Visfatin has shown to be increased in type 2 diabetes but to be unrelated to insulin sensitivity. We hypothesized that visfatin is associated with insulin secretion in humans. To this aim, a cross-sectional study was conducted in 118 nondiabetic men and 64 (35 men and 29 women) type 2 diabetic patients. Type 1 diabetic patients with long-standing disease (n ؍ 58; 31 men and 27 women) were also studied. In nondiabetic subjects, circulating visfatin (enzyme immunoassay) was independently associated with insulin secretion (acute insulin response to glucose [ V isfatin (also known as pre-B-cell colony-enhancing factor [1]) is a novel adipokine that is predominantly secreted by visceral adipose tissue (2), although controversy exists over the contribution of this fat depot to serum visfatin in humans (2,3). The protein exerts adipogenic effects in vitro and therefore is a good candidate to explain the accumulation of visceral adipose tissue that is associated with insulin resistance (2). Unexpectedly, insulin-mimetic effects were documented for this new adipokine, which are mediated by direct binding and activation of the insulin receptor (2).In humans, plasma visfatin is increased in type 2 diabetes (4); however, studies to date (3-6) have failed to demonstrate an association of the circulating protein with insulin sensitivity. Because abnormalities in insulin secretion also contribute to the development of the metabolic abnormalities observed in type 2 diabetes, we hypothesized that besides insulin sensitivity, plasma visfatin levels are related to insulin secretion. Our results not only support previous reports of a lack of association of circulating visfatin with measures of insulin sensitivity but also show that -cell dysfunction possibly mediates the link of this adipocytokine with diabetes. RESEARCH DESIGN AND METHODSOne hundred and eighteen nondiabetic men, consecutively enrolled in a prospective study of cardiovascular risk factors in our health area, were included in the present study. None of these participants had evidence of metabolic disease other than nonmorbid obesity. Indeed, type 2 diabetes was ruled out by an oral glucose tolerance test (OGTT) according to criteria from the American Diabetes Association. Exclusion criteria for this group were 1) BMI Ն40 kg/m 2 and 2) concurrence of any systemic disease or medication use.Sixty-four (35 men and 29 women) type 2 diabetic patients, defined according to the above-mentioned American Diabetes Association criteria and prospectively recruited from diabetes outpatient clinics at the Girona Hospital, were also studied. All type 2 diabetic patients had stable metabolic control in the previous 6 months. Pharmacological therapy for these subjects included insulin (34%), oral hypoglycemic agents (48%), statins (41%), fibrates (9%), blood pressure-lowering agents (48%), aspirin (27%), and allopurinol (5%). Exclusion criteria for this group were 1) clinically significant hepatic, renal, neurologic, endocrinologic, or other systemic disease, including malignancy;...
Objectives-␣-Defensins are natural antibiotics made by neutrophils that have been reported to modulate cholesterol metabolism and vascular function; however, their role in vivo remains largely unknown. We hypothesized that ␣-defensins 1 to 3 (DEFA1-3) are associated with serum lipids and vascular reactivity in humans. Methods and Results-One hundred thirteen apparently-healthy White men, participants in a prospective study of cardiovascular risk factors, were assessed for a lipid profile, insulin sensitivity (S I , frequently-sampled intravenous glucose tolerance test), and non-stressed circulating DEFA1-3 (ELISA). In a subset of 52 subjects, vascular reactivity (high-resolution ultrasound of the brachial artery) was also assessed. Subjects in the highest quartile for plasma DEFA1-3 were found to be leaner and more insulin sensitive, and to have significantly reduced total and LDL-cholesterol, compared with subjects in the lowest quartile for circulating DEFA1-3 (PϽ0.0001 to Pϭ0.002 for linear trend ANOVA). The associations with serum lipids persisted after adjustment for age, body mass index, insulin sensitivity, and smoking (which was associated with reduced plasma DEFA1-3 concentrations). Finally, endotheliumindependent vasodilation increased with increasing circulating DEFA1-3 (Pϭ0.003) and this association was not explained by age, body mass index, serum cholesterol, insulin sensitivity, or smoking. Conclusions-Circulating
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