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Insulin Resistance and Glucose Regulation
Published in Awanish Kumar, Ashwini Kumar, Diabetes, 2020
Resistin is a 12 kDa adipocyte-derived polypeptide. It is expressed and secreted not only by mature adipocytes but also expressed in macrophages in a much higher amount. It was named due to the fact that it was believed to be linked directly to insulin resistance. Resistin is perhaps the most controversial adipokine since many researchers supported the fact that it induces insulin resistance in animal models of obesity and diabetes but those working with human cells or subjects directly deny the fact. In an early breakthrough study published in 2001, researchers showed, using animal models and mouse adipocytes cell line, that resistin is the link between obesity and diabetes [32]. But, in fact, many human studies failed to link resistin to insulin resistance and it is even said that it is the adipose tissue macrophage rather than the human adipocytes that produce resistin [33].
Pathogenesis
Published in Aparna Palit, Arun C. Inamadar, Systemic Sclerosis, 2019
There are many mediators secreted by inflammatory cells and have been hypothesized to play role in the pathogenesis of SSc. Adipokines, chemical mediators synthesized by adipocytes, such as adiponectin, visfatin, retinol binding protein-4, apelin, and resistin, have demonstrated a potential role in the pathogenesis of SSc. Resistin, also secreted by inflammatory cells, triggers proliferative response in vascular smooth muscles resulting in angiogenesis in pulmonary vasculature. The significant increase in serum levels of resistin has been found in patients with SSc.27
Adipose Tissue as an Important Body Organ
Published in Roy J. Shephard, Obesity: A Kinesiologist’s Perspective, 2018
Resistin. Resistin is a cysteine-rich peptide hormone produced in adipose tissue and encoded by the RETN gene [52, 87]. It was called resistin because when injected it increased the insulin resistance of mice. Resistin is inversely correlated with serum levels of LDL cholesterol [66], and resistin deficiency exacerbates obesity in ob/ob mice. However, resistin also decreases the production of LDL cholesterol by liver cells and the hepatic export of VLDL [23, 77].
Correlation of plasma adipokines with endometrial atypical hyperplasia and type I/II endometrial cancer
Published in Journal of Obstetrics and Gynaecology, 2023
Xinxin Zhu, Linzhi Liu, Zonghao Feng, Yan Zhang
A study found that the resistin level is positively correlated with age, insulin, BMI, waist circumference, body-fat content, and HOMA in people with type 2 diabetic mellitus (Gharibeh et al.2010). Furthermore, researchers reported that patients with EC also have higher resistin levels, but no significant association between higher resistin levels and age and BMI was observed, which is consistent with the results of our study (Hlavna et al.2011). In addition, we found that after adjustments for confounders, resistin was not an independent risk factor for type I EC. Notably, no significant difference was found in plasma resistin levels between the EAH and control groups, whereas in the multiple logistic regression analysis, the p was on the threshold of significance after adjustments for confounders. This implies that a higher resistin level may be involved in type I EC development. Several mechanisms were reported for pathophysiologic pathway for resistin to cancer progression. Resistin increases cell proliferation by inducing phosphatidylinositol 3-kinase or it could be act as specific receptor inducers (Ilhan et al. 2015, Tarkowski et al.2010).
Changes in adipokine concentrations in antidepressant-resistant bipolar depression after ketamine infusion and electroconvulsive therapy
Published in The World Journal of Biological Psychiatry, 2023
Monika Dmitrzak-Weglarz, Marta Tyszkiewicz-Nwafor, Filip Rybakowski, Agnieszka Permoda-Pachuta
Resistin is a pro-inflammatory factor, mainly secreted by adipocytes in rodents, while in humans by monocytes and macrophages. It has been reported that resistin plays a role in obesity, insulin resistance, type II diabetes, inflammatory response, tumorigenesis, and atherosclerosis. Resistin attenuates the anti-inflammatory effect of adiponectin in vascular endothelial cells by stimulating the expression of adhesion molecules (vascular cell adhesion molecule 1 (VCAM-1), intercellular adhesion molecule 1 (ICAM-1), and pentraxin 3 (PTX3)), which are involved in leukocyte adhesion (Park HK et al. 2017; Fang and Judd 2018; Tripathi et al. 2020). Although the exact role of resistin in the pathogenesis of BD is unknown, its involvement in the pathogenesis of the disease has been suggested (Wędrychowicz et al. 2014). There are conflicting reports regarding serum resistin levels in patients with BD. Yumru et al. (2012) (Yumru et al. 2012) reported elevated resistin levels in BD patients compared to controls, while Akinlade et al. (2019) reported opposite results (Akinlade et al. 2019).
Peptide hormones and risk for future cardiovascular events among prediabetics: a 20-year follow-up in the OPERA study
Published in Annals of Medicine, 2020
Olli-Juhani Galla, Antti Ylitalo, Antti Kiviniemi, Heikki Huikuri, Y. Antero Kesäniemi, Olavi Ukkola
When NGT, IFG, IGT, and diabetes groups were compared, the IGT group stood out as significantly different from the other groups considering obesity-related peptide hormone plasma levels. When resistin levels were compared between NGT, prediabetes and diabetes groups, the highest value was seen among prediabetics, especially among IGT subjects. This is an interesting finding, because it seems that the resistin value rises when the glycemic state develops from normal to prediabetic state. After prediabetes has developed into diabetes, the resistin value drops to an even lower level than that observed among normoglycemics. Therefore, resistin, a hormone linked to insulin resistance, behaves like insulin – in prediabetic state, with compensatory increase and, eventually, a drop when beta-cell exhaustion has occurred. Higher resistin concentrations have been reported to be associated with all-cause and cardiovascular mortality among patients with CVD or diabetes [17]. In prediabetics, data are almost lacking. Adiponectin plasma level was remarkably lower and leptin value higher in IGT group than in normoglycemics. In type 2 diabetics, plasma adiponectin levels have been reported to be decreased [18]. In addition, leptin has been suggested to regulate glycemic control in addition to energy balance in both rodent models and clinical settings [19].