Abstract：
:Reducing obesity requires an elevation of energy expenditure and/or a suppression of food intake. Here we show that enhancing hepatic glycolysis reduces body weight and adiposity in obese mice. Overexpression of glucokinase or 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase is used to increase hepatic glycolysis. Either of the two treatments produces similar increases in rates of fatty acid oxidation in extrahepatic tissues, i.e., skeletal muscle, leading to an elevation of energy expenditure. However, only 6-phosphofructo-2-kinase/fructose-2,6-bisphosphatase overexpression causes a suppression of food intake and a decrease in hypothalamic neuropeptide Y expression, contributing to a more pronounced reduction of body weight with this treatment. Furthermore, the two treatments cause differential lipid profiles due to opposite effects on hepatic lipogenesis, associated with distinct phosphorylation states of carbohydrate response element binding protein and AMP-activated protein kinase. The step at which hepatic glycolysis is enhanced dramatically influences overall whole-body energy balance and lipid profiles.
journal_name
Cell Metabjournal_title
Cell metabolismauthors
Wu C,Kang JE,Peng LJ,Li H,Khan SA,Hillard CJ,Okar DA,Lange AJdoi
10.1016/j.cmet.2005.07.003keywords:
subject
Has Abstractpub_date
2005-08-01 00:00:00pages
131-40issue
2eissn
1550-4131issn
1932-7420pii
S1550-4131(05)00202-0journal_volume
2pub_type
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