Muscle metabolic reprogramming underlies the resistance of liver fatty acid-binding protein (LFABP)-null mice to high-fat feeding-induced decline in exercise capacity.

ABSTRACT: Liver fatty acid-binding protein (LFABP) binds long-chain fatty acids with high affinity and is abundantly expressed in the liver and small intestine. Although LFABP is thought to function in intracellular lipid trafficking, studies of LFABP-null (LFABP^-/-) mice have also indicated a role in regulating systemic energy homeostasis. We and others have reported that LFABP^-/- mice become more obese than wildtype (WT) mice upon high-fat feeding. Here, we show that despite increased body weight and fat mass, LFABP^-/- mice are protected from a high-fat feeding-induced decline in exercise capacity, displaying an approximate doubling of running distance compared with WT mice. To understand this surprising exercise phenotype, we focused on metabolic alterations in th

SUBMITTER: Xu H 

PROVIDER: S-EPMC6802512 | biostudies-literature | 2019 Oct

REPOSITORIES: biostudies-literature