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Am J Physiol Endocrinol Metab 293: E965-E969, 2007. First published July 10, 2007; doi:10.1152/ajpendo.00119.2007
0193-1849/07 $8.00
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Detection of adiponectin in cerebrospinal fluid in humans

Markus Neumeier,1 Johanna Weigert,1 Roland Buettner,1 Josef Wanninger,1 Andreas Schäffler,1 André Michael Müller,2 Stephan Killian,2 Sophie Sauerbruch,2 Felix Schlachetzki,2 Andreas Steinbrecher,2 Charalampos Aslanidis,3 Jürgen Schölmerich,1 and Christa Buechler1

Departments of 1Internal Medicine I and 2Neurology and 3Institute of Clinical Chemistry and Laboratory Medicine, Regensburg University Hospital, Regensburg, Germany

Submitted 22 February 2007 ; accepted in final form 23 June 2007

Adiponectin circulates in the body in high concentrations, and 100-fold lower amounts were described in the cerebrospinal fluid (CSF) of mice, whereas in humans, contradictory results have been published. To clarify whether adiponectin is present in human CSF and is derived from the circulation, it was determined in human CSF and plasma of 52 nonselected patients. Adiponectin was detected by immunoblot in CSF and was quantified in CSF and serum by ELISA. CSF adiponectin was positively correlated to systemic levels, and the CSF/serum adiponectin ratio was correlated to the CSF/serum albumin ratio. Furthermore, disturbed function of the blood-brain barrier (BBB) was associated with an elevated CSF/serum adiponectin ratio. Adiponectin mRNA was not found in the brain, indicating that adiponectin crosses the BBB and/or the blood-cerebrospinal fluid barrier (BCB). Rat adiponectin with a COOH-terminal tag was injected into the tail vein of rats and was detected 3 h later in CSF. However, CSF adiponectin in humans and rats was ~0.1% of the serum concentration and therefore was below the 0.5% expected in the CSF because of the residual leakage of an undisturbed BBB/BCB. Taken together, data from the present study show that adiponectin in human CSF is far below the level expected by the baseline BBB/BCB permeability, indicating that adiponectin enters the brain much less efficiently than albumin, thus supporting recent data that exclude adiponectin transport to the CSF. Additional studies are needed to reveal whether these low levels of adiponectin in CSF have a physiological function.

blood-brain barrier; inflammation



Address for reprint requests and other correspondence: C. Buechler, Dept. of Internal Medicine I, Regensburg Univ. Hospital, D-93042 Regensburg, Germany (e-mail: christa.buechler{at}klinik.uni-regensburg.de)







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