Abstract
The AMP-activated protein kinase (AMPK) cascade is a sensor of cellular energy charge that promotes catabolic and inhibits anabolic pathways. However, the role of AMPK in adipocytes is poorly understood. We show that transgenic expression of mitochondrial uncoupling protein 1 in white fat, which induces obesity resistance in mice, is associated with depression of cellular energy charge, activation of AMPK, downregulation of adipogenic genes, and increase in lipid oxidation. Activation of AMPK may explain the complex metabolic changes in adipose tissue of these animals and our results support a role for adipocyte AMPK in the regulation of storage of body fat.
Publication types
-
Research Support, Non-U.S. Gov't
MeSH terms
-
Adenylate Kinase / metabolism*
-
Adipose Tissue / enzymology
-
Adipose Tissue / physiopathology*
-
Animals
-
Animals, Genetically Modified
-
Base Sequence
-
Carrier Proteins / genetics
-
Carrier Proteins / metabolism*
-
DNA Primers
-
Epididymis
-
Immunity, Innate / genetics
-
Ion Channels
-
Male
-
Membrane Proteins / genetics
-
Membrane Proteins / metabolism*
-
Mice
-
Mice, Inbred C57BL
-
Mitochondrial Proteins
-
Obesity / genetics*
-
Oleic Acid / metabolism
-
Oxidation-Reduction
-
Oxygen Consumption
-
Reverse Transcriptase Polymerase Chain Reaction
-
Skin
-
Uncoupling Protein 1
Substances
-
Carrier Proteins
-
DNA Primers
-
Ion Channels
-
Membrane Proteins
-
Mitochondrial Proteins
-
Ucp1 protein, mouse
-
Uncoupling Protein 1
-
Oleic Acid
-
Adenylate Kinase