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J Biol Chem, Vol. 274, Issue 9, 5692-5700, February 26, 1999
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From the Departments of Uncoupling protein 2 (UCP2) uncouples respiration
from oxidative phosphorylation and may contribute to obesity through
effects on energy metabolism. Because basal metabolic rate is decreased in obesity, UCP2 expression is predicted to be reduced. Paradoxically, hepatic expression of UCP2 mRNA is increased in genetically obese (ob/ob) mice. In situ hybridization and immunohistochemical
analysis of ob/ob livers demonstrate that UCP2 mRNA and protein
expression are increased in hepatocytes, which do not express UCP2 in
lean mice. Mitochondria isolated from ob/ob livers exhibit an increased rate of H+ leak which partially dissipates the
mitochondrial membrane potential when the rate of electron transport is
suppressed. In addition, hepatic ATP stores are reduced and these
livers are more vulnerable to necrosis after transient hepatic
ischemia. Hence, hepatocytes adapt to obesity by up-regulating UCP2.
However, because this decreases the efficiency of energy trapping, the
cells become vulnerable to ATP depletion when energy needs increase acutely.
Surgery,
§ Medicine, ¶ Radiology, ** Pathology, and
Biological Chemistry, Johns Hopkins
University, Baltimore, Maryland 21205 and the Department of
Pathology, Anatomy and Cell Biology, Thomas Jefferson
University, Philadelphia, Pennsylvania 19107
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