Effect Of Abdominal Obesity Research Articles

TRIB3 Functional Q84R Polymorphism Is a Risk Factor for Metabolic Syndrome and Carotid Atherosclerosis

OBJECTIVETo determine the association of TRIB3 Q84R polymorphism with metabolic syndrome (MetS) and carotid atherosclerosis.RESEARCH DESIGN AND METHODSA case-control study enrolled 513 Chinese subjects in three groups: control, MetS, and obese. The functional TRIB3 Q84R polymorphism was genotyped among subjects undergoing carotid ultrasonography. The clinical and biochemical characteristics were determined.RESULTSFor individuals with the TRIB3 R84 allele, the odds ratio for developing MetS was 2.349 (P = 0.018), abdominal obesity 2.351 (P = 0.012), hypertriglyceridemia 2.314 (P = 0.00003), and insulin resistance 1.697 (P = 0.023). Likewise, the odds ratio for individuals with the TRIB3 R84 allele to develop thickened intima-media thickness was 2.208 (P = 0.040).CONCLUSIONSIndividuals with the functional TRIB3 Q84R polymorphism are at risk for MetS. The TRIB3 R84 allele especially predisposes to carotid atherosclerosis in part through the effects of abdominal obesity, hypertriglyceridemia, and insulin resistance.

A Pilot Study of the Association of Low Plasma Adiponectin and Barrett's Esophagus

Gastroesophageal reflux disease (GERD) and obesity are associated with esophageal adenocarcinoma (EAC). We hypothesized that the obesity-EAC relation is mediated by factors secreted from adipocytes. Adiponectin is a peptide secreted by adipocytes, and its plasma levels are inversely associated with obesity. We aimed to estimate the effect of circulating adiponectin on the risk of Barrett's esophagus (BE), an accepted precursor of EAC, controlling for GERD symptoms and other potential confounders. We conducted a case-control study in cases of BE compared with controls without BE; most controls had GERD. Odds ratios (OR), corresponding to associations with BE, were estimated from conditional and unconditional logistic regression analyses of 50 matched pairs. BE was inversely associated with plasma adiponectin level (OR for each 10-microg/mL decrement 4.7, 95% confidence interval [CI] 1.4-15.0) and positively associated with GERD duration >or=10 yr, male gender, tobacco smoking, body mass index (BMI), waist circumference, and waist-to-hip ratio. Further adjustment for GERD duration, tobacco use, and BMI increased the adiponectin-BE association (OR 6.4, 95% CI 1.1-37.0), but the estimated OR was reduced when adjusting for measures of abdominal obesity (e.g., OR 2.5, 95% CI 0.49-13.00) and further adjusting for gender (OR 1.8, 95% CI 0.66-4.70). Despite methodologic limitations, including the small sample size, our findings suggest that adiponectin may be involved in the etiology of BE. Rather than simply a mechanical effect of obesity promoting GERD, the effects of abdominal obesity on the risk of BE might be mediated by adiponectin and other circulating factors.

The effect of abdominal obesity on insulin sensitivity and serum lipid and cytokine concentrations in African women

Studies have shown clear associations of abdominal obesity with lipid and glucose metabolism and cytokine levels in a number of different population groups. However, no such studies have been performed in an African population in which visceral adipose tissue levels have been shown to be lower than in European subjects. Cross-sectional analysis in 124 African women. Fasting serum samples were taken from all subjects and anthropometric measurements obtained. Blood levels of glucose, insulin, total cholesterol, high-density lipoprotein (HDL) and low-density lipoprotein (LDL) cholesterol, triglyceride, interleukin (IL)-6, IL-8 and IL-18 were measured. Subjects were separated into normal and abnormal glucose tolerant groups and into tertiles according to waist circumference (WC). Insulin resistance was assessed using the homeostasis model assessment (HOMA). Abnormal glucose-tolerant subjects had higher WC, glucose and HOMA levels than the normal glucose-tolerant group. Increased WC was associated with higher triglyceride, insulin and HOMA levels and lower HDL levels. Multiple regression analyses showed that WC associated positively with HOMA and serum triglyceride levels and negatively with HDL levels. IL18 was a positive but weak determinant of the HOMA level and BMI correlated positively with serum IL-6 concentrations. Although previous studies have shown that African subjects have a lower visceral adipose depot size than European subjects, abdominal obesity is still associated with insulin resistance and dyslipidaemia. The association between abdominal obesity and metabolic dysfunction within this population is not dependent upon IL-6, IL-8 or IL-18.

Effect of abdominal obesity on insulin resistance and the components of the metabolic syndrome: evidence supporting obesity as the central feature.

Metabolic syndrome includes abdominal obesity, diabetes type 2, hypertension, dyslipidemia, derangements of fibrinolysis, and atherosclerosis. Since abdominal obesity is one of the major components of the insulin resistance syndrome (IRS), an attempt was made to evaluate the interrelationships between the magnitude of obesity and the components of the syndrome. A cross-sectional study of 123 subjects with type 2 diabetes, of whom 31 were normal body weight and 92 had varying degrees of obesity was conducted. The participants were investigated in terms of clinical and laboratory findings of IRS. Fasting and 30-min (early) plasma glucose and serum insulin excursions in response to oral glucose challenge (75 g) were determined. The peripheral and hepatic insulin resistance (insensitivity) was calculated by homeostasis model assessment (HOMA). Clinical and biochemical findings were compared with the components of the IRS, and demonstrated that a rise in fasting as well as 30-min insulin secretion increases as abdominal body fat (obesity) increases. There was also a significant and proportional correlation between the magnitude of abdominal obesity and the components of metabolic syndrome. Abdominal adiposity appears to have a pivotal role in the development of IRS.

Cross-sectional and prospective associations between abdominal adiposity and proinsulin concentration.

The objective of this study was to investigate the associations of total and abdominal obesity with variation in proinsulin concentration in a Native Canadian population experiencing an epidemic of type 2 diabetes mellitus (DM). Between 1993 and 1995, 728 members of a Native Canadian community participated in a population-based survey to determine the prevalence and risk factors for type 2 DM. Samples for glucose, C-peptide, and proinsulin were drawn after an overnight fast, and a 75-g oral glucose tolerance test was administered. Type 2 DM and impaired glucose tolerance (IGT) were diagnosed using World Health Organization criteria. Height, weight, waist circumference, and percent body fat were measured. In 1998, 95 individuals who, at baseline, had IGT or normal glucose tolerance with an elevated 2-h glucose level (> or = 7.0 mM) participated in a follow-up evaluation using the same protocol. After adjustment for age, sex, C-peptide concentration, per cent body fat, and waist circumference, proinsulin was found to be significantly elevated in diabetic subjects, relative to subjects with both impaired and normal glucose tolerance (both P < 0.0001); and the concentration in those with IGT was higher, compared with normals (P < 0.0001). Among nondiabetic subjects, proinsulin showed significant univariate associations with percent body fat, body mass index, and waist circumference (r = 0.34, 0.45, 0.41, respectively, all P < 0.0001). After adjustment for body fat and other covariates, waist circumference remained significantly associated with proinsulin concentration in nondiabetic subjects (r = 0.20, P < 0.0001). In prospective analysis, adjusted for covariates (including baseline IGT and follow-up glucose tolerance status), baseline waist circumference was positively associated with both follow-up and change in proinsulin concentration (r = 0.27, P = 0.01; r = 0.24, P = 0.03, respectively). These data highlight the detrimental effects of abdominal obesity on beta-cell function, and support the hypothesis that beta-cell dysfunction occurs early in the natural history of glucose intolerance.