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.
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.
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
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