The relationship of C‐reactive protein to obesity‐related depressive symptoms: A longitudinal study

Objective:

Obesity has been shown to produce a state of systematic low‐grade inflammation that may have detrimental neuropsychiatric effects.

Design and Methods:

Longitudinal associations between obesity, inflammation, and depressive symptoms amongst a cohort of older English adults over 4 years of follow‐up were examined. Participants were 3,891 obese and nonobese people drawn from the English longitudinal study of ageing (ELSA) [aged 64.9 (SD = 8.8) years, 44.6% men]. Depressive symptoms were assessed at baseline and after 4 years of follow‐up using the eight‐item center for epidemiological studies—depression scale (CES‐D).

Results:

Approximately 26.3% (N = 1,025) of the sample were categorized as obese at baseline. Obesity at baseline was associated with elevated levels of depressive symptoms at follow‐up (P < 0.001), in analyses that adjusted for depression levels at baseline and sociodemographic and background variables including the prevalence of permanent illness/disability, alcohol consumption, sedentary behavior, and smoking. In addition, C‐reactive protein (CRP) concentrations at baseline were independently associated with CES‐D depression scores at follow‐up (P = 0.008) in fully adjusted analyses. Subsequent mediation analyses revealed that CRP levels explained ～20% of the obesity‐related longitudinal change in depression scores.

Conclusion:

These data suggest that chronic inflammation may be a key determinant of depressive symptoms in obesity.     

Body mass index and depressive symptoms: instrumental‐variables regression with genetic risk score

The causal role of obesity in the development of depression remains uncertain. We applied instrumental‐variables regression (Mendelian randomization) to examine the association of adolescent and adult body mass index (BMI) with adult depressive symptoms. Participants were from the Young Finns prospective cohort study (n = 1731 persons, 2844 person‐observations), with repeated measurements of BMI and depressive symptoms (modified Beck's Depression Inventory). Genetic risk score of 31 single nucleotide polymorphisms previously identified as robust genetic markers of body weight was used as a proxy for variation in BMI. In standard linear regression analysis, higher adult depressive symptoms were predicted by higher adolescent BMI (B = 0.33, CI = 0.06–0.60, P = 0.017) and adult BMI (B = 0.47, CI = 0.32–0.63, P < 0.001). These associations were replicated in instrumental‐variables analysis with genetic risk score as instrument (B = 1.96, CI = 0.03–3.90, P = 0.047 for adolescent BMI; B = 1.08, CI = 0.11–2.04, P = 0.030 for adult BMI). The association for adolescent BMI was significantly stronger in the instrumented analysis compared to standard regression (P = 0.04). These findings provide additional evidence to support a causal role for high BMI in increasing symptoms of depression. However, the present analysis also demonstrates potential limitations of applying Mendelian randomization when using complex phenotypes.     

School level contextual factors are associated with the weight status of adolescent males and females

Objective: To determine whether school context influences the BMI of adolescent males and females. Methods and Procedures: Our sample was 17,007 adolescents (aged 12–19) from the National Longitudinal Study of Adolescent Health (Add Health). We used gender‐stratified multilevel modeling to examine the contribution of schools to the overall variance in adolescent BMIs, calculated from self‐reported weight and height. We then examined the associations of individual attributes with BMI after controlling for the average BMI of the school and the association of two school‐level variables with BMI. Results: Participants attended schools that were segregated by race/ethnicity and socioeconomic status (SES). In females, when controlling only for individual‐level attributes, individual household income was inversely associated (β = ?0.043, P = 0.01) while Hispanic (β = 0.89, P < 0.001) and black (β = 1.61, P < 0.001) race/ethnicity were positively associated with BMI. In males, Hispanic (β = 0.67, P < 0.001) race/ethnicity was positively associated with BMI; there was no difference in the BMIs of blacks compared with whites (β = 0.24, P = 0.085). After controlling for the school racial/ethnic makeup and the school level median household income, the relationship between individual race/ethnicity and BMI was attenuated in both male and female adolescents. Higher school level median household income was associated with lower individual BMIs in adolescent girls (γ = ?0.37, P < 0.001) and boys (γ = ?0.29, P < 0.001) suggesting a contextual effect of the school. Discussion: Male and female adolescents attending schools with higher median household incomes have on average lower BMIs. Resources available to or cultural norms within schools may constitute critical mechanisms through which schools impact the BMI of their students.     

RETRACTION: C-reactive Protein and Metabolic Syndrome in Youth: A Strong Relationship?

Retraction: Note from the Editor‐in‐Chief: This paper is retracted Objective: Metabolic syndrome (MS) is on the rise in youth. As high‐sensitivity C‐reactive protein (hs‐CRP) is associated with cardiovascular/metabolic disorders, we evaluated the association between MS and its components and hs‐CRP in a sample of Brazilian overweight and obese youth. Methods and Procedures: A total of 407 students (229 girls, 273 with excessive weight, 11.3 ± 3.2 years) were evaluated. Measurement included BMI, waist circumference (WC), blood pressure, lipids, insulin, and hs‐CRP. Excessive weight was defined using BMI z ‐score; MS by the modified National Cholesterol Education Program—Adult Treatment Panel III. Results: Subjects were classified into two groups: with MS (n = 72) and without (n = 335). hs‐CRP means and medians were higher in MS group (1.41 mg/l vs. 1.06 mg/l, P < 0.001; 2.21 mg/l vs. 1.23 mg/l, P < 0.001). Associations between hs‐CRP quartiles and insulin resistance (IR) (P < 0.001), MS (P < 0.001), WC (P < 0.000), BMI z‐score (P < 0.001), hypertension (P < 0.001), hypertriglyceridemia (P < 0.001), and low HDL‐c (P = 0.023) were significant; adjustment of hs‐CRP for BMI z‐score eliminated the previous association, except for the number of MS components (nMSc) (P < 0.001). Adjusting for homeostasis model assessment method of IR (HOMA‐IR) did not eliminate the relation between hs‐CRP and MS components. Furthermore, increases in BMI z ‐score and nMSc were associated with an increased hs‐CRP. Excessive weight (odds ratio (OR), 7.9; confidence interval (CI), 4.7–13.4; P = 0.000), hypertension (OR, 2.3; CI, 1.3–4.2; P = 0.003), and hypertriglyceridemia (OR, 2.3; CI, 1.5–3.7; P < 0.001) were independently associated with hs‐CRP. Discussion: In youth, hs‐CRP is strongly related with MS and its components, and is also determined by the body composition. This association indicates a precocious proinflammatory state.     

The influence of body composition, fat distribution, and sustained weight loss on left ventricular mass and geometry in obesity

Alterations in left ventricular mass and geometry vary along with the degree of obesity, but mechanisms underlying such covariation are not clear. In a case–control study, we examined how body composition and fat distribution relate to left ventricular structure and examine how sustained weight loss affects left ventricular mass and geometry. At the 10‐year follow‐up of the Swedish obese subjects (SOS) study cohort, we identified 44 patients with sustained weight losses after bariatric surgery (surgery group) and 44 matched obese control patients who remained weight stable (obese group). We also recruited 44 matched normal weight subjects (lean group). Dual‐energy X‐ray absorptiometry, computed tomography, and echocardiography were performed to evaluate body composition, fat distribution, and left ventricular structure. BMI was 42.5 kg/m², 31.5 kg/m², and 24.4 kg/m² for the obese, surgery, and lean groups, respectively. Corresponding values for left ventricular mass were 201.4 g, 157.7 g, and 133.9 g (P < 0.001). In multivariate analyses, left ventricular diastolic dimension was predicted by lean body mass (β = 0.03, P < 0.001); left ventricular wall thickness by visceral adipose tissue (β = 0.11, P < 0.001) and systolic blood pressure (β = 0.02, P = 0.019); left ventricular mass by lean body mass (β = 1.23, P < 0.001), total body fat (β = 1.15, P < 0.001) and systolic blood pressure (β = 2.72, P = 0.047); and relative wall thickness by visceral adipose tissue (β = 0.02, P < 0.001). Left ventricular adjustment to body size is dependent on body composition and fat distribution, regardless of blood pressure levels. Obesity is associated with concentric left ventricular remodeling and sustained 10‐year weight loss results in lower cavity size, wall thickness and mass.     

Plasma MR‐proADM Correlates to BMI and Decreases in Relation to Leptin After Gastric Bypass Surgery

Adrenomedullin (ADM) is a vasoactive peptide found to be related to obesity and its comorbidities: type 2 diabetes, hypertension, atherosclerosis, and coronary heart disease. ADM is increased both in plasma and in adipose tissue of obese individuals when compared to lean subjects and is considered as a member of the adipokine family. We determined plasma midregional proadrenomedullin (MR‐proADM) concentrations in a cohort of 357 subjects with BMI ranging from 17.5 to 42.3 kg/m² and no additional medical history. In parallel, 28 severely obese patients scheduled to undergo laparoscopic Roux‐en‐Y gastric bypass (RYGB) surgery were studied at two time points: before and 1 year after surgery. Outcome measurements were: MR‐proADM, cortisol, leptin, C‐reactive protein (CRP) thyroid‐stimulating hormone (TSH), creatinine and metabolic parameters. BMI correlated significantly to plasma MR‐proADM levels (r = 0.714, P < 0.001), also after adjustment for age and gender (r = 0.767, P < 0.001). In obese subjects, there was a positive relationship between MR‐proADM and leptin (r = 0.511, P = 0.006). Following RYGB, plasma MR‐proADM decreased from 0.76 ± 0.03 to 0.62 ± 0.02 pg/ml (P < 0.0001). RYGB‐induced changes in MR‐proADM correlated significantly to changes in leptin (r = 0.533, P = 0.004) and in CRP (r = 0.429, P = 0.023). We conclude that BMI is an independent predictor of circulating MR‐proADM levels. Weight loss after RYGB is associated with a significant decrease in plasma MR‐proADM, which is related to surgery‐induced changes in both circulating leptin and systemic inflammation.     

Sleep apnea modifies the long‐term impact of surgically induced weight loss on cardiac function and inflammation

Objective:

Obesity is frequently associated with obstructive sleep apnea (OSA). Both conditions are proinflammatory and proposed to deteriorate cardiac function. We used a nested cohort study design to evaluate the long‐term impact of bariatric surgery on OSA and how weight loss and OSA relate to inflammation and cardiac performance.

Design and Methods:

At 10‐year follow‐up in the Swedish Obese Subjects (SOS) study, we identified 19 obese subjects (BMI 31.2 ± 5.3 kg m^?2), who following bariatric surgery at SOS‐baseline had displayed sustained weight losses (surgery group), and 20 obese controls (BMI 42.0 ± 6.2 kg m^?2), who during the same time‐period had maintained stable weight (control group). All study participants underwent overnight polysomnography examination, echocardiography and analysis of inflammatory markers.

Results:

The surgery group displayed a lower apnea hypopnea index (AHI) (19.9 ± 21.5 vs. 37.8 ± 27.7 n/h, P = 0.013), lower inflammatory activity (hsCRP 2.3 ± 3.0 vs. 7.2 ± 5.0 mg L^?1, P < 0.001), reduced left ventricular mass (165 ± 22 vs. 207 ± 22 g, P < 0.001) and superior left ventricular diastolic function (E/A ratio 1.24 ± 1.10 vs. 1.05 ± 0.20, P = 0.006) as compared with weight stable obese controls. In multiple regression analyses including all subjects (n = 39) and controlling for BMI, the AHI remained independently associated with hsCRP (β = 0.09, P < 0.001), TNF‐α (β = 0.03, P = 0.031), IL‐6 (β = 0.01, P = 0.007), IL 10 (β = ?0.06; P = 0.018), left ventricular mass (β = 0.64, P < 0.001), left atrial area (β = 0.08, P = 0.002), pulmonary artery pressure (β = 0.08, P = 0.011) and E/E_a ratio (β = 0.04, P = 0.021).

Conclusions:

Patients with sustained weight loss after bariatric surgery display less severe sleep apnea, reduced inflammatory activity, and enhanced cardiac function. Persisting sleep apnea appears to limit the beneficial effect of weight loss on inflammation and cardiac performance.

     

Relation of BMI and physical activity to sex hormones in postmenopausal women

Objective: Levels of estrogen, androgen, and prolactin have been related to risk of postmenopausal breast cancer. However, the determinants of these hormone concentrations are not established. The purpose of this study was to examine correlates of endogenous sex hormones. Research Methods and Procedures: Associations among adiposity, physical activity, and diet and concentrations of estradiol, free estradiol, estrone, testosterone, free testosterone, sex hormone‐binding globulin (SHBG), androstenedione, dehydroepiandrosterone, dehydroepiandrosterone sulfate, and prolactin were evaluated in 267 postmenopausal women randomly selected from the Women's Health Initiative Dietary Modification Trial. Results: In multiple regression analyses on log‐transformed hormones, BMI was positively associated with estrone (β = 0.031, p < 0.001), estradiol (β = 0.048, p < 0.001), free estradiol (β = 0.062, p < 0.001), free testosterone (β = 0.017, p = 0.02), and prolactin (β = 0.012, p = 0.02) and negatively associated with SHBG (β = ?0.02, p = 0.001). Total physical activity (metabolic equivalent tasks per week) was negatively associated with concentrations of estrone, estradiol, and androstenedione (β = ?0.006, ?0.007, and ?0.005, respectively, all p ≤ 0.05). Using a composite variable of BMI and physical activity dichotomized by median values, women with high BMI/low physical activity had a mean estrone concentration of 28.8 pg/mL, compared with 24.1, 19.9, and 18.4 pg/mL for women with high BMI/high physical activity, low BMI/low physical activity, and low BMI/high physical activity, respectively (p trend < 0.001). Similar trends were observed for estradiol and free estradiol and, in inverse, for SHBG. Discussion: These associations may, in part, explain the positive associations between overweight/obesity and a sedentary lifestyle on breast cancer risk.     

Maternal obesity is associated with younger age at obesity onset in U.S. adolescent offspring followed into adulthood

Objective: The objective was to test the hypothesis that maternal obesity is associated with younger age of offspring's obesity onset. Research Methods and Procedures: We used prospective, nationally representative, longitudinal data collected across Waves I (1995; 12 to 20 years), II (1996; 13 to 20 years), and III (2001; 18 to 28 years) of the National Longitudinal Study of Adolescent Health (N = 14,654; 49% female). Interval regression analysis was used to assess the association between maternal obesity and age at offspring's obesity onset (International Obesity Task Force BMI ≥30 equivalent age‐ and sex‐specific cut‐off points for adolescents and BMI ≥30 for young adults) using self‐reported heights and weights, adjusting for race/ethnicity, sex, parental education, and family income, accounting for complex sampling design. Results: The net effect of having an obese mother varied by race/ethnicity and was associated with a significantly earlier age at obesity onset (p = 0.0001) for whites [β= ?8.1 year, 95% confidence interval (CI), ?9.3; ?6.9)], blacks (β = ?10.8 years, 95% CI, ?12.4; ?9.2), Hispanics (β = ?7.0 years, 95% CI, ?9.2; ?4.8), and Asians (β = ?8.6 years, 95% CI, ?13.3; ?3.9). Earlier obesity onset (<18 years) was associated with increased severity at young adulthood (mean BMI, 36.0 ± 0.3 kg/m²) vs. onset after age 18 (mean BMI, 34.4 ± 0.2 kg/m²; p = 0.0001). There were no sex differences in the association of maternal obesity to age at obesity onset. Conclusions: Having an obese mother was associated with earlier age at obesity onset across all race/ethnic groups, particularly non‐Hispanic blacks. Early obesity onset has important health consequences because of its association with more severe adult obesity.     

Obesity and C-reactive protein levels among white, black, and hispanic US adults

Objective: Studies suggest that obesity's adverse impact on cardiovascular mortality may be reduced in African Americans relative to white Americans. We examined whether obesity's association with novel cardiovascular risk factors such as C‐reactive protein (CRP) also varies by race and ethnicity. Methods and Procedures: We analyzed data from 10,492 white, African‐American, and Hispanic‐American participants of the 1999–2004 National Health and Nutrition Examination Survey, who were aged 20 years and older, with a BMI ≥18.5 kg/m² and CRP ≤10 mg/l. We fit sex‐specific multivariable models of the association of BMI or waist circumference with log CRP levels and tested for interactions of BMI or waist circumference with race/ethnicity. Results: Higher BMI was significantly associated with higher CRP in all racial/ethnic groups for both men and women (P > 0.05 for BMI–race/ethnicity interaction) before and after adjustment for age, education, and health behaviors. Larger waist circumference was also associated with higher CRP levels in all racial/ethnic groups before and after adjustment; among women, the relationship was strongest for Mexican Hispanics (P < 0.01 for waist circumference–race/ethnicity interaction). Results were similar after additional adjustment for medications that might affect CRP levels. Discussion: The association between obesity and CRP is at least as strong in African Americans and Hispanic Americans as in white Americans. Racial differences in the relationship between obesity and cardiovascular mortality are unlikely to be due to racial differences in obesity's impact on CRP.     

ADIPOQ Polymorphisms,Monounsaturated Fatty Acids,and Obesity Risk: The GOLDN Study

Serum adiponectin levels have been positively associated with insulin sensitivity and are decreased in type 2 diabetes (T2D) and obesity. Genetic and environmental factors influence serum adiponectin and may contribute to risk of metabolic syndrome and T2D. Therefore, we investigated the effect of ADIPOQ single‐nucleotide polymorphisms (SNPs), ?11377C>G and ?11391G>A, on metabolic‐related traits, and their modulation by dietary fat in white Americans. Data were collected from 1,083 subjects participating in the Genetics of Lipid Lowering Drugs and Diet Network study. Mean serum adiponectin concentration was higher for carriers of the ?11391A allele (P = 0.001) but lower for the ?11377G allele carriers (P = 0.017). Moreover, we found a significant association with obesity traits for the ?11391G>A SNP. Carriers of the ?11391A allele had significantly lower weight (P = 0.029), BMI (P = 0.019), waist (P = 0.003), and hip circumferences (P = 0.004) compared to noncarriers. Interestingly, the associations of the ?11391G>A with BMI and obesity risk were modified by monounsaturated fatty acids (MUFAs) intake (P‐interaction = 0.021 and 0.034 for BMI and obesity risk, respectively). In subjects with MUFA intake above the median (≥13% of energy intake), ?11391A carriers had lower BMI (27.1 kg/m² for GA+AA vs. 29.1 kg/m² for GG, P = 0.002) and decreased obesity risk (odds ratio for ?11391A = 0.52, 95% confidence interval (CI); 0.28–0.96; P = 0.031). However, we did not detect genotype‐related differences for BMI or obesity in subjects with MUFA intake <13%. Our findings support a significant association between the ?11391G>A SNPs and obesity‐related traits and the potential to moderate such effects using dietary modification.     

Treadmill desks: A 1‐year prospective trial

Objective: Sedentariness is associated with weight gain and obesity. A treadmill desk is the combination of a standing desk and a treadmill that allow employees to work while walking at low speed. Design and Methods: The hypothesis was that a 1‐year intervention with treadmill desks is associated with an increase in employee daily physical activity (summation of all activity per minute) and a decrease in daily sedentary time (zero activity). Employees (n = 36; 25 women, 11 men) with sedentary jobs (87 ± 27 kg, BMI 29 ± 7 kg/m², n = 10 Lean BMI < 25 kg/m², n = 15 Overweight 25 < BMI < 30 kg/m², n = 11 Obese BMI > 30 kg/m²) volunteered to have their traditional desk replaced with a treadmill desk to promote physical activity for 1 year. Results: Daily physical activity (using accelerometers), work performance, body composition, and blood variables were measured at Baseline and 6 and 12 months after the treadmill desk intervention. Subjects who used the treadmill desk increased daily physical activity from baseline 3,353 ± 1,802 activity units (AU)/day to, at 6 months, 4,460 ± 2,376 AU/day (P < 0.001), and at 12 months, 4,205 ± 2,238 AU/day (P < 0.001). Access to the treadmill desks was associated with significant decreases in daily sedentary time (zero activity) from at baseline 1,020 ± 75 min/day to, at 6 months, 929 ± 84 min/day (P < 0.001), and at 12 months, 978 ± 95 min/day (P < 0.001). For the whole group, weight loss averaged 1.4 ± 3.3 kg (P < 0.05). Weight loss for obese subjects was 2.3 ± 3.5 kg (P < 0.03). Access to the treadmill desks was associated with increased daily physical activity compared to traditional chair‐based desks; their deployment was not associated with altered performance. For the 36 participants, fat mass did not change significantly, however, those who lost weight (n = 22) lost 3.4 ± 5.4 kg (P < 0.001) of fat mass. Weight loss was greatest in people with obesity. Conclusions: Access to treadmill desks may improve the health of office workers without affecting work performance.     

Associations of leukocyte telomere length with body anthropometric indices and weight change in chinese women

Objective: This study evaluated associations of telomere length with various anthropometric indices of general and abdominal obesity, as well as weight change. Design and Methods: The study included 2,912 Chinese women aged 40‐70 years. Monochrome multiplex quantitative polymerase chain reaction was applied to measure relative telomere length. Results: Telomere length was inversely associated with body mass index (BMI), waist circumference, waist‐to‐height ratio, weight, and hip circumference (P_trend = 0.005, 0.004, 0.004, 0.010, and 0.026, respectively), but not waist‐to‐hip ratio (P_trend = 0.116) or height (P_trend = 0.675). Weight change since age 50 was further evaluated among women over age 55. Women who maintained their weight within ±5% since age 50, particularly within a normal range (BMI = 18.5‐24.9 kg/m²), or reduced their weight from overweight (BMI = 25‐29.9 kg/m²) or obesity (BMI ≥30 kg/m²) to normal range, had a longer mean of current telomere length than women who gained weight since age 50 (P_trend = 0.025), particularly those who stayed in obesity or gained weight from normal range or overweight to obesity (P = 0.023). Conclusion: Our findings show that telomere shortening is associated with obesity and that maintaining body weight within a normal range helps maintain telomere length.     

The Effect of Obesity and Weight Loss on Aortic Pulse Wave Velocity as Assessed by Magnetic Resonance Imaging

Obesity is an escalating global health problem associated with both an increased risk of death and an increased risk of cardiovascular events. Our goal was to use magnetic resonance imaging (MRI) to determine the effect of obesity and weight loss, in the absence of the traditional cardiovascular risk factors, on aortic pulse wave velocity (PWV) a reliable, reproducible, and accurate clinical measure of aortic stiffness linked to increased mortality. Fifty obese (BMI 38.3 ± 6.8 kg/m²) and eighteen normal‐weight controls (BMI 22.0 ± 1.7 kg/m²) with no identifiable cardiovascular risk factors underwent vascular MRI to assess PWV between the ascending aorta at the level of the pulmonary artery and the abdominal aorta (AA). Twenty‐eight subjects underwent repeat imaging after a 1‐year period of weight loss. Both groups were well matched for age, systolic blood pressure, fasting glucose, and total cholesterol. Obesity was associated with a 14% increase in PWV (P = 0.021), and with elevated C‐reactive protein (CRP) (P < 0.01) and leptin levels (P < 0.001) factors known to cause increase arterial stiffness. Weight loss (average 50% excess weight) was associated with a 14% improvement in PWV (P = 0.03), and with reductions in serum leptin levels (P < 0.01). Obesity, in the absence of the traditional cardiovascular risk factors, is associated with increased aortic PWV, a noninvasive clinical measure of aortic stiffness independently predictive of cardiovascular mortality. Significant weight loss results in improvements in aortic PWV. This may provide a potential link between both obesity and increased mortality, and the reduction in mortality that occurs with weight loss.     

Obesity and body fat classification in the metabolic syndrome: Impact on cardiometabolic risk metabotype

Objective:

Obesity is a key factor in the development of the metabolic syndrome (MetS), which is associated with increased cardiometabolic risk. We investigated whether obesity classification by BMI and body fat percentage (BF%) influences cardiometabolic profile and dietary responsiveness in 486 MetS subjects (LIPGENE dietary intervention study).

Design and Methods:

Anthropometric measures, markers of inflammation and glucose metabolism, lipid profiles, adhesion molecules, and hemostatic factors were determined at baseline and after 12 weeks of four dietary interventions (high saturated fat (SFA), high monounsaturated fat (MUFA), and two low fat high complex carbohydrate (LFHCC) diets, one supplemented with long chain n‐3 polyunsaturated fatty acids (LC n‐3 PUFAs)).

Results:

About 39 and 87% of subjects classified as normal and overweight by BMI were obese according to their BF%. Individuals classified as obese by BMI (≥30 kg/m²) and BF% (≥25% (men) and ≥35% (women)) (OO, n = 284) had larger waist and hip measurements, higher BMI and were heavier (P < 0.001) than those classified as nonobese by BMI but obese by BF% (NOO, n = 92). OO individuals displayed a more proinflammatory (higher C reactive protein (CRP) and leptin), prothrombotic (higher plasminogen activator inhibitor‐1 (PAI‐1)), proatherogenic (higher leptin/adiponectin ratio) and more insulin resistant (higher HOMA‐IR) metabolic profile relative to the NOO group (P < 0.001). Interestingly, tumor necrosis factor‐α (TNF‐α) concentrations were lower post‐intervention in NOO individuals compared with OO subjects (P < 0.001).

Conclusions:

In conclusion, assessing BF% and BMI as part of a metabotype may help to identify individuals at greater cardiometabolic risk than BMI alone.     

Association of Two CETP Polymorphisms With HDL Levels in the Chinese Obese Population

The association of two cholesterol ester transfer protein (CETP) polymorphisms, D442G and TAQIB (B1→B2), with high‐density lipoprotein (HDL) levels in 932 Chinese obese individuals (BMI ≥ 27) was investigated in comparison with normal controls (BMI ≤ 24). Independent association was demonstrated for TAQIB minor allele B2 and CETP442 minor allele G with elevated HDL levels. The CETP D442G polymorphism was associated with a much greater increase in HDL levels in subjects with BMI exceeding 27 kg/m² (+5.42 mg/dl, P = 0.0007) compared to normal controls (+1.97 mg/dl, P = 0.275), and the increase in HDL reached the highest level among subjects with BMI exceeding 30 kg/m² (+6.80 mg/dl, P = 0.016). TAQIB showed significant association with HDL levels only in normal BMI subgroup (P = 0.0017). TAQIB significantly interacted with serum triglyceride (TG) on modulating HDL levels (P = 0.027). The TAQIB–TG interaction effect remained marginally significant after controlling for BMI (P = 0.057). We conclude that D442G polymorphism is associated with more HDL elevation in obesity. TAQIB interacts with serum TG on modulating HDL levels, and the interaction is partly independent of BMI.     

Effects of Obesity and Body Fat Distribution on Lipids and Lipoproteins in Nondiabetic American Indians: The Strong Heart Study

Objectives: To examine the relationship between obesity and lipoprotein profiles and compare the effects of total obesity and central adiposity on lipids/lipoproteins in American Indians. Research Methods and Procedures: Participants were 773 nondiabetic American Indian women and 739 men aged 45 to 74 years participating in the Strong Heart Study. Total obesity was estimated using body mass index (BMI). Central obesity was measured as waist circumference. Lipoprotein measures included triglycerides, high‐density lipoprotei in (HDL) cholesterol, low‐density lipoprotein (LDL) cholesterol, apolipoprotein AI (apoAI), and apolipoprotein B (apoB). Partial and canonical correlation analyses were used to examine the associations between obesity and lipids/lipoproteins. Results: Women were more obese than men in Arizona (median BMI 32.1 vs. 29.2 kg/m²) and South Dakota and North Dakota (28.3 vs. 28.0 kg/m²), but there was no sex difference in waist circumference. Men had higher apoB and lower apoAI levels than did women. In women, when adjusted for center, gender, and age, BMI was significantly related to HDL cholesterol (r = ?0.24, p < 0.001). There was a significant but weak relation with apoAI (r = ?0.14 p < 0.001). Waist circumference was positively related to triglycerides (r = 0.14 p < 0.001) and negatively related to HDL cholesterol (r = ?0.23, p < 0.001) and apoAI (r = ?0.13, p < 0.001). In men, BMI was positively correlated with triglycerides (r = 0.30, p < 0.001) and negatively correlated with HDL cholesterol (r = ?0.35, p < 0.001) and apoAI (r = ?0.23, p < 0.001). Triglycerides increased with waist circumference (r = 0.30, p < 0.001) and HDL cholesterol decreased with waist circumference (r = ?0.36 p < 0.001). In both women and men there was an inverted U‐shaped relationship between obesity and waist with LDL cholesterol and apoB. In canonical correlation analysis, waist circumference received a greater weight (0.86) than did BMI (0.17) in women. However, the canonical weights were similar for waist (0.46) and BMI (0.56) in men. Only HDL cholesterol (?1.02) carried greater weight in women, whereas in men, triglycerides (0.50), and HDL cholesterol (?0.64) carried a large amount of weight. All the correlation coefficients between BMI, waist circumference, and the first canonical variable of lipids/lipoproteins or between the individual lipid/lipoprotein variables and the first canonical variable of obesity were smaller in women than in men. Triglycerides and HDL cholesterol showed clinically meaningful changes with BMI and waist circumference in men. All lipid/lipoprotein changes in women in relation to BMI and waist circumference were minimal. Discussion: The main lipoprotein abnormality related to obesity in American Indians was decreased HDL cholesterol, especially in men. Central adiposity was more associated with abnormal lipid/lipoprotein profiles than general obesity in women; both were equally important in men.     

Cord blood ASP is predicted by maternal lipids and correlates with fetal birth weight

Background: The acylation stimulating protein (ASP) is a potent lipogenic adipokine that correlates with postprandial triglyceride (TG) clearance and is linked to the pathophysiology of obesity and related disorders. Objective: To investigate ASP levels in cord blood and its relation to maternal and cord blood lipid parameters and fetal birth weight. Methods and Procedures: Thirty nondiabetic pregnant women, their newborns, and thirty‐three nonpregnant controls were included in this study. Fasting maternal and cord blood ASP, TGs, nonesterified fatty acids (NEFAs), cholesterol, glucose levels, in addition to maternal BMI and fetal birth weight were measured. Results: No significant difference was found between cord blood ASP (16.3 ± 0.96 nmol/l) and ASP levels in the adult controls (15.7 ± 1.0 nmol/l). Cord blood ASP, however, was lower than maternal plasma ASP levels (25.4 ± 1.6 nmol/l, P < 0.001). Yet, lipid levels in cord blood, particularly TGs were markedly decreased compared to control and maternal TG levels (threefold and 7.4‐fold, P < 0.001 respectively). Maternal TGs significantly correlated with fetal birth weight (r = 0.54, P = 0.002). Multiple regression analysis showed that maternal TGs (β = 0.57, P = 0.01) and NEFAs (β = 0.43, P = 0.024) predicted 45% variation in cord blood ASP levels, independent of all measured maternal and cord blood parameters. Cord blood ASP showed a positive correlation with fetal birth weight (r = 0.524, P = 0.037) in neonates above average fetal birth weight of the studied population. Discussion: This is the first study investigating ASP in cord blood. We suggest that maternal hypertriglyceridemia is associated with increased fetal ASP production, thus enhancing fetal fat storage independent of maternal glucose variations in nondiabetic women.     

Meta‐analysis Added Power to Identify Variants in FTO Associated With Type 2 Diabetes and Obesity in the Asian Population

Several common variants in the intron 1 of FTO (fat mass and associated obesity) gene have been reliably associated with BMI and obesity in European populations. We analyzed two variants (rs9939609 and rs8050136) in 4,189 Chinese Han individuals and conducted a meta‐analysis of published studies in Asian population to investigate whether these variants are associated with type 2 diabetes (T2D) and obesity in Asian population. In this study, both the minor allele A of rs9939609 and the minor allele A of rs805136 were associated with increased risk of T2D, independent of measures of BMI; the odds ratios (ORs) per copy of the risk allele were 1.19 for rs9939609 (95% confidence interval (CI), 1.04–1.37; P = 0.01) and 1.22 for rs8050136 (95% CI, 1.07–1.40; P = 0.004) after adjusting for age, sex, and BMI. Our results also showed association with risk of obesity (rs9939609: OR = 1.39 (95% CI 1.04–1.85), P = 0.02; rs8050136: OR = 1.45 (95% CI 1.09–1.93), P = 0.01) but no association with overweight. These results were consistent with the pooled results from our meta‐analysis study (for diabetes, rs8050136, P = 1.3 × 10^?3; rs9939609, P = 9.8 × 10^?4; for obesity, rs8050136, P = 2.2 × 10^?7; rs9939609, P = 9.0 × 10^?9). Our findings indicate that the two variants (rs9939609 and rs8050136) in the FTO gene contribute to obesity and T2D in the Asian populations.