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A role for the endogenous opioid beta-endorphin in energy homeostasis.

Abstract：

:Proopiomelanocortin (POMC) neurons in the hypothalamus are direct targets of the adipostatic hormone leptin and contribute to energy homeostasis by integrating peripheral and central information. The melanocortin and beta-endorphin neuropeptides are processed from POMC and putatively coreleased at axon terminals. Melanocortins have been shown by a combination of pharmacological and genetic methods to have inhibitory effects on appetite and body weight. In contrast, pharmacological studies have generally indicated that opioids stimulate food intake. Here we report that male mice engineered to selectively lack beta-endorphin, but that retained normal melanocortin signaling, were hyperphagic and obese. Furthermore, beta-endorphin mutant and wild-type mice had identical orexigenic responses to exogenous opioids and identical anorectic responses to the nonselective opioid antagonist naloxone, implicating an alternative endogenous opioid tone to beta-endorphin that physiologically stimulates feeding. These genetic data indicate that beta-endorphin is required for normal regulation of feeding, but, in contrast to earlier reports suggesting opposing actions of beta-endorphin and melanocortins on appetite, our results suggest a more complementary interaction between the endogenously released POMC-derived peptides in the regulation of energy homeostasis.

journal_name

Endocrinology

journal_title

Endocrinology

authors

Appleyard SM,Hayward M,Young JI,Butler AA,Cone RD,Rubinstein M,Low MJ

doi

10.1210/en.2002-221096

subject

Has Abstract

pub_date

2003-05-01 00:00:00

pages

1753-60

issue

5

eissn

0013-7227

issn

1945-7170

journal_volume

144

pub_type

杂志文章

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