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

ABSTRACT:

Objective

Glycogen is a major energy reserve in liver and skeletal muscle. The master metabolic regulator AMP-activated protein kinase (AMPK) associates with glycogen via its regulatory β subunit carbohydrate-binding module (CBM). However, the physiological role of AMPK-glycogen binding in energy homeostasis has not been investigated in vivo. This study aimed to determine the physiological consequences of disrupting AMPK-glycogen interactions.

Methods

Glycogen binding was disrupted in mice via whole-body knock-in (KI) mutation of either the AMPK β1 (W100A) or β2 (W98A) isoform CBM. Systematic whole-body, tissue and molecular phenotyping was performed in KI and respective wild-type (WT) mice.

Results

While β1 W100A KI did not affect whole-body metabolism or exercise ca

SUBMITTER: Hoffman NJ 

PROVIDER: S-EPMC7393401 | biostudies-literature | 2020 Nov

REPOSITORIES: biostudies-literature