Journal
CELL METABOLISM
Volume 6, Issue 3, Pages 181-194Publisher
CELL PRESS
DOI: 10.1016/j.cmet.2007.08.003
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Funding
- NIAAA NIH HHS [AA12814, R01 AA012814] Funding Source: Medline
- NIDDK NIH HHS [R01 DK062880-06, DK053843, R01 DK053843, R01 DK062880-07, R01 DK053843-09, DK34738, R01 DK034738, R01 DK062880, DK062880, R56 DK034738] Funding Source: Medline
- NIGMS NIH HHS [GM39722] Funding Source: Medline
- NINDS NIH HHS [R01 NS038641, NS038641] Funding Source: Medline
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Leucine is recognized as a nutrient signal; however, the long-term in vivo consequences of leucine signaling and the role of branched-chain amino acid (BCAA) metabolism in this signaling remain unclear. To investigate these questions, we disrupted the BCATm gene, which encodes the enzyme catalyzing the first step in peripheral BCAA metabolism. BCATm(-/-) mice exhibited elevated plasma BCAAs and decreased adiposity and body weight, despite eating more food, along with increased energy expenditure, remarkable improvements in glucose and insulin tolerance, and protection from diet-induced obesity. The increased energy expenditure did not seem to be due to altered locomotor activity, uncoupling proteins, sympathetic activity, or thyroid hormones but was strongly associated with food consumption and an active futile cycle of increased protein degradation and synthesis. These observations suggest that elevated BCAAs and/or loss of BCAA catabolism in peripheral tissues play an important role in regulating insulin sensitivity and energy expenditure.
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