CAMP (Cathelicidin antimicrobial peptide) is synthesized and secreted by adipocytes and involved in adipose tissue (AT) innate immune response and host defense of subcutaneous AT against Gram positive bacteria. Data on the regulation of CAMP in obesity and during weight loss are scarce and reference values do not exist. Serum CAMP levels (ELISA) and AT gene expression levels (quantitative real time PCR) were investigated in two large and longitudinal (12 months) cohorts of severely obese patients undergoing either a low calorie diet (LCD; n=79) or bariatric surgery (BS; n=156). The impact of metabolic factors on CAMP expression in vitro was investigated in differentiated 3T3-L1 adipocytes. CAMP serum levels significantly increased after BS but not during LCD. Females had lower CAMP serum levels and lower gene expression levels in subcutaneous AT. CAMP was positively correlated to unfavorable metabolic factors/adipokines and negatively to favorable factors/adipokines. CAMP gene expression was higher in subcutaneous than in visceral AT but serum CAMP levels were not correlated to levels of AT gene expression. While certain bile acids upregulated CAMP expression in vitro, high glucose/insulin as well as GLP-1 had an inhibitory effect. There exist gender-specific and AT compartment-specific effects on the regulation of CAMP gene expression. Weight loss induced by BS (but not by LCD) upregulated CAMP serum levels suggesting the involvement of weight loss-independent mechanisms in CAMP regulation such as bile acids, incretins and metabolic factors. CAMP might represent an adipokine at the interface between metabolism and innate immune response.

Resistin and progranulin represent novel and putative regulators of the fat-brain axis by their ability to cross the BBB under physiological and pathophysiological conditions. The presented data provide insight into the characteristics of BBB function regarding progranulin and resistin and the basis for future establishment of normal values for CSF concentrations and CSF/serum ratios.

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The novel adipokine CTRP-3 is detectable in human cerebrospinal fluid (proof of principle). Due to its blood-brain barrier permeability, CTRP-3 represents a novel putative candidate for a physiological regulator molecule affecting central nervous functions.

Context Data on quantification and regulation of adipsin in human cerebrospinal fluid (CSF) are sparse, and the physiological role of adipsin as an adipokine crossing the blood-brain barrier (BBB) is uncertain. Objectives This study quantified adipsin concentrations in paired serum and CSF samples of patients undergoing neurological evaluation and spinal puncture. Design A total of 270 consecutive patients with specified neurological diagnosis were included in this study without prior selection. Main outcome measures Adipsin serum and CSF concentrations were measured by ELISA. A variety of serum and CSF routine parameters were measured by standard procedures. Anthropometric data, medication and patient history were available. Results Adipsin concentrations ranged between 467 and 5148 ng/ml in serum and between 4Á2 and 133Á5 ng/ml in CSF. Serum adipsin concentrations were correlated positively with respective CSF concentrations and were approximately 40-fold higher when compared to CSF. The mean CSF/serum ratio for adipsin was 27 AE 22 9 10 À3 . Serum and CSF adipsin levels were independent of gender and significantly higher in overweight/obese individuals. Serum and CSF adipsin levels correlated significantly with age and were higher in patients suffering from diabetes mellitus or hypertension. CSF adipsin concentrations showed a significant correlation with markers of inflammation in CSF, but not with CSF total cell count or the presence of oligoclonal bands. Patients suffering from infectious diseases had higher CSF levels of adipsin than multiple sclerosis patients. Conclusions Adipsin is present in human CSF under pathophysiological conditions. The positive correlation between serum and CSF concentrations, the positive correlation between the CSF/serum ratios for adipsin and total protein and the lack of association with CSF cell count argue against an autochthonous production in the central nervous system. In contrast, the present data argue for a significant BBB permeability to adipsin.