To investigate the association of serum resistin levels with metabolic syndrome (MS) and early atherosclerosis in obese children.
A total of 176 obese children and 88 healthy children were enrolled in this study, and were gender and age matched. Obesity was defined as a body mass index (BMI) of ≥ the 95th percentile for age and sex. All children had a physical examination and routine hematology testing for fasting blood glucose, insulin, and lipids profile. Homeostasis model of assessment of insulin resistance (HOMA-IR) was calculated, as insulin resistance has a central role in the pathophysiology of MS. Non-invasive ultrasound measurement was obtained to investigate carotid intima-media thickness (IMT) as the markers of early atherosclerosis. Path analysis was used to evaluate the value of resistin levels to early atherosclerosis.
The resistin levels were higher in obese children compared to healthy children (23.14 ± 7.35 vs. 17.1 ± 5.7 ng/mL, p<0.05), and it is positively correlated with BMI, waist circumference, systolic blood pressure, fasting insulin, HOMA-IR, IMT and high sensitive CRP (Hs-CRP), but not related to diastolic blood pressure, blood lipids and fasting glucose. A positive linear correlation was observed between resistin and the number of MS components. Path analysis indicated serum resistin can directly (β=0.304, p=0.001), and indirectly via HOMA-IR (β=0.085, p=0.008) and Hs-CRP (β=0.047, p=0.029), contribute to early atherosclerosis.
Resistin not only play a certain role in the presence of MS, but also indirectly via insulin resistance and Hs-CRP to contribute to early atherosclerosis in obese children.
"Moreover, genetic studies showed that two single nucleotide polymorphisms (SNPs: −537A > C and −420C > G) were associated with increased resistin levels in diabetic patients, but not in control subjects . Recently, associations have been reported between resistin and metabolic syndrome components on one hand and early atherosclerosis in obese children on the other hand . Finally, resistin has been demonstrated to stimulate the secretion of several inflammatory factors (e.g., TNF-α, IL-6, IL-8, and MCP-1) known to play a role in the induction of insulin resistance . "
[Show abstract][Hide abstract] ABSTRACT: Adipose tissue is a complex organ that comprises a wide range of cell types with diverse energy storage, metabolic regulation, and neuroendocrine and immune functions. Because it contains various immune cells, either adaptive (B and T lymphocytes; such as regulatory T cells) or innate (mostly macrophages and, more recently identified, myeloid-derived suppressor cells), the adipose tissue is now considered as a bona fide immune organ, at the cross-road between metabolism and immunity. Adipose tissue disorders, such as those encountered in obesity and lipodystrophy, cause alterations to adipose tissue distribution and function with broad effects on cytokine, chemokine, and hormone expression, on lipid storage, and on the composition of adipose-resident immune cell populations. The resulting changes appear to induce profound consequences for basal systemic inflammation and insulin sensitivity. The purpose of this review is to synthesize the current literature on adipose cell composition remodeling in obesity, which shows how adipose-resident immune cells regulate inflammation and insulin resistance-notably through cytokine and chemokine secretion-and highlights major research questions in the field.
[Show abstract][Hide abstract] ABSTRACT: Hyperlipidemia is a well-recognized risk factor for atherosclerosis and can be regulated by adipokines. Expression of the adipokine resistin-like molecule alpha (Retnla) is regulated by food intake; whether Retnla has a role in the pathogenesis of hyperlipidemia and atherosclerosis is unknown. Here we report that Retnla has a cholesterol-lowering effect and protects against atherosclerosis in low-density lipoprotein receptor-deficient mice. On a high-fat diet, Retnla deficiency promotes hypercholesterolaemia and atherosclerosis, whereas Retnla overexpression reverses these effects and improves the serum lipoprotein profile, with decreased cholesterol in the very low-density lipoprotein fraction concomitant with reduced serum apolipoprotein B levels. We show that Retnla upregulates cholesterol-7-α-hydroxylase, a key hepatic enzyme in the cholesterol catabolic pathway, through induction of its transcriptional activator liver receptor homologue-1, leading to increased excretion of cholesterol in the form of bile acids. These findings define Retnla as a novel therapeutic target for treating hypercholesterolaemia and atherosclerosis.
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