| Free fatty acids (FFA) |
Splanchnic FFA levels may contribute to liver fat accumulation leading to abdominal obesity. Acute exposure of skeletal muscle to elevated FFA levels induces IR by inhibiting the insulin-mediated glucose uptake. Chronic exposure of the pancreas to the elevated FFA impairs a pancreatic β-cell function. FFAs increase both fibrinogen and PAI-1 production.
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| Tumor necrosis factor alpha (TNF α) |
Paracrine mediator in adipocytes to act locally reducing insulin sensitivity. TNF-α induces adipocytes apoptosis and promotes IR by the inhibition of the insulin RS 1 signaling pathway. Also, it exacerbates FFA release, inducing atherogenic dyslipidemia. Plasma TNFα is positively associated with BW, WC, TGs while, negatively associated with plasma TNFα and HDL-C.
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| C-reactive protein (CRP) |
Elevated CRP level is associated with an increased WC, IR, BMI, and HG and increased number of MetS components. More likely to be elevated in obese insulin-resistant, but, not in obese insulin-sensitive subjects. CRP levels independently predict occurrence of future CVD events.
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| Interleukin 6 (IL-6) |
Released by both adipose tissue and skeletal muscle in humans with inflammatory and anti-inflammatory actions. IL-6 receptor is also expressed in the hypothalamus controlling appetite and energy intake. IL-6 suppresses lipoprotein lipase activity. Systemic adipokine that not only impairs insulin sensitivity, but also regulates the hepatic production of CRP. Positively associated with BMI, fasting insulin, and the development of T2DM and negatively associated HDL-C.
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| Plasminogen activator inhibitor-1 (PAI-1) |
A serine protease inhibitor is secreted from intra-abdominal adipocytes, platelets, and the vascular endothelium. It exerts its effects by inhibiting the tissue plasminogen activator (tPA) and thus it is considered as a marker of impaired fibrinolysis and atherothrombosis. Plasma PAI-1 levels are increased in abdominally obese subjects and inflammatory states, increasing the risk of an intravascular thrombus and adverse cardiovascular outcomes.
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| Adiponectin |
It regulates the lipid and glucose metabolism, increases insulin sensitivity, regulates food intake and BW, protects against a chronic inflammation, inhibits hepatic gluconeogenic enzymes as well as the rate of endogenous glucose production in the liver. It increases glucose transport in muscles and enhances FFA oxidation. Multifactorial antiatherogenic action which includes inhibition of endothelial activation, reduced conversion of macrophages to foam cells, and inhibition of the smooth muscle proliferation and arterial remodeling. Adiponectin is inversely associated with CVD risk factors such as blood pressure, LDL-C, and TGs. Anti-inflammatory molecule is negatively associated with BW, WC, TGs, fasting insulin, IR, BMI, and BP, whereas a positive association exists between adiponectin and HDL-C. Its expressions and secretions are reduced by TNFα, possibly through a stimulated production of IL-6, which also inhibits adiponectin secretion; hence, it is seen to be “protective.”
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| Leptin |
Adipokine involved in the regulation of satiety and energy intake. Plasma leptin levels increase during the development of obesity and decline during the weight loss. Thus, most overweight and obese individuals have elevated leptin levels that do not suppress appetite. This leptin resistance is thought to be a fundamental pathology in obesity. Leptin receptors are located mostly in the hypothalamus and the brain stem and signals through these receptors controls satiety, energy expenditure, and neuroendocrine function. Increases in the BP through activation of the sympathetic nervous system. Leptin is a NO dependent vasodilator but also increases the PVR and the sympathetic nerve activity. Concentration of plasma leptin correlates with adiposity and hyperleptinemia is an independent CVD risk factor.
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