Resistin and obesity, mortality, testing by
Ray Sahelian, M.D.
February 5 2014
Resistin is a 12.5-kDa polypeptide hormone produced by adipocytes and immunocompetent cells. Resistin was originally proposed as a link between obesity and insulin resistance / diabetes. Later, studies revealed that substantial inter-species differences exist between the major sites of resistin production in rodents (adipocytes) and humans (immunocompetent cells). While in rodents resistin appears to have an important role in the development of liver insulin resistance, its role in humans is less clear, and it is probably involved in the regulation of inflammatory processes rather than in insulin sensitivity. Adipose tissue is a highly active metabolic and endocrine organ. Adipose cells secrete leptin, resistin, adiponectin, adipsin, acylation-stimulating protein, angiotensinogen, tumour necrosis factor a, interleukin-6, retinol-binding protein, plasminogen activator inhibitor-1, tissue factor, fasting-induced adipose factor, fibrinogen / angiopoetin-related protein, and metallothionein.
Resistin in health and disease
Resistin may be an inflammatory marker associated with CAD. Resistin and adiponectin are also implicated in insulin resistance and atherosclerosis.
Adipokines, factors produced by adipose tissue, may be proinflammatory (such as leptin and resistin) or anti-inflammatory (such as adiponectin). Effects of these adipokines on the lungs have the potential to evoke or exacerbate asthma. This review summarizes basic mechanistic data through population-based and clinical studies addressing the potential role of adipokines in asthma. Augmenting circulating concentrations of adiponectin attenuates allergic airway inflammation and airway hyperresponsiveness in mice. Murine data is supported by human data that suggest that low serum adiponectin is associated with greater risk for asthma among women and peripubertal girls. Further, higher serum total adiponectin may be associated with lower clinical asthma severity among children and women with asthma. In contrast, exogenous administration of leptin results in augmented allergic airway hyperresponsiveness in mice. Alveolar macrophages obtained from obese asthmatics are uniquely sensitive to leptin in terms of their potential to augment inflammation. Consistent with this basic mechanistic data, epidemiologic studies demonstrate that higher serum leptin is associated with greater asthma prevalence and/or severity and that these associations may be stronger among women, postpubertal girls, and prepubertal boys. The role of adipokines in asthma is still evolving, and it is not currently known whether modulation of adipokines may be helpful in asthma prevention or treatment.
adiponectin, and risk of heart failure the framingham offspring study.
J Am Coll Cardiol. 2009; Frankel DS, Vasan RS, D'Agostino RB Sr, Benjamin EJ, Levy D, Wang TJ, Meigs JB. Department of Medicine, Massachusetts General Hospital, Boston, Massachusetts.
We tested the association of the adipokines resistin and adiponectin with incident heart failure. Abnormal concentrations of adipokines may partially explain the association between obesity and heart failure. We related circulating adipokine concentrations to the incidence of heart failure in 2,739 participants in the Framingham Offspring Study. During 6 years of follow-up, 58 participants developed new-onset heart failure. In proportional hazards models (adjusting for age, sex, blood pressure, antihypertensive treatment, diabetes, smoking, total/high-density lipoprotein cholesterol ratio, prevalent coronary heart disease, valvular heart disease, left ventricular hypertrophy, and estimated glomerular filtration rate) using the lowest third of the resistin distribution as the referent, the hazard ratios for heart failure in the middle and top thirds were 2.8 and 4 respectively. Increased circulating concentrations of resistin were associated with incident heart failure, even after accounting for prevalent coronary heart disease, obesity, and measures of insulin resistance and inflammation. The findings suggest a role for resistin in human disease and a novel pathway to heart failure.