AMPK (A2/B1/G1) plays a key role in insulin signaling pathway and is a major therapeutic target for the treatment of diabetes. AMPK is viewed as a fuel sensor for glucose and lipid metabolism by modulating the activity of the autonomous nervous system in vivo. Short-term overexpression of a constitutively active form of AMPK in the liver leads to mild hypoglycemia and fatty liver due to increased fatty acid utilization.
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AMP-activated protein kinase (AMPK) is a major therapeutic target for the treatment of diabetes. We investigated the effect of a short-term overexpression of AMPK specifically in the liver by adenovirus-mediated transfer of a gene encoding a constitutively active form of
Biochemical Society transactions, 31(Pt 1), 216-219 (2003-01-28)
AMP-activated protein kinase (AMPK) is viewed as a fuel sensor for glucose and lipid metabolism. To understand better the physiological role of the catalytic AMPK subunit isoforms, we generated two knockout mouse models with the alpha1 (AMPK alpha 1(-/-)) and
Tumour cell metabolic plasticity is essential for tumour progression and therapeutic responses, yet the underlying mechanisms remain poorly understood. Here, we identify Prospero-related homeobox 1 (PROX1) as a crucial factor for tumour metabolic plasticity. Notably, PROX1 is reduced by glucose
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