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October 27, 1999

Public Health History

Author Affiliations
 

Margaret A.WinkerMD, Deputy EditorIndividualAuthorPhil B.FontanarosaMD, Interim CoeditorIndividualAuthor

JAMA. 1999;282(16):1517-1518. doi:10-1001/pubs.JAMA-ISSN-0098-7484-282-16-jbk1027

To the Editor: The protein hormone leptin appears to act as an afferent signal from adipose tissue to the brain indicating the state of energy reserves.1 Both serum and cerebrospinal fluid (CSF) leptin concentrations increase with body fat2; however, CSF concentrations are generally 2 orders of magnitude lower than serum concentrations. The transport of leptin across the blood-brain barrier appears to occur via a saturable system, as has been demonstrated in mice.3 This suggests a mechanism by which obese people can be "resistant" to their higher circulating levels of leptin2 and suggests that exogenous administration of leptin to treat obesity might be ineffective.2 Results of a double-blind clinical trial demonstrated that exogenous leptin (daily bolus subcutaneous injections of up to 0.3 mg/kg) has a biologic effect.4 We report here data from a separate cohort of this clinical trial indicating that recombinant leptin enters the CSF.

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