title: Chemerin and adiponectin contribute reciprocally to metabolic syndrome.
abstract: Obesity and metabolic syndrome (MetS) are considered chronic inflammatory states. Chemerin, a novel adipokine, may play an important role in linking MetS and inflammation. We investigated the association of chemerin with inflammatory markers and with characteristics of MetS in apparently healthy overweight and obese adults. We studied 92 adults; 59 men and 33 women whose average body mass index (BMI) was 28.15 ± 5.08 kg/m(2). Anthropometric parameters, insulin resistance indices, lipid profiles, and inflammatory markers including high sensitivity C-reactive protein (hsCRP), pentraxin 3 (PTX3), adiponectin, and chemerin were measured. Controlling for age, gender, and BMI, serum chemerin level was positively correlated with body fat and serum triglyceride, and negatively correlated with adiponectin and high density lipoprotein cholesterol (HDL- C), and was not correlated with altered hsCRP or PTX3 levels. Among the low, moderate and high chemerin groups, high chemerin individuals are more likely to have lower HDL-C. Conversely, individuals in the low adiponectin group are more likely to have lower HDL-C and show more MetS phenotypic traits than moderate and high adiponectin subjects. To determine the relationships of chemerin and adiponectin to MetS and its components, participants were stratified into four groups based on their chemerin and adiponectin levels (high chemerin/high adiponectin, high chemerin/low adiponectin, low chemerin/high adiponectin, or low chemerin/low adiponectin). Participants who were in the high chemerin/low adiponectin group more likely to have dyslipidemia and MetS (OR: 5.79, 95% CI:1.00-33.70) compared to the other three group. Our findings suggest that chemerin and adiponectin may reciprocally participate in the development of MetS.
authors.affiliation: Department of Clinical Nursing Science, Yonsei University College of Nursing, Nursing Policy and Research Institute, Biobehavioral Research Center, Seoul, Korea.
authors.forename: Sang Hui
authors.initials: SH
authors.lastname: Chu
authors.forename: Mi Kyung
authors.initials: MK
authors.lastname: Lee
authors.forename: Ki Yong
authors.initials: KY
authors.lastname: Ahn
authors.forename: Jee-Aee
authors.initials: JA
authors.lastname: Im
authors.forename: Min Soo
authors.initials: MS
authors.lastname: Park
authors.forename: Duk-Chul
authors.initials: DC
authors.lastname: Lee
authors.forename: Justin Y
authors.initials: JY
authors.lastname: Jeon
authors.forename: Ji Won
authors.initials: JW
authors.lastname: Lee
mesh_terms: D052242:Adiponectin / Q000097:blood*; D000273:Adipose Tissue / Q000378:metabolism; D000328:Adult; D015992:Body Mass Index; D002097:C-Reactive Protein / Q000032:analysis; D018925:Chemokines / Q000097:blood*; D008076:Cholesterol, HDL / Q000097:blood; D005260:Female; D006801:Humans; D036341:Intercellular Signaling Peptides and Proteins; D008297:Male; D024821:Metabolic Syndrome / Q000175:diagnosis / Q000378:metabolism*; D009765:Obesity / Q000175:diagnosis / Q000378:metabolism*; D000683:Serum Amyloid P-Component / Q000032:analysis; D014280:Triglycerides / Q000097:blood; D000099153:Pentraxins
chemical_list: D052242:Adiponectin; D002097:C-Reactive Protein; D018925:Chemokines; D008076:Cholesterol, HDL; D036341:Intercellular Signaling Peptides and Proteins; D000683:Serum Amyloid P-Component; D014280:Triglycerides; D000099153:Pentraxins; C478630:RARRES2 protein, human