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;...
OBJECTIVE -We hypothesized that burden of infection could be associated with chronic low-grade inflammation, resulting in insulin resistance. We aimed to study the effect of exposure to four infections on insulin sensitivity in apparently healthy middle-aged men (n ϭ 124).RESEARCH DESIGN AND METHODS -By inclusion criteria, all subjects were hepatitis C virus antibody seronegative. Each study subject's serum was tested for specific IgG class antibodies against herpes simplex virus (HSV)-1, HSV-2, enteroviruses, and Chlamydia pneumoniae through the use of quantitative in vitro enzyme-linked immunosorbent assays. Insulin sensitivity was evaluated using minimal model analysis.RESULTS -The HSV-2 titer was negatively associated with insulin sensitivity even after controlling for BMI, age, and C-reactive protein (CRP). The associations were stronger when considering the infection burden. In particular, in those subjects who were seropositive for C. pneumoniae, the relationship between the quantitative seropositivity index (a measure of the exposure to various pathogens) and insulin sensitivity was strengthened (r ϭ Ϫ0.50, P Ͻ 0.0001). We also observed decreasing mean insulin sensitivity index with increasing seropositivity score in subjects positive for enteroviruses. In the latter, the relationship between insulin sensitivity and seropositivity was especially significant (r ϭ Ϫ0.71, P Ͻ 0.0001). In a multivariate regression analysis, both BMI and quantitative seropositivity index (7%) independently predicted insulin sensitivity variance in subjects with C. pneumoniae seropositivity. When controlling for CRP, this association was no longer significant. CONCLUSIONS -Pathogen burden showed the strongest association with insulin resistance, especially with enteroviruses and C. pneumoniae seropositivity. We hypothesize that exposure to multiple pathogens could cause a chronic low-grade inflammation, resulting in insulin resistance.
The Asp358Ala and CA-repeat polymorphisms in the IL-6R gene are associated with obesity and characteristics of the metabolic syndrome in our population of Mediterranean subjects.
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