Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Review
. 2010 Oct;17(5):441-5.
doi: 10.1097/MED.0b013e32833c3013.

Molecular neuroendocrine targets for obesity therapy

Annette D de Kloet  1 , Stephen C Woods
Affiliations
Review

Molecular neuroendocrine targets for obesity therapy

Annette D de Kloet et al. Curr Opin Endocrinol Diabetes Obes. 2010 Oct.

Abstract

Purpose of review: Although energy balance is tightly regulated in order to maintain a specific level of adiposity, the incidence of obesity continues to increase. Consequently, it is essential that effective therapeutics for the treatment and prevention of obesity be developed. This review provides a brief update on some recent advances in the characterization of neuroendocrine targets for obesity therapy.

Recent findings: During the review period, considerable progress occurred in the understanding of previously described neuroendocrine regulators of energy balance, and several novel targets have been identified. Moreover, the understanding of the neural circuitry and molecular mechanisms of the neuroendocrine regulation of energy homeostasis has been expanded.

Summary: Energy balance is maintained by neuroendocrine signals arising from many tissues including the gastrointestinal tract and adipose tissue. These signals are integral to the cessation of meals and to the ability of the brain to monitor energy status and respond accordingly. Many current targets for obesity therapy are based on manipulating the activity of these signals and their receptors; however, to date, clinical-weight loss based on this strategy has been minimal and alternative approaches such as combinatorial therapies are emerging.

PubMed Disclaimer

References

    1. Schwartz MW, Woods SC, Porte D, et al. Central nervous system control of food intake. Nature. 2000;404(6778):661. - PubMed
    1. Woods SC, Seeley RJ, Porte D, Jr., Schwartz MW. Signals That Regulate Food Intake and Energy Homeostasis. Science. 1998;280(5368):1378–1383. - PubMed
    1. Tamashiro KL, Terrillion CE, Hyun J, et al. Prenatal stress or high-fat diet increases susceptibility to diet-induced obesity in rat offspring. Diabetes. 2009;58(5):1116–25. [This study demonstrates that exposure to prenatal stress and/or a high-fat diet results in enhanced susceptibility to diet-induced weight gain. This highlights the impact of the intrauterine environment on life-long metabolism.] - PMC - PubMed
    1. Woods SC. The control of food intake: behavioral versus molecular perspectives. Cell Metab. 2009;9(6):489–98. [This article provides a novel perspective on the molecular and behavioral control of food intake and on the potential of targeting neuroendocrine regulators of energy balance for obesity therapy.] - PMC - PubMed
    1. Raybould HE. Gut chemosensing: interactions between gut endocrine cells and visceral afferents. Auton Neurosci. 2010;153(1-2):41–6. - PMC - PubMed

Publication types