期刊
CELLULAR AND MOLECULAR NEUROBIOLOGY
卷 31, 期 7, 页码 985-989出版社
SPRINGER/PLENUM PUBLISHERS
DOI: 10.1007/s10571-011-9663-8
关键词
Olanzapine; Weight gain; Hyperphagia; AMP-activated protein kinase; Hypothalamus
资金
- JSPS, Japan [17390159, 18890227, 20800066, 19790199, 21790102, 21790255, 21790257, 21790526]
- Ministry of Health, Labour and Welfare of Japan [H19-nanchiippan-006]
- Nakatomi Foundation, Research Foundation ITSUU Laboratory
- Kakihara Science and Technology Foundation
- Grants-in-Aid for Scientific Research [20800066, 18890227, 21790102, 23790311, 19790199, 22590255, 17390159, 21790257, 21790526, 21790255] Funding Source: KAKEN
Olanzapine is known to be advantageous with respect to outcome and drug compliance in patients with schizophrenia. However, olanzapine has adverse effects, including a higher incidence of weight gain and metabolic disturbances, when compared with those of other antipsychotic agents. The mechanisms underlying these adverse events remain obscure. Female rats were orally administered olanzapine (2 mg/kg) or vehicle once a day for 2 weeks to ascertain if hypothalamic AMP-activated protein kinase (AMPK) mediates olanzapine-induced weight gain and hyperphagia. Body weight and food intake in each rat were evaluated every day and every two days, respectively. After the termination of drug treatment, we measured the protein levels of AMPK and phosphorylated AMPK in the hypothalamus using western blot analyses. Olanzapine significantly increased body weight and food intake. The phosphorylation levels of AMPK were significantly elevated by olanzapine. These results suggest that activation of hypothalamic AMPK may mediate hyperphagia and weight gain induced by chronic treatment with olanzapine.
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