cerulenin and Weight-Loss

cerulenin has been researched along with Weight-Loss* in 1 studies

Other Studies

1 other study(ies) available for cerulenin and Weight-Loss

Article	Year
Reduced food intake and body weight in mice treated with fatty acid synthase inhibitors. Science (New York, N.Y.), 2000, Jun-30, Volume: 288, Issue:5475 With the escalation of obesity-related disease, there is great interest in defining the mechanisms that control appetite and body weight. We have identified a link between anabolic energy metabolism and appetite control. Both systemic and intracerebroventricular treatment of mice with fatty acid synthase (FAS) inhibitors (cerulenin and a synthetic compound C75) led to inhibition of feeding and dramatic weight loss. C75 inhibited expression of the prophagic signal neuropeptide Y in the hypothalamus and acted in a leptin-independent manner that appears to be mediated by malonyl-coenzyme A. Thus, FAS may represent an important link in feeding regulation and may be a potential therapeutic target. Topics: Acetyl-CoA Carboxylase; Animals; Appetite; Appetite Depressants; Cerulenin; Dose-Response Relationship, Drug; Eating; Enzyme Inhibitors; Fasting; Fatty Acid Synthases; Female; Hypothalamus; Injections, Intraventricular; Leptin; Liver; Male; Malonyl Coenzyme A; Mice; Mice, Inbred BALB C; Neurons; Neuropeptide Y; RNA, Messenger; Weight Loss	2000

Article

Year

Reduced food intake and body weight in mice treated with fatty acid synthase inhibitors.

Science (New York, N.Y.), 2000, Jun-30, Volume: 288, Issue:5475

With the escalation of obesity-related disease, there is great interest in defining the mechanisms that control appetite and body weight. We have identified a link between anabolic energy metabolism and appetite control. Both systemic and intracerebroventricular treatment of mice with fatty acid synthase (FAS) inhibitors (cerulenin and a synthetic compound C75) led to inhibition of feeding and dramatic weight loss. C75 inhibited expression of the prophagic signal neuropeptide Y in the hypothalamus and acted in a leptin-independent manner that appears to be mediated by malonyl-coenzyme A. Thus, FAS may represent an important link in feeding regulation and may be a potential therapeutic target.

Topics: Acetyl-CoA Carboxylase; Animals; Appetite; Appetite Depressants; Cerulenin; Dose-Response Relationship, Drug; Eating; Enzyme Inhibitors; Fasting; Fatty Acid Synthases; Female; Hypothalamus; Injections, Intraventricular; Leptin; Liver; Male; Malonyl Coenzyme A; Mice; Mice, Inbred BALB C; Neurons; Neuropeptide Y; RNA, Messenger; Weight Loss

2000