Serum Levels and Adipose Tissue Gene Expression of Cathelicidin Antimicrobial Peptide (CAMP) in Obesity and During Weight Loss

Abstract

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.

Deficiency of Cathelicidin Attenuates High-Fat Diet Plus Alcohol-Induced Liver Injury through FGF21/Adiponectin Regulation

“…Studies have shown that mice fed with a high-fat diet developed obesity and leptin resistance [ 68 ]. Importantly, Hochberg et al demonstrated in a human study that CAMP expression was negatively correlated with leptin level in subcutaneous adipose tissue of obese subjects undergoing a bariatric surgery [ 69 ]. It will be interesting to investigate how does the deficiency of CRAMP affect leptin expression and whether it can contribute to the protective effects on fatty liver in our animal model.…”

Identification and Interaction Analysis of Molecular Markers in Myocardial Infarction by Integrated Bioinformatics Analysis

“…EDNRB (endothelin receptor type B) [181], FGF10 [182], WNK3 [183], KNG1 [184], FCN3 [185], AQP3 [186], HPR (haptoglobin-related protein) [187], CTH (cystathionine gamma-lyase) [188], SPARCL1 [189], MAOA (monoamine oxidase A) [190], BMPR1B (bone morphogenetic protein receptor type 1B) [191], FGF7 [192], CALCRL (calcitonin receptor like receptor) [193], MARK3 [194], ADH1B [195], AMH (anti-Mullerian hormone) [196], RET (ret proto-oncogene) [197], IGF2 [198], SLC6A9 [199], NPPA (natriuretic peptide A) [200], SCT (secretin) [201], DCX (doublecortin) [202], ASIC1 [203], LMX1B [204], DBP (D-box binding PAR bZIP transcription factor) [205] and SLC6A9 [206] levels are correlated with disease severity in patients with hypertension. CAMP (cathelicidin antimicrobial peptide) [207], SPP1 [208]. CXCL11 [209], TFRC (transferrin receptor) [210], IRAK3 [211], C3AR1 [212], GLI2 [213], THY1 [214], FOXO6 [215], RGS4 [216], WNT10B [217] and AEBP1 [218] were found to be involved in progression of obesity, but these genes might be novel target for MI.…”

Role of the Steroid Sulfate Uptake Transporter Soat (Slc10a6) in Adipose Tissue and 3T3-L1 Adipocytes

“…Murine 3T3-L1 preadipocytes were cultured at 37 °C and 5% CO 2 in DMEM (Dulbecco’s modified Eagle medium, Biochrom AG, Berlin, Germany) supplemented with 10% newborn calf serum (NCS; Sigma-Aldrich) and 1% penicillin/streptomycin (PAN-Biotech, Aidenbach, Germany). At confluence, the cells were differentiated into mature adipocytes by culturing in DMEM/F12/glutamate medium (Lonza, Basel, Switzerland) supplemented with 20 μM 3-Isobutylmethylxanthine (Serva, Heidelberg, Germany), 1 μM corticosterone, 100 nM insulin, 200 μM ascorbate, 2 μg/ml apo-transferrin, 5% fetal calf serum (FCS, PAN-Biotech), 1 μM biotin, 17 μM pantothenate, 1% penicillin/streptomycin, and 300 μg/ml Pedersen fetuin (MP Biomedicals, Illkirch, France) ( Zaitsu and Serrero, 1990 ; Bachmeier and Löffler, 1994 ) for 9 days using a slightly modified protocol as reported previously ( Hochberg et al, 2021 ). The cell cultures were supplemented with adipogenesis-inducing medium (AIM) from day 0 to day 8 of differentiation, when the cell culture medium was switched to serum-free conditions (with increased insulin supplementation to a concentration of 1 μM).…”