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Linking resistin, inflammation, and cardiometabolic diseases
The Korean Journal of Internal Medicine ; : 239-247, 2017.
Article in English | WPRIM | ID: wpr-82850
ABSTRACT
Adipose tissue secretes a variety of bioactive substances that are associated with chronic inflammation, insulin resistance, and an increased risk of type 2 diabetes mellitus. While resistin was first known as an adipocyte-secreted hormone (adipokine) linked to obesity and insulin resistance in rodents, it is predominantly expressed and secreted by macrophages in humans. Epidemiological and genetic studies indicate that increased resistin levels are associated with the development of insulin resistance, diabetes, and cardiovascular disease. Resistin also appears to mediate the pathogenesis of atherosclerosis by promoting endothelial dysfunction, vascular smooth muscle cell proliferation, arterial inflammation, and the formation of foam cells. Thus, resistin is predictive of atherosclerosis and poor clinical outcomes in patients with cardiovascular disease and heart failure. Furthermore, recent evidence suggests that resistin is associated with atherogenic dyslipidemia and hypertension. The present review will focus on the role of human resistin in the pathogeneses of inflammation and obesity-related diseases.
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Full text: Available Index: WPRIM (Western Pacific) Main subject: Arteritis / Rodentia / Insulin Resistance / Cardiovascular Diseases / Adipose Tissue / Cell Proliferation / Diabetes Mellitus, Type 2 / Atherosclerosis / Dyslipidemias / Resistin Type of study: Prognostic study Limits: Humans Language: English Journal: The Korean Journal of Internal Medicine Year: 2017 Type: Article

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Full text: Available Index: WPRIM (Western Pacific) Main subject: Arteritis / Rodentia / Insulin Resistance / Cardiovascular Diseases / Adipose Tissue / Cell Proliferation / Diabetes Mellitus, Type 2 / Atherosclerosis / Dyslipidemias / Resistin Type of study: Prognostic study Limits: Humans Language: English Journal: The Korean Journal of Internal Medicine Year: 2017 Type: Article