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The aim of this case-control study was to assess the relationship between resistin levels and obesity and insulin resistance in type 2 diabetic patients.
The study involved a sample of the Jordanian population that included 140 type 2 diabetic patients and 125 control subjects.
Serum resistin levels were higher in type 2 diabetic patients compared with the controls (P<0.01). Markers of adiposity [body mass index (BMI) and waist circumference (WC)] and insulin resistance, as well as fasting blood glucose, glycated haemoglobin, urea and blood pressure were considerably higher among the studied diabetics than in the controls. When diabetic patients were subdivided into age-group categories of 10-year intervals, resistin levels significantly increased with increased age, with a significant proportion in the group aged>60 years (P<0.01). Similarly, there was a significant association between plasma resistin and blood urea with growing older in diabetic patients. Pearson's analysis revealed positive correlations between plasma resistin and age, urea, creatinine, insulin, BMI, WC, body-fat content and homoeostasis model assessment (HOMA). Furthermore, plasma resistin concentrations were higher in type 2 diabetic obese patients than in non-diabetic obese subjects (P<0.01), whereas no such difference was found between overweight and normal-weight controls.
These results suggest that variations in resistin concentrations are not directly related to susceptibility to type 2 diabetes. However, it may be that resistin plays a role in the pathogenesis of obesity and insulin resistance, both of which could, indirectly, contribute to the development of type 2 diabetes.
Department of Medical Laboratory Sciences, Jordan University of Science and Technology, P.O. Box 3030, Irbid 22110, Jordan.
This article was published in the following journal.
Name: Diabetes & metabolism
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Diminished effectiveness of INSULIN in lowering blood sugar levels: requiring the use of 200 units or more of insulin per day to prevent HYPERGLYCEMIA or KETOSIS. It can be caused by the presence of INSULIN ANTIBODIES or the abnormalities in insulin receptors (RECEPTOR, INSULIN) on target cell surfaces. It is often associated with OBESITY; DIABETIC KETOACIDOSIS; INFECTION; and certain rare conditions. (from Stedman, 25th ed)
A 12-kDa cysteine-rich polypeptide hormone secreted by FAT CELLS in the ADIPOSE TISSUE. It is the founding member of the resistin-like molecule (RELM) hormone family. Resistin suppresses the ability of INSULIN to stimulate cellular GLUCOSE uptake.
A 30-kDa COMPLEMENT C1Q-related protein, the most abundant gene product secreted by FAT CELLS of the white ADIPOSE TISSUE. Adiponectin modulates several physiological processes, such as metabolism of GLUCOSE and FATTY ACIDS, and immune responses. Decreased plasma adiponectin levels are associated with INSULIN RESISTANCE; TYPE 2 DIABETES MELLITUS; OBESITY; and ATHEROSCLEROSIS.
A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
A syndrome with excessively high INSULIN levels in the BLOOD. It may cause HYPOGLYCEMIA. Etiology of hyperinsulinism varies, including hypersecretion of a beta cell tumor (INSULINOMA); autoantibodies against insulin (INSULIN ANTIBODIES); defective insulin receptor (INSULIN RESISTANCE); or overuse of exogenous insulin or HYPOGLYCEMIC AGENTS.
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