Effect of diet with and without exercise training on markers of inflammation and fat distribution in overweight women

The independent effects of exercise and weight loss on markers of inflammation (MOI) in obese individuals have not been clearly characterized. The objectives of this study were to: (i) identify the independent effects of exercise and weight loss on MOI and (ii) determine whether changes in MOI were associated with changes in fat distribution. Subjects were 126 healthy, premenopausal women, BMI 27–30 kg/m². They were randomized to one of three groups: diet only, diet + aerobic‐, or diet + resistance training until a BMI <25 kg/m² was achieved. Fat distribution was measured with computed tomography, and body composition with dual‐energy X‐ray absorptiometry. Serum concentrations of tumor necrosis factor (TNF)‐α, soluble TNF receptor 1 (sTNF‐R1), soluble TNF receptor 2 (sTNF‐R2), C‐reactive protein (CRP), and interleukin (IL)‐6 were assessed. Results of repeated‐measures ANOVA indicated a significant effect of time on MOI, such that MOI decreased with weight loss. Results of mixed‐model analysis indicated that adjusting for intra‐abdominal adipose tissue (IAAT) and total fat mass explained the decreases in TNF‐α and sTNF‐R1, whereas only total fat mass explained the decreases in sTNF‐R2, IL‐6, and CRP. In conclusion, weight loss was associated with decreases in MOI. The effect of weight loss appeared to be mediated by changes in total fat mass or IAAT. Addition of exercise did not alter the response, suggesting that weight loss has a more profound impact for reducing MOI in overweight women than exercise.     

Diet‐induced Changes in Intra‐abdominal Adipose Tissue and CVD Risk in American Women

The aim of the study was to determine what effect weight loss had on intra‐abdominal adipose tissue (IAAT) and cardiovascular disease (CVD) risk in 135 premenopausal overweight African‐American (AA) and European‐American (EA) women matched for BMI. Blood lipids, systolic blood pressure (SBP), diastolic BP (DBP), and IAAT (computed tomography determined) were examined prior to and after an 800 kcal/day diet producing 12 kg‐weight loss. Significant decreases in IAAT (～38%), total cholesterol (TC; 3%), low‐density lipoproteins (LDLs: 6%), triglycerides (TGs: 27%), cholesterol/high‐density lipoprotein ratio (C/HDL ratio: 18%), SBP (3%), and DBP (3%) occurred while HDL increased (16%), following weight loss and 1 month energy balance. Significant interactions between time and race showed that AA women decreased TG and increased HDL proportionately less than EA women. After adjusting for ΔIAAT, none of the CVD variables significantly changed after weight loss with the exception of HDL and C/HDL ratio. After adjusting for ΔLF (leg fat), ΔTC, ΔTG, ΔLDL, and ΔC/HDL ratio were significantly different. Multiple regression showed that independent of each other, ΔIAAT was significantly and positively related to ΔTC (adjusted β = 0.24) and ΔTG (adjusted β = 0.47), and ΔLF was negatively related to ΔTC (adjusted β = ?0.19) and ΔTG (adjusted β = ?0.18). Overweight and premenopausal AA and EA women benefitted from weight loss by decreasing IAAT and improving CVD risk. The changes in IAAT were significantly related to blood lipids, but loss of LF seems to be related to reduced improvement in TC and TG. Based on these results, interventions should focus on changes on IAAT.     

Intra-abdominal adipose tissue is independently associated with sex-hormone binding globulin in premenopausal women

Lower serum concentrations of sex-hormone binding globulin (SHBG) are associated with increased risk for several obesity-related diseases in women including hormone-sensitive cancers, type 2 diabetes, metabolic syndrome, and cardiovascular disease. Previous investigations have reported that body composition, specifically central obesity, and/or higher insulin concentrations are key factors associated with lower SHBG in overweight and obese women; however, these studies were limited by their cross-sectional design. We hypothesized that intra-abdominal adipose tissue (IAAT), a fat depot linked with an abnormal metabolic profile, is inversely and independently associated with SHBG. Therefore, we determined the longitudinal associations among SHBG, insulin, and IAAT in 107 premenopausal women enrolled in a weight loss study. Overweight (BMI 27-30 kg/m(2)) women were weight reduced until BMI of ≤ 24 was achieved. Body composition and IAAT were measured at baseline and after weight loss with dual-energy X-ray absorptiometry and computed tomography, respectively. Serum concentrations of insulin and SHBG were determined. Paired t-test showed that insulin and IAAT decreased significantly and SHBG increased significantly following weight loss (P < 0.0001 for all). Simple correlations from baseline showed no association with insulin and SHBG (r = -0.142, P = 0.143) and a significant inverse association between IAAT and SHBG (r = -0.43, P < 0.0001). Repeated measures mixed-model showed that after adjusting for age and time (weight loss), IAAT was significantly inversely associated with SHBG (P = 0.0002) and there was no association with insulin and SHBG (P = 0.180). We conclude that SHBG concentrations are influenced by IAAT and not insulin in premenopausal women.     

Age-related changes in insulin sensitivity and β-cell function among European-American and African-American women

Type 2 diabetes (T2D) is more prevalent among African-American (AA) than European-American (EA) women for reasons that are unknown. Ethnic differences in physiological processes related to insulin sensitivity (S(I)) and secretion, and age-related changes in these processes, may play a role. The purpose of this study was to identify ethnicity- and age-related differences in S(I) and β-cell responsivity among AA and EA females, and to determine whether these differences are independent of body composition and fat distribution. Healthy, normoglycemic females aged 7-12 years (n = 62), 18-32 years (n = 57), and 40-70 years (n = 49) were recruited for entry into this study. Following an overnight fast, S(I), intravenous glucose tolerance (Kg), acute C-peptide secretion (X0), and basal, first-phase, second-phase, and total β-cell responsivity to glucose (PhiB, Phi1, Phi2, and Phi(TOT), respectively) were measured by an intravenous glucose tolerance test. Total % body fat was assessed by dual-energy X-ray absorptiometry, and intra-abdominal adiposity (IAAT) by computed tomography. Main effects of age group and ethnicity were measured with analysis of covariance, adjusting for % fat, IAAT, and S(I) as indicated. AA had lower S(I), and higher Kg, X0, Phi1, and Phi(TOT) (P < 0.05), which remained after adjustment for % fat and IAAT. Greater X0, Phi1, and Phi(TOT) among AA were independent of S(I). Advancing age was associated with greater Phi2 among both EA and AA. To conclude, inherent ethnic differences in β-cell function exist independently of adiposity and S(I). Future research should examine whether ethnic differences in β-cell physiology contribute to disparities in T2D risk.     

Insulin Sensitivity in African‐American and White Women: Association With Inflammation

Whether the contribution of inflammation to risk for chronic metabolic disease differs with ethnicity is not known. The objective of this study was to determine: (i) whether ethnic differences exist in markers of inflammation and (ii) whether lower insulin sensitivity among African Americans vs. whites is due to greater inflammatory status. Subjects were African‐American (n = 108) and white (n = 105) women, BMI 27–30 kg/m². Insulin sensitivity was assessed with intravenous glucose tolerance test and minimal modeling; fat distribution with computed tomography; body composition with dual‐energy X‐ray absorptiometry; markers of inflammation (tumor necrosis factor (TNF)‐α, soluble tumor necrosis factor receptor (sTNFR)‐1, sTNFR‐2, C‐reactive protein (CRP), and interleukin (IL)‐6) with enzyme‐linked immunosorbent assay (ELISA). Whites had greater intra‐abdominal adipose tissue (IAAT), insulin sensitivity, and concentrations of TNF‐α, sTNFR‐1, and sTNFR‐2 than African Americans. Greater TNF‐α in whites vs. African Americans was attributed to greater IAAT in whites. Among whites, but not African Americans, CRP was independently and inversely associated with insulin sensitivity, after adjusting for IAAT (r = ?0.29 P < 0.05, and r = ?0.13 P = 0.53, respectively). Insulin sensitivity remained lower in African Americans after adjusting for CRP (P < 0.001). In conclusion, greater IAAT among whites may be associated with greater inflammation. Insulin sensitivity was lower among African Americans, independent of obesity, fat distribution, and inflammation.     

Fat Distribution,Aerobic Fitness,Blood Lipids,and Insulin Sensitivity in African‐American and European‐American Women

The purpose of this study was to determine independent relationships of intra‐abdominal adipose tissue (IAAT), leg fat, and aerobic fitness with blood lipids and insulin sensitivity (S_i) in European‐American (EA) and African‐American (AA) premenopausal women. Ninety‐three EA and ninety‐four AA with BMI between 27 and 30 kg/m² had IAAT by computed tomography, total fat and leg fat by dual‐energy X‐ray absorptiometry, aerobic fitness by a graded exercise test, African admixture (AFADM) by ancestry informative markers, blood lipids by the Ektachem DT system, and S_i by glucose tolerance test. Independent of age, aerobic fitness, AFADM, and leg fat, IAAT was positively related to low‐density lipoprotein–cholesterol (LDL‐C), cholesterol‐high‐density lipoprotein (HDL) ratio, triglycerides (TGs), and fasting insulin (standardized β varying 0.16–0.34) and negatively related to HDL‐cholesterol (HDL‐C) and S_i (standardized β ?0.15 and ?0.25, respectively). In contrast, independent of age, aerobic fitness, AFADM, and IAAT, leg fat was negatively related to total cholesterol, LDL‐C, cholesterol‐HDL ratio, TGs, and fasting insulin (standardized β varying ?0.15 to ?0.21) and positively related to HDL‐C and S_i (standardized β 0.16 and 0.23). Age was not independently related to worsening of any blood lipid but was related to increased S_i (standardized β for S_i 0.25, insulin ?0.31). With the exception of total cholesterol and LDL‐C, aerobic fitness was independently related to worsened blood lipid profile and increased S_i (standardized β varying 0.17 to ?0.21). Maintenance of favorable fat distribution and aerobic fitness may be important strategies for healthy aging, at least in premenopausal EA and AA women.     

Relationship of Intramyocellular Lipid to Insulin Sensitivity May Differ With Ethnicity in Healthy Girls and Women

The prevalence of type 2 diabetes is greater among African Americans (AA) vs. European Americans (EA), independent of obesity and lifestyle. We tested the hypothesis that intramyocellular lipid (IMCL) or extramycellular lipid (EMCL) would be associated with insulin sensitivity among healthy young women, and that the associations would differ with ethnic background. We also explored the hypothesis that adipokines and estradiol would be associated with muscle lipid content. Participants were 57 healthy, normoglycemic, women and girls mean age 26 (±10) years; mean BMI 27.3 (±4.8) kg/m²; 32 AA, 25 EA. Soleus IMCL and EMCL were assessed with ¹H magnetic resonance spectroscopy (MRS); insulin sensitivity with an insulin‐modified frequently sampled intravenous glucose tolerance test and minimal modeling; body composition with dual‐energy X‐ray absorptiometry; and intra‐abdominal adipose tissue (IAAT) with computed tomography. Adiponectin, leptin, and estradiol were assessed in fasting sera. Analyses indicated that EMCL, but not IMCL, was greater in AA vs. EA (2.55 ± 0.16 vs. 1.98 ± 0.18 arbitrary units, respectively, P < 0.05; adjusted for total body fat). IMCL was associated with insulin sensitivity in EA (r = ?0.54, P < 0.05, adjusted for total fat, IAAT, and age), but not AA (r = 0.16, P = 0.424). IMCL was inversely associated with adiponectin (r = ?0.31, P < 0.05, adjusted for ethnicity, age, total fat, and IAAT). In conclusion, IMCL was a significant determinant of insulin sensitivity among healthy, young, EA but not AA women. Further research is needed to determine whether the component lipids of IMCL (e.g., diacylglycerol (DAG) or ceramide) are associated with insulin sensitivity in an ethnicity specific manner.     

Ethnicity and weight status affect the accuracy of proxy indices of insulin sensitivity

This study tested the hypotheses that correlations between direct measures of insulin sensitivity and proxy indices of insulin sensitivity derived from fasting values, (i) would not be affected by ethnicity, and (ii) would be stronger in overweight vs. weight-reduced states. We further hypothesized that associations between proxy indices and fat distribution would be similar to those between directly measured insulin sensitivity and fat distribution. Testing was performed in weight-stable conditions in 59 African-American (AA) and 62 white-American (WA) overweight, premenopausal women before and after a weight loss intervention. Subjects were retested 1 year following weight loss. Proxy indices were correlated against the insulin sensitivity index S(I) determined via minimal modeling. Fat distribution was assessed using computed tomography. Correlations between Si and proxy indices were consistently stronger among overweight women (r = 0.44-0.52) vs. weight-reduced women (r = 0.18-0.32), and among AA (r = 0.49-0.56, baseline; 0.24-0.36, weight-reduced) vs. WA (r = 0.38-0.46, baseline; 0.19-0.31, weight-reduced). Among subjects who regained >3 kg after 1 year, correlations between S(I) and proxy indices were similar to those observed at baseline, whereas correlations were weak among women who maintained their reduced body weight. S(I) and all proxy indices were similarly correlated with intra-abdominal adipose tissue (IAAT) at baseline, but not after weight loss. In conclusion, correlations between S(I) and proxy indices were affected by both ethnicity and weight status. If proxy indices are used in multiethnic populations, or in populations including both lean and overweight/obese subjects, data should be interpreted with caution.     

Dietary Calcium Intake Is Associated With Less Gain in Intra‐Abdominal Adipose Tissue Over 1 Year

Calcium intake is reported to enhance weight loss with a preferential loss in trunk fat. Discrepant findings exist as to the effects of calcium intake on longitudinal changes in total fat mass and central fat deposition. Therefore, the purpose of this study was to determine associations between dietary calcium intake and 1‐year change in body composition and fat distribution, specifically intra‐abdominal adipose tissue (IAAT). A total of 119 healthy, premenopausal women were evaluated at baseline and 1 year later. Average dietary calcium was determined via 4‐day food records. Total fat was determined by dual‐energy X‐ray absorptiometry (DXA) and subcutaneous abdominal adipose tissue (SAAT) and IAAT by computed tomography. Over the study period, participants' reported daily calcium and energy intakes were 610.0 ± 229.9 mg and 1,623.1 ± 348.5 kcal, respectively. The mean change in weight, total fat, IAAT, and SAAT was 4.9 ± 4.4 kg, 5.3 ± 4.0 kg, 7.7 ± 19.5 cm², and 49.3 ± 81.1 cm², respectively. Average calcium intake was significantly, inversely associated with 1‐year change in IAAT (standardized β: ?0.23, P < 0.05) after adjusting for confounding variables. For every 100 mg/day of calcium consumed, gain in IAAT was reduced by 2.7 cm². No significant associations were observed for average calcium intake with change in weight, total fat, or SAAT. In conclusion, dietary calcium intake was significantly associated with less gain in IAAT over 1 year in premenopausal women. Further investigation is needed to verify these findings and determine the calcium intake needed to exert beneficial effects on fat distribution.     

Adipokine serum concentrations, anthropometric measurements and socio-economic status in two ethnic groups with different prevalence levels for cardiovascular diseases and type 2 diabetes

Obesity is more common in African than Asian-Indian populations and yet type 2 diabetes and cardiovascular diseases are more common in the latter populations. The main purpose of the current study was therefore to determine whether ethnic differences in body fat distribution, adipokine levels, and socio-economic status may explain population differences in the prevalence of these metabolic disorders. Leptin, IL-6, CRP, visceral fat, education level, and socio-economic status were measured in 50 African and the same number of Indian women residing in Johannesburg, South Africa. Serum leptin levels were significantly higher in Indian than African subjects (41.3±2.0 and 34.2±2.9?ng/ml, respectively; p<0.05). TNF-α levels were significantly higher in the African group, (5.22±0.86 vs. 2.54±0.52?pg/ml; p<0.05), whilst visceral fat levels were significantly lower (56.1±5.5 vs. 77.9±6.5?cm(2); p<0.05). The CRP and IL-6 levels were not different between groups. Education levels (p<0.005) and socio-economic status (p<0.0001) were both lower in the African subjects, however, adjusting for these variables in ANCOVA did not attenuate differences in adipokine or visceral fat levels. We hypothesise that one of the reasons for the higher prevalence of obesity in the African than Indian population may be related to lower leptin levels, whilst ethnic differences in the prevalence of metabolic disorders cannot be explained by differences in adipokine levels, but maybe related to higher visceral adiposity in the Indian group.     

IAAT, catecholamines, and parity in African-American and European-American women

Objective: We have recently reported that parous European‐American (EA) women have disproportionately more intra‐abdominal adipose tissue (IAAT) than their nulliparous counterparts. Mediating mechanisms for IAAT accumulation remain unknown; however, some evidence suggests a possible catecholamine link. The objective of this study was to determine whether the IAAT‐parity relationship found in EA women exists in African‐American (AA) women and to determine whether catecholamines play a mediating role. Methods and Procedures: Subjects included 44 EA and 47 AA premenopausal women. Free‐living physical activity by doubly labeled water (activity‐related time equivalent (ARTE)), body composition (air plethysmography, computed tomography), and 24‐h fractionated urinary catecholamines were measured. Results: Repeated measures ANOVA revealed parous EA and AA women had significantly higher IAAT than their nulliparous counterparts (100.1 ± 28.5 and 76.2 ± 34.8 cm² vs. 75.9 ± 29.1 and 59.6 ± 15.0 cm²). In AA women and nulliparous women, 24‐h urinary dopamine was significantly higher (AA parous 260.8 ± 88; EA parous 197.2 ± 78.8; AA nulliparous 376.5 ± 81; EA nulliparous 289.6 ± 62). Multiple regression analysis for modeling IAAT indicated that race, parity, dopamine, ARTE, and VO_2max were all significant and independent contributors to the model (Unstandardized βs: race ?32.6 ± 7.4; parity (number of births) 10.0 ± 3.4; 24‐h urinary dopamine 0.08 ± 0.04; ARTE (min/day) ?0.09 ± 0.04; VO_2max (ml/kg/min) ?2.8 ± 1.0). Discussion: Independent of the potential confounders: age, race, percent body fat, IAAT, 24‐h fractionated urinary catecholamines, physical activity, and VO_2max, parous EA and AA women had more IAAT than their nulliparous counterparts. Of the catecholamines, dopamine was found to be significantly lower in parous women and higher in AA's. Dopamine, however, did not explain racial or parity differences in IAAT.     

Resistance training conserves fat-free mass and resting energy expenditure following weight loss

Objective: To determine what effect diet‐induced ～12 kg weight loss in combination with exercise training has on body composition and resting energy expenditure (REE) in premenopausal African‐American (AA) and European‐American (EA) women. Methods and Procedures: This study was a longitudinal, randomized weight loss clinical intervention, with either aerobic (AT), resistance (RT), or no exercise training (NT). Forty‐eight AA and forty‐six EA premenopausal overweight (BMI between 27 and 30) women underwent weight loss to a BMI <25. Body composition (densitometry), REE (indirect calorimetry), maximal oxygen uptake (VO₂max), and muscular strength (isometric elbow flexion) were evaluated when subjects were in energy balance. Results: AA women lost less fat‐free mass (FFM, P ≤ 0.05) (47.0 ± 4.6 to 46.9 ± 5.0 kg) than EA women (46.4 ± 4.9 to 45.2 ± 4.6 kg). Regardless of race, RT maintained FFM (P ≤ 0.05) following weight loss (46.9 ± 5.2 to 47.2 ± 5.0 kg) whereas AT (45.4 ± 4.2 to 44.4 ± 4.1 kg) and NT (47.9 ± 4.7 to 46.4 ± 5.1 kg) decreased FFM (P ≤ 0.05). Both AT and NT decreased in REE with weight loss but RT did not. Significant time by group interactions (all P ≤ 0.05) for strength indicated that RT maintained strength and AT did not. Discussion: AA women lost less FFM than EA women during equivalent weight losses. However, following weight loss in both AA and EA, RT conserved FFM, REE, and strength fitness when compared to women who AT or did not train.     

Longitudinal associations of the endocrine environment on fat partitioning in postmenopausal women

Among postmenopausal women, declining estrogen may facilitate fat partitioning from the periphery to the intra-abdominal space. Furthermore, it has been suggested that excess androgens contribute to a central fat distribution pattern in women. The objective of this longitudinal study was to identify independent associations of the hormone milieu with fat distribution in postmenopausal women. Fifty-three healthy postmenopausal women, either using or not using hormone replacement therapy (HRT) were evaluated at baseline and 2 years. The main outcomes were intra-abdominal adipose tissue (IAAT), subcutaneous abdominal adipose tissue, and total thigh fat analyzed by computed tomography scanning and leg fat and total body fat mass measured by dual-energy X-ray absorptiometry. Serum estradiol, estrone, estrone sulfate, total testosterone, free testosterone, androstenedione, dehydroepiandrosterone sulfate), sex hormone-binding globulin (SHBG), and cortisol were assessed. On average, in all women combined, IAAT increased by 10% (10.5 cm(2)) over 2 years (P < 0.05). Among HRT users, estradiol was inversely associated with, and estrone was positively associated with, 2-year gain in IAAT. Among HRT nonusers, free testosterone was inversely associated with, and SHBG was positively associated with, 2-year gain in IAAT. These results suggest that in postmenopausal women using HRT, greater circulating estradiol may play an integral role in limiting lipid deposition to the intra-abdominal cavity, a depot associated with metabolically detrimental attributes. However, a high proportion of weak estrogens may promote fat partitioning to the intra-abdominal cavity over time. Furthermore, among postmenopausal women not using HRT, greater circulating free testosterone may limit IAAT accrual.     

Ibuprofen does not affect levels of tumor necrosis factor alpha and soluble tumor necrosis factor receptor types I and II in Gabonese children with uncomplicated Plasmodium falciparum malaria

We assessed the ability of ibuprofen to modulate tumor necrosis factor alpha (TNF-alpha), soluble tumor necrosis factor receptor type I (sTNFR-I), and soluble tumor necrosis factor receptor type II (sTNFR-II) responses during the treatment of fever in uncomplicated Plasmodium falciparum malaria, in a placebo-controlled, randomized, double-blind study of 50 pediatric patients in Lambaréné, Gabon. Treatment of the malaria involved the patients receiving intravenous quinine (12 mg/kg of quinine dihydrochloride every 12 h for 72 h) followed by a single dose of oral sulfadoxine/pyrimethamine (25 mg and 1.25 mg/kg). Fever was treated by mechanical treatment plus either ibuprofen (7 mg/kg every 8 h) or placebo during the hospitalization period. We determined serum concentrations of TNF-alpha, sTNFR-I, and sTNFR-II in peripheral blood throughout the treatment period in the two groups: ibuprofen and placebo groups. TNF-alpha levels were found to be positively correlated with body temperature. In contrast, TNF receptors levels did not differ between the two groups and the antipyretic effect of ibuprofen was not correlated with specific changes in sTNFR-I and sTNFR-II production. Our data suggest that TNF-alpha is involved in malarial fever, but soluble TNF receptors play no major role in fever modulation.     

Soluble TNF-Alpha-Receptors I Are Prognostic Markers in TIPS-Treated Patients with Cirrhosis and Portal Hypertension

Background

TNFα levels are increased in liver cirrhosis even in the absence of infection, most likely owing to a continuous endotoxin influx into the portal blood. Soluble TNFα receptors (sTNFR type I and II) reflect release of the short-lived TNFα, because they are cleaved from the cells after binding of TNFα. The aims were to investigate the circulating levels of soluble TNFR-I and -II in cirrhotic patients receiving TIPS.

Methods

Forty-nine patients with liver cirrhosis and portal hypertension (12 viral, 37 alcoholic) received TIPS for prevention of re-bleeding (n = 14), therapy-refractory ascites (n = 20), or both (n = 15). Portal and hepatic venous blood was drawn in these patients during the TIPS procedure and during the control catheterization two weeks later. sTNFR-I and sTNFR-II were measured by ELISA, correlated to clinical and biochemical characteristics.

Results

Before TIPS insertion, sTNFR-II levels were lower in portal venous blood than in the hepatic venous blood, as well as in portal venous blood after TIPS insertion. No significant differences were measured in sTNFR-I levels. Hepatic venous levels of sTNFR-I above 4.5 ng/mL (p = 0.036) and sTNFR-II above 7 ng/mL (p = 0.05) after TIPS insertion were associated with decreased survival. A multivariate Cox-regression survival analysis identified the hepatic venous levels of sTNFR-I (p = 0.004) two weeks after TIPS, and Child score (p = 0.002) as independent predictors of mortality, while MELD-score was not.

Conclusion

Hepatic venous levels of sTNFR-I after TIPS insertion may predict mortality in patients with severe portal hypertension.     

Substantial changes in epicardial fat thickness after weight loss in severely obese subjects

We sought to evaluate the effect of weight loss on echocardiographic epicardial fat thickness, as index of visceral adiposity, and whether epicardial fat change after the weight loss can be proportionally different from overall body weight changes and related to cardiac parameters changes in severely obese subjects. This was an interventional study in 20 severely obese subjects (12 women, 8 men, BMI 45+/-5 kg/m(2), 35+/-10 years) who underwent 6-month very low calorie diet weight loss program. Baseline and after 6-month weight loss anthropometrics, echocardiographic epicardial fat thickness, left ventricular mass (LVM), and diastolic function parameters were assessed. Subjects lost 20% of original body weight, BMI reduced by 19% of original BMI, waist circumference decreased by 23% of initial waist circumference. Epicardial fat thickness decreased from 12.3+/-1.8 to 8.3+/-1 mm P<0.001 after the 6-month very low calorie diet, as -32% of baseline epicardial fat thickness. LVM and diastolic function changes were better correlated with epicardial fat changes. We showed that significant weight loss can be associated with significant reduction in the epicardial fat thickness, marker of visceral adiposity in severely obese subjects. Epicardial fat decrease, therefore visceral fat decrease, can be proportionally higher than overall adiposity decrease. Epicardial fat changes are significantly associated with obesity-related cardiac morphological and functional changes during weight loss. Measurement of echocardiographic epicardial fat thickness may provide an additional tool in understanding the metabolic risk associated with variation in fat distribution.     

Greater weight loss and hormonal changes after 6 months diet with carbohydrates eaten mostly at dinner

This study was designed to investigate the effect of a low-calorie diet with carbohydrates eaten mostly at dinner on anthropometric, hunger/satiety, biochemical, and inflammatory parameters. Hormonal secretions were also evaluated. Seventy-eight police officers (BMI >30) were randomly assigned to experimental (carbohydrates eaten mostly at dinner) or control weight loss diets for 6 months. On day 0, 7, 90, and 180 blood samples and hunger scores were collected every 4 h from 0800 to 2000 hours. Anthropometric measurements were collected throughout the study. Greater weight loss, abdominal circumference, and body fat mass reductions were observed in the experimental diet in comparison to controls. Hunger scores were lower and greater improvements in fasting glucose, average daily insulin concentrations, and homeostasis model assessment for insulin resistance (HOMA(IR)), T-cholesterol, low-density lipoprotein (LDL) cholesterol, high-density lipoprotein (HDL) cholesterol, C-reactive protein (CRP), tumor necrosis factor-α (TNF-α), and interleukin-6 (IL-6) levels were observed in comparison to controls. The experimental diet modified daily leptin and adiponectin concentrations compared to those observed at baseline and to a control diet. A simple dietary manipulation of carbohydrate distribution appears to have additional benefits when compared to a conventional weight loss diet in individuals suffering from obesity. It might also be beneficial for individuals suffering from insulin resistance and the metabolic syndrome. Further research is required to confirm and clarify the mechanisms by which this relatively simple diet approach enhances satiety, leads to better anthropometric outcomes, and achieves improved metabolic response, compared to a more conventional dietary approach.     

The missing risk: MRI and MRS phenotyping of abdominal adiposity and ectopic fat

Individual compartments of abdominal adiposity and lipid content within the liver and muscle are differentially associated with metabolic risk factors, obesity and insulin resistance. Subjects with greater intra-abdominal adipose tissue (IAAT) and hepatic fat than predicted by clinical indices of obesity may be at increased risk of metabolic diseases despite their "normal" size. There is a need for accurate quantification of these potentially hazardous depots and identification of novel subphenotypes that recognize individuals at potentially increased metabolic risk. We aimed to calculate a reference range for total and regional adipose tissue (AT) as well as ectopic fat in liver and muscle in healthy subjects. We studied the relationship between age, body-mass, BMI, waist circumference (WC), and the distribution of AT, using whole-body magnetic resonance imaging (MRI), in 477 white volunteers (243 male, 234 female). Furthermore, we used proton magnetic resonance spectroscopy (MRS) to determine intrahepatocellular (IHCL) and intramyocellular (IMCL) lipid content. The anthropometric variable which provided the strongest individual correlation for adiposity and ectopic fat stores was WC in men and BMI in women. In addition, we reveal a large variation in IAAT, abdominal subcutaneous AT (ASAT), and IHCL depots not fully predicted by clinically obtained measurements of obesity and the emergence of a previously unidentified subphenotype. Here, we demonstrate gender- and age-specific patterns of regional adiposity in a large UK-based cohort and identify anthropometric variables that best predict individual adiposity and ectopic fat stores. From these data we propose the thin-on-the-outside fat-on-the-inside (TOFI) as a subphenotype for individuals at increased metabolic risk.