Abstract
The global epidemic of obesity and its strong association to Atherosclerotic Cardiovascular Diseases (ASCVD), including coronary heart disease, has lead to extensive research into the causes of obesity mediated ASCVD. Currently, there is a great deal of interest on the role of adipose tissue derived adipokines as obesity induced ASCVD risk factors. The present review focuses on the current state of knowledge of the recently discovered adipokine, resistin, and the role of resistin as an emerging ASCVD risk factor. Studies investigating the relationship between elevated serum resistin levels, which is characteristic of obese individuals, and atherosclerosis progression and clinical ASCVD events are discussed. Investigations on the actions of resistin as a direct cellular mediator of pro-atherosclerotic processes in the arterial wall are summarized. We further examine the evidence for resistin in inducing the atherogenic dyslipidemia, a major ASCVD risk factor in obesity. The novel role of human resistin in stimulating hepatic dysregulation of Low- Density Lipoprotein (LDL) and Very-Low Density Lipoprotein (VLDL) metabolism, two key pro-atherogenic components of the atherogenic dyslipidemia are featured. The important therapeutic implications of the pathophysiological effects of human resistin on LDL and VLDL metabolism are delineated. Finally, the overall potential of resistin as an ASCVD risk factor and therapeutic target in mitigating ASCVD in human obesity is examined.
Highlights
The global epidemic of obesity and its strong association to Atherosclerotic Cardiovascular Diseases (ASCVD), including coronary heart disease, has lead to extensive research into the causes of obesity mediated ASCVD
We recently identified a novel role of resistin in directly increasing the levels of the pro-atherogenic lipid and lipoprotein components of the atherogenic dyslipidemia in humans – that is, elevated triglycerides and increased LowDensity Lipoprotein (LDL) particle concentration [44,45]
A cause had not been identified until we reported that human resistin, at the levels seen in obese individuals, almost completely ablates the LDL receptor upregulatory effect of statins, the major mechanism of action of the statins [45]
Summary
Obesity is a growing global epidemic, with more than 1 billion individuals worldwide characterized as being overweight or obese [1]. Recent attempts at identifying such novel obesity ASCVD risk factors have focused on the secretory products of adipose tissue in obesity. There has been strong rodent data on the pathophysiological effects of resistin in mediating a multitude of metabolic impairments, including insulin resistance and type 2 diabetes [13] These findings have not been necessarily translatable to humans. Consistent with this, there are strong positive correlations between plasma resistin levels and increases in both BMI and the quantity of abdominal visceral adipose tissue, the most metabolically adverse type of fat, in humans [14,17,18,19,20]. Highlighting its clinical importance, is the observation that elevated serum resistin levels in humans correlate strongly with ASCVD and has been identified as a link between obesity and the resulting accelerated development of cardiovascular diseases in obese individuals. With the accumulating body of evidence of the strong association between resistin and ASCVD, resistin has emerged as a novel risk factor and strong potential biomarker for ASCVD
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