Human resistin: Found in translation from mouse to man

Division of Endocrinology, Diabetes, and Metabolism, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.
Trends in Endocrinology and Metabolism (Impact Factor: 9.39). 04/2011; 22(7):259-65. DOI: 10.1016/j.tem.2011.03.005
Source: PubMed


The discovery of resistin 10 years ago as a fat cell-secreted factor that modulates insulin resistance suggested a link to the current obesity-associated epidemics of diabetes and cardiovascular disease, which are major human health concerns. Although adipocyte-derived resistin is indisputably linked to insulin resistance in rodent models, the relevance of human resistin is complicated because human resistin is secreted by macrophages rather than adipocytes, and because of the descriptive nature of human epidemiology. In this review, we examine the recent and growing evidence that human resistin is an inflammatory biomarker and a potential mediator of diabetes and cardiovascular disease.

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Available from: Mitchell A Lazar, Jul 08, 2015
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    • "There are also other reports indicating that increased serum resistin levels are associated with increased obesity, visceral fat [14] [15], insulin resistance, and Type 2 diabetes [16] [17], but these findings have not been consistent [18] [19]. Owing to these inconsistencies [20], the association of resistin with MetS and its components has remained controversial. Therefore, the present study aimed to compare serum concentrations of resistin in Iranian subjects with "
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    ABSTRACT: Background: The aim of the study is to determine the association of resistin with each MetS component. Methods: This study had a case-control design, and its data was retrieved from the Isfahan Healthy Heart Program (IHHP), Serum samples from 44 subjects with MetS (diagnosed according to the NCEP-ATPIII criteria) and 46 healthy controls were analyzed for resistin using enzyme-linked immunosorbent assay. Association between serum resistin and levels of total (TC), low- (LDL-C) and high-density (HDL-C) lipoprotein cholesterol, triglycerides (TG), fasting blood sugar (FBS), waist circumference, body mass index, and systolic and diastolic blood pressures was determined. Results: Serum resistin levels were significantly higher in the MetS compared with control group (3.64±1.63, P=0.040). Serum levels of resistin were found to be significantly correlated with levels of TC (r=-0.347; P=0.027) and LDL-C (r=-0.311; P=0.050), but not other components of MetS including systolic and diastolic blood pressure, TG, HDL-C and FBS (P>0.05) in the MetS group, after adjustment for age, gender and BMI. No significant correlation between resistin and MetS components was observed in the control group (P>0.05). Conclusion: Serum resistin levels are elevated in subjects with MetS and may be associated with the severity of this syndrome.
    Diabetes and Metabolic Syndrome Clinical Research and Reviews 10/2014; DOI:10.1016/j.dsx.2014.09.007
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    • "Adipocyte-derived resistin is linked to insulin resistance in rodent models of depression-like behavior while in humans, the role of resistin is less defined (Schwartz and Lazar, 2011; Hryhorczuk et al., 2013). In genetic and diet induced obese mice circulating resistin levels are elevated (Steppan et al., 2001). "
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    ABSTRACT: Food is a potent natural reward and food intake is a complex process. Reward and gratification associated with food consumption leads to dopamine (DA) production, which in turn activates reward and pleasure centers in the brain. An individual will repeatedly eat a particular food to experience this positive feeling of gratification. This type of repetitive behavior of food intake leads to the activation of brain reward pathways that eventually overrides other signals of satiety and hunger. Thus, a gratification habit through a favorable food leads to overeating and morbid obesity. Overeating and obesity stems from many biological factors engaging both central and peripheral systems in a bi-directional manner involving mood and emotions. Emotional eating and altered mood can also lead to altered food choice and intake leading to overeating and obesity. Research findings from human and animal studies support a two-way link between three concepts, mood, food, and obesity. The focus of this article is to provide an overview of complex nature of food intake where various biological factors link mood, food intake, and brain signaling that engages both peripheral and central nervous system signaling pathways in a bi-directional manner in obesity.
    Frontiers in Psychology 09/2014; 5:925. DOI:10.3389/fpsyg.2014.00925 · 2.80 Impact Factor
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    • "The protein resistin is related to insulin resistance in rodents (Schwartz and Lazar, 2011). Some studies found elevated peripheral resistin levels in human obesity (Degawa-Yamauchi et al., 2003; Owecki et al., 2011), whereas other investigations found resistin down-regulated in obesity (Way et al., 2001). "
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    ABSTRACT: Adiponectin, leptin and resistin may play a role in the pathophysiology of major depressive disorder (MDD). However, differences in peripheral levels of these hormones are inconsistent across diagnostic and intervention studies. Therefore, we performed meta-analyses of diagnostic studies (i.e., MDD subjects versus healthy controls) and intervention investigations (i.e., pre-vs. post-antidepressant treatment) in MDD. Adiponectin (N = 1278; Hedge's g = -0.35; P = 0.16) and leptin (N = 893; Hedge's g = -0.018; P = 0.93) did not differ across diagnostic studies. Meta-regression analyses revealed that gender and depression severity explained the heterogeneity observed in adiponectin diagnostic studies, while BMI and the difference in BMI between MDD individuals and controls explained the heterogeneity of leptin diagnostic studies. Subgroup analyses revealed that adiponectin peripheral levels were significantly lower in MDD participants compared to controls when assayed with RIA, but not ELISA. Leptin levels were significantly higher in individuals with mild/moderate depression versus controls. Resistin serum levels were lower in MDD individuals compared to healthy controls (N = 298; Hedge's g = -0.25; P = 0.03). Leptin serum levels did not change after antidepressant treatment. However, heterogeneity was significant and sample size was low (N = 108); consequently meta-regression analysis could not be performed. Intervention meta-analyses could not be performed for adiponectin and resistin (i.e., few studies met inclusion criteria). In conclusion, this systematic review and meta-analysis underscored that relevant moderators/confounders (e.g., BMI, depression severity and type of assay) should be controlled for when considering the role of leptin and adiponectin as putative MDD diagnostic biomarkers.
    Journal of Psychiatric Research 08/2014; 59. DOI:10.1016/j.jpsychires.2014.08.002 · 3.96 Impact Factor
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