STATE-OF-THE-ART PAPER
Adiponectin and Cardiovascular Disease
Response to Therapeutic Interventions
Seung Hwan Han, MD, PhD*,
Michael J. Quon, MD, PhD ,
Jeong-a Kim, PhD and
Kwang Kon Koh, MD, PhD, FACC*,*
* Division of Cardiology, Gil Heart Center, Gachon Medical School, Incheon, Korea
Diabetes Unit, Laboratory of Clinical Investigation, NCCAM, NIH, Bethesda, Maryland
Manuscript received June 29, 2006;
revised manuscript received August 17, 2006,
accepted August 21, 2006.
* Reprint requests and correspondence: Dr. Kwang Kon Koh, Vascular Medicine and Atherosclerosis Unit, Division of Cardiology, Gil Heart Center, Gachon Medical School, 1198 Kuwol-dong, Namdong-gu, Incheon, South Korea 405-760. (Email: kwangk{at}gilhospital.com).
Adiponectin is a protein secreted specifically by adipose cells that may couple regulation of insulin sensitivity with energy metabolism and serve to link obesity with insulin resistance. Obesity-related disorders including the metabolic syndrome, diabetes, atherosclerosis, hypertension, and coronary artery disease are associated with decreased plasma levels of adiponectin, insulin resistance, and endothelial dysfunction. Adiponectin has insulin-sensitizing effects as well as antiatherogenic properties. Lifestyle modifications and some drug therapies to treat atherosclerosis, hypertension, and coronary heart disease have important effects to simultaneously increase adiponectin levels, decrease insulin resistance, and improve endothelial dysfunction. In this review, we discuss insights into the relationships between adiponectin levels, insulin resistance, and endothelial dysfunction that are derived from various therapeutic interventions. The effects of lifestyle modifications and cardiovascular drugs on adiponectin levels and insulin resistance suggest plausible mechanisms that may be important for treating atherosclerosis and coronary heart disease.
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Abbreviations and Acronyms
| | AMP = adenosine monophosphate | | CRP = C-reactive protein | | HMW = high molecular weight | | IL = interleukin | | LMW = low molecular weight | NF- B = nuclear transcription factor kappa B | | NO = nitric oxide | | PPAR = peroxisome proliferator-activated receptor | | TNF = tumor necrosis factor |
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