the-aps.org>meetings>eb

Transport-Metabolism Coupling through AMPK
Sponsored by APS Cell & Molecular Physiology Section
Transporters Track

It has long been recognized that the coupling of membrane transport to underlying cellular metabolic status is critical because transport processes consume a large portion of total cellular energy.  Recently, the finely tuned metabolic sensor AMP-activated protein kinase (AMPK), which has a wide variety of cellular targets and functions, has emerged as a novel regulator of membrane transport.  This regulation may permit sensitive transport-metabolism crosstalk.  Recent studies suggest that AMPK, which activates under conditions of cellular metabolic stress, promotes the cellular uptake of nutrients such as glucose and fatty acids to promote ATP generation and inhibits ion transport proteins, thereby potentially limiting the dissipation of transmembrane ion gradients.  Thus, as found for its actions on other cellular targets, the effects of AMPK on membrane transport proteins are consonant with its role as a homeostatic regulator of cellular energy balance.  An understanding of the underlying cellular and molecular mechanisms for AMPK-dependent regulation of transport proteins is beginning to emerge.  The talks in this session will present recent work exploring the molecular mechanisms and functions for AMPK-dependent regulation of membrane transport proteins, including the cystic fibrosis transmembrane conductance regulator (CFTR), the epithelial Na⁺ channel (ENaC), Na⁺-dependent co-transporters, and glucose (GLUT) transporters.  Work in this exciting area has relevance to normal exercise physiology, diseases such as cystic fibrosis, hypertension, and diabetes, and the pathophysiology of hypoxic and ischemic injury and adaptation in epithelia and other tissues.