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Adiponectin Does Not Cross the Blood-Brain Barrier but Modifies Cytokine Expression of Brain Endothelial Cells

¹ Department of Clinical Nutrition, German Institute of Human Nutrition, Potsdam, Germany
² Department of Endocrinology, Diabetes and Nutrition, Charité-Universitymedicine Berlin, Berlin, Germany
³ Geriatric Research Educational Clincal Center, Veterans Affairs Medical Center, St. Louis, Missouri
⁴ Division of Geriatrics, Department of Internal Medicine, Saint Louis University School of Medicine, St. Louis, Missouri
⁵ Department of Neurology, Charité-Universitymedicine Berlin, Berlin, Germany
⁶ Department of Physiology and Pharmacology, West Virginia University, Morgantown, West Virginia
⁷ Department of Psychiatry, Obesity Research Center, University of Cincinnati, Genome Research Institute, Cincinati, Ohio

Address correspondence and reprint requests to Joachim Spranger, MD, Dept. of Clinical Nutrition, German Institute of Human Nutrition Potsdam, Arthur-Scheunert-Allee 114-116, 14558 Nuthetal, Germany. E-mail: spranger{at}mail.dife.de or joachim.spranger{at}charite.de

Abbreviations: AMPK, cAMP kinase; BBB, blood-brain barrier; CNS, central nervous system; CSF, cerebrospinal fluid; IL, interleukin

Adiponectin has recently been reported to generate a negative energy balance by increasing energy expenditure. However, it is unclear whether such effects require the presence and direct action of the adiponectin protein in the central nervous system. In this study, neither radiolabeled nonglycosylated nor glycosylated globular adiponectin crossed the blood-brain barrier (BBB) in mice. In addition, adiponectin was not detectable in human cerebrospinal fluid using various established methods. Using murine cerebral microvessels, we demonstrated expression of adiponectin receptors, which are upregulated during fasting, in brain endothelium. Interestingly, treatment with adiponectin reduced secretion of the centrally active interleukin-6 from brain endothelial cells, a phenomenon that was paralleled by a similar trend of other proinflammatory cytokines. In summary, our data suggest that direct effects of endogenous adiponectin on central nervous system pathways are unlikely to exist. However, the identification of adiponectin receptors on brain endothelial cells and the finding of a modified secretion pattern of centrally active substances from BBB cells provides an alternate explanation as to how adiponectin may evoke effects on energy metabolism.

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