Aims/hypothesis: Inflammation is implicated in the development of type 2 diabetes and CHD, but the trigger of inflammation is unclear. Although in vitro and animal studies support a role of elevated levels of atherosclerotic lipoproteins in the activation of inflammation, plasma cholesterol cannot predict inflammatory markers in humans. Moreover, the association between inflammatory markers and other traditional risk factors of diabetes and CHD is unclear. To increase our knowledge of in vivo regulation of inflammation, we examined the association between several traditional risk factors and inflammatory markers. We hypothesised that because apolipoprotein B (ApoB) reflects atherogenic particle number, it is the primary predictor of inflammatory status. Subjects, materials and methods: We examined the association between several traditional risk factors and plasma high-sensitivity (hs) C-reactive protein (CRP), hsTNF-α, soluble TNF receptor 1, IL-6, orosomucoid, haptoglobin and α 1 -antitrypsin in 77 non-diabetic overweight and obese postmenopausal women. Results: The inflammatory markers correlated positively with total and abdominal adiposity, blood pressure, 2-h OGTT glucose, insulin resistance, triglyceride, total/HDL cholesterol, ApoB, ApoB:apolipoprotein A1 (ApoA1) ratio and Framingham CHD risk points. They correlated negatively with ApoA1, and total, LDL and HDL cholesterol. ApoB was an independent predictor of the interindividual variation in IL-6, hsCRP, orosomucoid, haptoglobin and α 1 -antitrypsin (R 2 range 8-40%); other risk factors were less predictive. Compared with BMI-matched control subjects, women with hyperapobetalipoproteinaemia (hyperapoB) had higher hsTNF-α, IL-6, hsCRP and orosomucoid (increase 17-104%). Conclusions/interpretation: ApoB is the primary predictor of inflammatory markers in postmenopausal overweight and obese women. Given elevated levels of inflammatory markers in hyperapoB women, we hypothesise that hyperapoB women may have an increased risk of developing both CHD and diabetes.

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OBJECTIVEThe objective of the present study was to analyze the association between neighborhood deprivation and self-reported disability in a community sample of people with type 2 diabetes.RESEARCH DESIGN AND METHODSRandom digit dialing was used to select a sample of adults with self-reported diabetes aged 18–80 years in Quebec, Canada. Health status was assessed by the World Health Organization Disability Assessment Schedule II. Material and social deprivation was measured using the Pampalon index, which is based on the Canadian Census. Potential risk factors for disability included sociodemographic characteristics, socioeconomic status, social support, lifestyle-related factors (smoking, physical activity, and BMI), health care–related problems, duration of diabetes, insulin use, and diabetes-specific complications.RESULTSThere was a strong association between disability and material and social deprivation in our sample (n = 1,439): participants living in advantaged neighborhoods had lower levels of disability than participants living in disadvantaged neighborhoods. The means ± SD disability scores for men were 7.8 ± 11.8, 12.0 ± 11.8, and 18.1 ± 19.4 for low, medium, and high deprivation areas, respectively (P < 0.001). The disability scores for women were 13.4 ± 12.4, 14.8 ± 15.9, and 18.9 ± 16.2 for low, medium, and high deprivation areas, respectively (P < 0.01). Neighborhood deprivation was associated with disability even after controlling for education, household income, sociodemographic characteristics, race, lifestyle-related behaviors, social support, diabetes-related variables, and health care access problems.CONCLUSIONSThe inclusion of neighborhood characteristics might be an important step in the identification and interpretation of risk factors for disability in diabetes.

Objective: Chronic subclinical inflammation and regular physical activity have opposing relationships to obesity-related metabolic diseases. Yet, the association between chronic inflammation and physical activity has rarely been examined in obese subjects. We examined the association between physical activity energy expenditure (PAEE), total (TEE) and resting energy expenditure (REE) and cardiorespiratory fitness (VO 2 peak) with inflammatory markers in overweight/obese women. Design: Cross-sectional study. Methods: The study included 152 overweight/obese postmenopausal women who were sedentary and free of chronic/ inflammatory diseases (mean age: 57.5 (95% confidence interval (CI) 56.7-58.3) years, body mass index (BMI): 32.5 (95% CI 31.8-33.2) kg m À2 ). The following parameters were measured: TEE (doubly labeled water), REE (indirect calorimetry), PAEE (as (TEE Â 0.90)ÀREE), VO 2 peak (ergocycle) and serum high-sensitive C-reactive protein (hsCRP), haptoglobin, soluble tumor necrosis factor-a receptor 1 (sTNFR1), interleukin-6, orosomucoid and white blood cells. Results: Sedentary women with the highest tertile of PAEE (1276 (1233-1319) kcal day À1 ) had lower concentrations of hsCRP and haptoglobin than those in the lowest tertile (587 (553-621) kcal day À1 ) after adjustment for fat mass (Po0.05). Soluble TNFR1 was positively correlated with VO 2 peak, TEE and REE (Po0.05), and hsCRP and orosomucoid were positively associated with REE (Po0.01), whereas haptoglobin was negatively associated with PAEE (Po0.05). In stepwise regression analyses that examined the concomitant associations of components of energy expenditure with inflammatory markers, PAEE remained the only predictor of hsCRP and haptoglobin (Po0.05), explaining 14 and 5%, respectively, of their variation,whereas REE was the only predictor of orosomucoid (r 2 ¼ 0.05, P ¼ 0.02) after adjustment for fat mass. Adding leptin to the regression models results in similar relationships between inflammatory markers and components of energy expenditure. Conclusion: PAEE is an independent predictor of hsCRP and haptoglobin in sedentary overweight/obese postmenopausal women free of chronic disease. Our data support the role of physical activity in reducing subclinical inflammation and risk of metabolic and cardiovascular diseases.

The objective of this cross-sectional study was to examine the relationship between the triglyceride-HDL-cholesterol ratio (TG:HDL-C) and insulin sensitivity in overweight and obese sedentary postmenopausal women. The study population consisted of 131 non-diabetic overweight and obese sedentary postmenopausal women (age; 57.7+/-5.0 y; body mass index (BMI), 32.2+/-4.3 kg/m2). Subjects were characterized by dividing the entire cohort into tertiles based on the TG:HDL-C (T1<0.86 vs. T2=0.86 to 1.35 vs. T3>1.35, respectively). We measured (i) insulin sensitivity (using the hyperinsulinenic-euglycemic clamp and homeostasis model assessment (HOMA)), (ii) body composition (using dual-energy X-ray absorptiometry), (iii) visceral fat (using computed tomography), (iv) plasma lipids, C-reactive protein, 2 h glucose concentration during an oral glucose tolerance test (2 h glucose), as well as fasting glucose and insulin, (v) peak oxygen consumption, and (vi) lower-body muscle strength (using weight training equipment). Significant correlations were observed between the TG:HDL-C and the hyperinsulinemic-euglycemic clamp (r=-0.45; p<0.0001), as well as with HOMA (r=0.42; p<0.0001). Moreover, the TG:HDL-C significantly correlated with lean body mass, visceral fat, 2 h glucose, C-reactive protein, and muscle strength. Stepwise regression analysis showed that the TG:HDL-C explained 16.4% of the variation in glucose disposal in our cohort, which accounted for the greatest source of unique variance. Other independent predictors of glucose disposal were 2 h glucose (10.1%), C-reactive protein (CRP; 7.6%), and peak oxygen consumption (5.8%), collectively (including the TG:HDL-C) explaining 39.9% of the unique variance. In addition, the TG:HDL-C was the second predictor for HOMA, accounting for 11.7% of the variation. High levels of insulin sensitivity were associated with low levels of the TG:HDL-C. In addition, the TG:HDL-C was a predictor for glucose disposal rates and HOMA values in our cohort of overweight and obese postmenopausal women.

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The objective of the present study was to examine anthropometric, metabolic, psychosocial and dietary factors associated with dropout in a 6-month weight loss intervention aimed at reducing body weight by 10 %. The study sample included 137 sedentary, overweight and obese postmenopausal women, participating in a weight loss intervention that consisted of either energy restriction (ER) or ER with resistance training (ER+RT). Anthropometric (BMI, percent lean body mass, percent fat mass, visceral adipose tissue and waist circumference), metabolic (total energy expenditure, RMR, insulin sensitivity and fasting plasma levels of leptin and ghrelin), psychosocial (body esteem, self-esteem, stress, dietary restraint, disinhibition, hunger, quality of life, self-efficacy, perceived benefits for controlling weight and perceived risk) and dietary (3-d food record) variables were measured. Thirty subjects out of 137 dropped out of the weight loss programme (22 %), with no significant differences in dropout rates between those in the ER and the ER+RT groups. Overall, amount of weight loss was significantly lower in dropouts than in completers ( - 1.7 (sd 3.5) v. - 5.6 (sd 4.3) kg, P < 0.05); weekly weight loss during the first 4 weeks was also significantly lower. Dropouts consumed fewer fruit servings than completers (1.7 (sd 1.1) v. 2.7 (sd 1.53), P < 0.05) and had higher insulin sensitivity levels (12.6 (sd 3.8) v. 11.1 (sd 2.8) mg glucose/min per kg fat-free mass, P < 0.05). The present results suggest that the rate of weight loss during the first weeks of an intervention plays an important role in the completion of the programme. Thus, participants with low rates of initial weight loss should be monitored intensely to undertake corrective measures to increase the likelihood of completion.