Article

Therapy insight: Adipocytokines in metabolic syndrome and related cardiovascular disease

Sumitomo Hospital, Osaka, Japan.
Nature Clinical Practice Cardiovascular Medicine (Impact Factor: 7.04). 02/2006; 3(1):35-42. DOI: 10.1038/ncpcardio0380
Source: PubMed

ABSTRACT Abdominal fat accumulation has been shown to play crucial roles in the development of metabolic syndrome. Visceral fat accumulation particularly is closely correlated to the development of cardiovascular disease and obesity-related disorders such as diabetes mellitus, hyperlipidemia and hypertension. Given these clinical findings, the functions of adipocytes have been intensively investigated in the past 10 years, and have been revealed to act as endocrine cells that secrete various bioactive substances termed adipocytokines. Among adipocytokines, tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor are produced in adipocytes as well as other organs, and contribute to the development of vascular diseases. Visfatin has been identified as a visceral-fat-specific protein that might be involved in the development of obesity-related diseases, such as diabetes mellitus and cardiovascular disease. In contrast to these adipocytokines, adiponectin, which is an adipose-tissue-specific, collagen-like protein, has been noted as an important antiatherogenic and antidiabetic protein, or as an anti-inflammatory protein. The functions of adipocytokine secretion might be regulated dynamically by nutritional state. Visceral fat accumulation causes dysregulation of adipocyte functions, including oversecretion of tumor-necrosis factor-alpha, plasminogen activator inhibitor type 1 and heparin-binding epidermal growth factor-like growth factor, and hyposecretion of adiponectin, which results in the development of a variety of metabolic and circulatory diseases. In this review, the importance of adipocytokines, particularly adiponectin, is discussed with respect to cardiovascular diseases.

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    • "Adiponectin is a hormone secreted by adipocytes that plays a key role as an antidiabetic and anti-atherogenic adipokine [26]. Patients with obesity, insulin resistance, and/or MetS have been shown to have lower adiponectin levels [27]. Non-MetS patients showed normal levels of Fig. 2. Changes in the sterol/TC ratio treatment with ezetimibe in the MetS and non-MetS groups. "
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    ABSTRACT: Background Ezetimibe may be more effective in patients with high cholesterol absorption than in patients with low cholesterol absorption. This prospective study was performed to evaluate the effect of ezetimibe on hypercholesterolemia in patients with metabolic syndrome (MetS). Methods and results 81 patients with hypercholesterolemia in the presence or absence of MetS (MetS or non-MetS group) initially received ezetimibe (10 mg/day). In both groups, the levels of total cholesterol (TC), triglyceride, low-density lipoprotein cholesterol (LDL-C), non-high-density lipoprotein cholesterol (non-HDL-C) and the ratio of LDL-C to HDL-C (L/H) significantly decreased with treatment. A ratio of lathosterol to TC (lathosterol/TC) in the MetS group was significantly higher than that in the non-MetS group before treatment. Lathosterol/TC significantly increased after treatment in both groups, and campesterol/TC and sitosterol/TC significantly decreased. The non-MetS group, but not the MetS group, showed a significant increase in cholesterol/TC after treatment. Finally, we divided all of the patients into two groups (responders and non-responders) according to the percent changes in LDL-C after treatment. Male gender (p = 0.037), the presence of MetS (p = 0.026) and lower levels of L/H (p = 0.006) were independent factors that predicted a response to ezetimibe. Conclusions The lipid-lowering effect of ezetimibe in MetS was comparable to that in non-MetS. Treatment with ezetimibe may be effective in males with MetS and relatively lower levels of L/H.
    12/2013; 1:7–12. DOI:10.1016/j.ijcme.2013.10.001
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    • "These two fat depots, the subcutaneous and the omental fat, exhibit unique biochemical and cellular properties, such as response to sex hormones, and different secretion profiles [4], including a different lipolytic program [5]. Moreover, the omental, but not the subcutaneous, fat drains directly into the portal circulation, and some data point out to excessive free fatty acid release from the omental adipose tissue in central obesity [6]. In fact, it is well established that the size of the omental, more than the subcutaneous, fat is strongly related to a higher risk of obesity-related co-morbidities, including insulin resistance, type 2 diabetes, dyslipidemia and CVD. "
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    • "To note, targeted disruption of AdipoR1 and AdipoR2 causes abrogation of adiponectin binding and all its metabolic actions [30]. TheScientificWorldJOURNAL (2011) 11, 1932–1947 Actually, some evidences, indicates that adiponectin has a wide range of effects in pathologies with inflammatory component, such as cardiovascular disease, endothelial dysfunction, type 2 diabetes, metabolic syndrome, OA, and RA [31]. Adiponectin acts as a potent modulator of both B and T cells; moreover, it modulates the activity of immune innate response by inducing relevant anti-inflammatory factors such as IL-1 receptor antagonist and IL-10 [26] "
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    ABSTRACT: The cloning of leptin in 1994 by Zhang et al. introduced a novel concept about white adipose tissue (WAT) as a very dynamic organ that releases a plethora of immune and inflammatory mediators, such as adipokines and cytokines, which are involved in multiple diseases. Actually, adipokines exert potent modulatory actions on target tissues involved in rheumatic diseases including cartilage, synovial, bone and immune cells. The goal of this paper is to elucidate the recent findings concerning the involvement of adipokines in rheumatic diseases, such as rheumatoid arthritis (RA), osteoarthritis (OA), and systemic lupus erythematosus (SLE).
    The Scientific World Journal 10/2011; 11:1932-47. DOI:10.1100/2011/290142 · 1.73 Impact Factor
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