Leptin-to-Adiponectin Ratio as a Potential Atherogenic Index in Obese Type 2 Diabetic Patients
- Noriko Satoh, MD, PHD1,
- Mitsuhide Naruse, MD, PHD1,
- Takeshi Usui, MD, PHD1,
- Tetsuya Tagami, MD, PHD1,
- Takayoshi Suganami, MD, PHD2,
- Kazunori Yamada, MD, PHD3,
- Hideshi Kuzuya, MD, PHD3,
- Akira Shimatsu, MD, PHD1 and
- Yoshihiro Ogawa, MD, PHD24
- 1Clinical Research Institute for Endocrine Metabolic Disease, Kyoto Medical Center, Fushimi-ku, Kyoto, Japan
- 2Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, Chiyoda-ku, Tokyo, Japan
- 3Diabetes Center, National Hospital Organization, Kyoto Medical Center, Fushimi-ku, Kyoto, Japan
- 4Center of Excellence Program for Frontier Research on Molecular Destruction and Reconstitution of Tooth and Bone, Tokyo Medical and Dental University, Chiyoda-ku, Tokyo, Japan
- Address correspondence and reprint requests to Yoshihiro Ogawa, MD, PhD, Department of Molecular Medicine and Metabolism, Medical Research Institute, Tokyo Medical and Dental University, 2-3-10 Kanda-surugadai, Chiyoda-ku, Tokyo 101-0062, Japan. E-mail: ogawa.mmm{at}mri.tmd.ac.jp
Obesity promotes the progression of atherosclerosis by inducing multiple cardiovascular and metabolic derangements such as diabetes, hypertension, and dyslipidemia, all of which have high atherogenic potential. Adipose tissue has been considered an important endocrine organ that secretes many biologically active substances, collectively known as adipocytokines (1). Two major adipocytokines, leptin and adiponectin, are thought to play important roles in the regulation of cardiovascular and metabolic homeostasis. Leptin acts directly on the hypothalamus, thereby regulating food intake and energy expenditure (2). Plasma leptin concentrations are significantly elevated in obese subjects in proportion to the degree of adiposity (3), suggesting that hyperleptinemia may play a role in the pathogenesis of obesity-related complications. On the other hand, adiponectin increases tissue fat oxidation, leading to reduced levels of fatty acids and tissue triglyceride content, thus increasing insulin sensitivity (4). Paradoxically, plasma adiponectin concentrations are decreased in obese subjects (5), suggesting that hypoadiponectinemia is involved in the pathophysiology of obesity. Two recent studies have demonstrated that vascular remodeling and neointimal formation are markedly attenuated in leptin-deficient ob/ob mice and db/db mice with leptin receptor mutation (6,7), suggesting that leptin may accelerate the development of vascular injury. Conversely, studies with adiponectin-deficient mice have revealed that adiponectin plays a protective role in the development of atherosclerosis (8,9). In obese type 2 diabetic patients who are susceptible to atherosclerosis, plasma concentrations of leptin are increased, whereas those of adiponectin …
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