Serum adiponectin level is not only decreased in metabolic syndrome but also in borderline metabolic abnormalities.

Abstract:

OBJECTIVE:Along with the increasing prevalence of obesity and related diseases, particularly atherosclerotic diseases, metabolic syndrome (MetS) is now a common and major public health issue in many countries around the world. Adiponectin, a protein secreted by the adipose tissue, has become recognized as a key player in the development of MetS. These days, not only MetS but also borderline metabolic/physiological abnormalities, such as impaired fasting glucose, high normal blood pressure and high normal plasma cholesterol, have been reported to be risk factors for atherosclerotic disease. Therefore, we undertook this study to determine the relationship between adiponectin and borderline metabolic/physiological abnormalities, as well as MetS. DESIGN:A cross-sectional study performed from April 2007 to November 2009. SUBJECTS:In 16 892 Japanese adults (10 008 men and 6884 women), we examined the relationship between the serum adiponectin concentration and borderline metabolic/physiological abnormalities or MetS by a questionnaire survey about medical treatment, body size measurement and measurement of laboratory parameters including the serum adiponectin concentration. RESULTS:Adiponectin showed a significant negative correlation with the number of MetS components. In subjects without overt diabetes mellitus, hypertension or dyslipidemia, the adiponectin concentration also showed a significant negative correlation with the number of borderline metabolic abnormalities. CONCLUSION:The decrease of circulating adiponectin may start before the development of diabetes mellitus, hypertension, dyslipidemia or MetS. Adiponectin is an important biomarker for reflecting the adverse influence of visceral fat in persons with MetS, and also in these subclinical states.

journal_name

Nutr Diabetes

journal_title

Nutrition & diabetes

authors

Baden MY,Yamada Y,Obata Y,Hosakawa Y,Saisho K,Tamba S,Yamamoto K,Umeda M,Furubayashi A,Tsukamoto Y,Matsuzawa Y

doi

10.1038/nutd.2011.13

subject

Has Abstract

pub_date

2011-10-10 00:00:00

pages

e18

issn

2044-4052

pii

nutd201113

journal_volume

1

pub_type

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