Data seem to suggest that lower levels of adiponectin, and higher levels of resistin can be predictive of a future diabetes in obese people, even years before the disease onset.
Both systemic and adipose tissue resistin are linked to dysglycemia in these individuals and may be a potential biomarker for diabetes in this population.
Several of these activities, together with the effect of ellagic acid on insulin, glycogen, phosphatases, aldose reductase, sorbitol accumulation, advanced glycation end-product formation, and resistin secretion, may explain its effects on metabolic syndrome and diabetes.
Adipose tissue is an important endocrine organ that secretes a number of adipokines, like Resistin (RETN); it's an adipocytes-secreted cytokine and has been proposed as a link between obesity and diabetes.
In experiments reported among different human genetic groups as well as the patients with various disease such as diabetes, no significant correlation is shown between FBG and resistin level.
Resistin levels in patients with CP and systemic inflammatory disorders such as diabetes, obesity, or rheumatoid arthritis was not significantly higher than the levels in patients with only CP.
Thirty-seven patients (35.6%) had high aortic stiffness and higher percentages of diabetes (p = 0.001), were of older age (p = 0.001) and had higher waist circumference (p < 0.001), systolic blood pressure (p = 0.027), pulse pressure (p = 0.013), high-sensitivity C-reactive protein (p < 0.001) and resistin levels (p < 0.001) but lower estimated glomerular filtration rate (p = 0.009) compared to subjects with low aortic stiffness.
This finding suggested an essential role of resistin in linking IR and hypertension, which may offer a novel target in clinic on the study of the association between diabetes and hypertension.
In this review knowledge on resistin, including its structure, physiological role related to obesity and diabetes, as well as, gene sequence and phenotypic effects of the identified polymorphisms in human and domestic mammals is discussed.
Using comprehensive linkage disequilibrium mapping, we genotyped tag single nucleotide polymorphisms (SNPs) in RETN and tested associations with plasma resistin levels, risk of diabetes, and glycemic traits.
Transgenic mice that overexpress the resistin gene (Retn) in adipose tissue are insulin-resistant, whereas Retn (-/-) mice show lower fasting blood glucose, suggesting that the altered Retn promoter function could cause diabetes.
Resistin, founding member of the resistin-like molecule (RELM) hormone family, is secreted selectively from adipocytes and induces liver-specific antagonism of insulin action, thus providing a potential molecular link between obesity and diabetes.