutation) primarily increases hepatic fat deposition without affecting whole-body glucose handling.

This research highlights that the body's energy sensors (AMPK) rely on glycogen stores for stability. Disrupting this link impairs metabolic health. While this is a genetic model, it suggests that maintaining healthy glycogen stores through balanced carbohydrate intake and regular physical activity is crucial for optimal metabolic function and preventing ectopic fat accumulation.

GoodSupportsHIGH confidence
b2 W98A KI mice displayed increased adiposity and impairments in whole-body glucose handling and maximal exercise capacity relative to WT... Destabilisation of AMPK was associated with increased fat deposition in b1 W100A liver and b2 W98A skeletal muscle versus WT.
Nolan J. Hoffman et al. · Molecular Metabolism · 2020

Why this rating

High-quality in vivo mouse models with systematic phenotyping, though translational to humans requires caution.

Source

Genetic loss of AMPK-glycogen binding destabilises AMPK and disrupts metabolism

Nolan J. Hoffman et al. · Molecular Metabolism · 2020

DOI 10.1016/j.molmet.2020.101048

mechanism_onlyCited 38×
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DOI resolved against Crossref · corpus check 2026-06-10

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