Increase In Visceral Fat Research Articles

Association of estrogen with glucocorticoid levels in visceral fat in postmenopausal women

The aim of this study is to clarify the association between estrogen and glucocorticoid levels in adipose tissues of premenopausal and postmenopausal women. Forty (15 premenopausal and 25 postmenopausal) women aged 22 to 79 years were recruited through elective gynecological surgical operation, and both subcutaneous and visceral fat were collected during the surgical operation. Messenger RNA (mRNA) expressions of 11β hydroxysteroid dehydrogenase type 1 (HSD1), which catalyzes cortisone to cortisol, and 17β-HSD1 and 17β hydroxysteroid dehydrogenase type 2 (HSD2), which catalyze the interconversion of estrone (E1) and estradiol (E2), were measured by real-time reverse transcription polymerase chain reaction. The levels of E1, E2, cortisol, and cortisone in adipose tissues were measured by liquid chromatography tandem mass spectrometry. The visceral fat area was significantly increased (P < 0.01) in postmenopausal women compared with that in premenopausal women. The cortisol/cortisone ratio (P < 0.01) and the expression of 11β-HSD1 mRNA (P < 0.001) in visceral fat, but not in subcutaneous fat, in postmenopausal women were significantly higher than those in premenopausal women. There was a significant correlation (r = 0.69, P < 0.05) between the E1/E2 ratio of visceral fat and body mass index in postmenopausal women. A significant correlation (r = 0.54, P < 0.05) between the cortisol/cortisone ratio and the E1/E2 ratio of visceral fat was observed in postmenopausal women. The expression of 11β-HSD1 mRNA in visceral fat increases in postmenopausal women, and the E1/E2 ratio in visceral fat may be associated with local glucocorticoid levels after menopause.

Renal Denervation Abolishes the Age-Dependent Increase in Blood Pressure in Female Intrauterine Growth-Restricted Rats at 12 Months of Age

Perinatal insults program sex differences in blood pressure, with males more susceptible than females. Aging may augment developmental programming of chronic disease, but the mechanisms involved are not clear. We previously reported that female growth-restricted offspring are normotensive after puberty. Therefore, we tested the hypothesis that age increases susceptibility to hypertension in female growth-restricted offspring. Blood pressure remained similar at 6 months of age; however, blood pressure was significantly elevated in female growth-restricted offspring relative to control by 12 months of age (137±3 vs 117±4 mm Hg; P<0.01, respectively). Body weight did not differ at 6 or 12 months of age; however, total fat mass and visceral fat were significantly increased at 12 months in female growth-restricted offspring (P<0.05 vs control). Glomerular filtration rate remained normal, yet renal vascular resistance was increased at 12 months of age in female growth-restricted offspring (P<0.05 vs control). Plasma leptin, which can increase sympathetic nerve activity, did not differ at 6 months but was increased at 12 months of age in female growth-restricted offspring (P<0.05 vs control). Because of the age-dependent increase in leptin, we hypothesized that the renal nerves may contribute to the age-dependent increase in blood pressure. Bilateral renal denervation abolished the elevated blood pressure in female growth-restricted offspring normalizing it relative to denervated female control offspring. Thus, these data indicate that age induces an increase in visceral fat and circulating leptin associated with a significant increase in blood pressure in female growth-restricted offspring, with the renal nerves serving as an underlying mechanism.

Effects of weight gain and weight loss on regional fat distribution

Normal-weight adults gain lower-body fat via adipocyte hyperplasia and upper-body subcutaneous (UBSQ) fat via adipocyte hypertrophy. We investigated whether regional fat loss mirrors fat gain and whether the loss of lower-body fat is attributed to decreased adipocyte number or size. We assessed UBSQ, lower-body, and visceral fat gains and losses in response to overfeeding and underfeeding in 23 normal-weight adults (15 men) by using dual-energy X-ray absorptiometry and abdominal computed tomography scans. Participants gained ∼5% of weight in 8 wk and lost ∼80% of gained fat in 8 wk. We measured abdominal subcutaneous and femoral adipocyte sizes and numbers after weight gain and loss. Volunteers gained 3.1 ± 2.1 (mean ± SD) kg body fat with overfeeding and lost 2.4 ± 1.7 kg body fat with underfeeding. Although UBSQ and visceral fat gains were completely reversed after 8 wk of underfeeding, lower-body fat had not yet returned to baseline values. Abdominal and femoral adipocyte sizes, but not numbers, decreased with weight loss. Decreases in abdominal adipocyte size and UBSQ fat mass were correlated (ρ = 0.76, P = 0.001), as were decreases in femoral adipocyte size and lower-body fat (ρ = 0.49, P = 0.05). UBSQ and visceral fat increase and decrease proportionately with a short-term weight gain and loss, whereas a gain of lower-body fat does not relate to the loss of lower-body fat. The loss of lower-body fat is attributed to a reduced fat cell size, but not number, which may result in long-term increases in fat cell numbers.

The effect of the menopausal transition on body composition and cardiometabolic risk factors

Cardiovascular disease is the first cause of mortality in women in North America. The risk of cardiovascular disease increases sharply after middle age in women, especially after menopause. The aim was to investigate changes in body composition and cardiometabolic profile throughout the menopausal transition. This was a 5-year observational, longitudinal study on the menopausal transition. The study included 102 premenopausal women at baseline (age, 49.9 ± 1.9 y; body mass index, 23.3 ± 2.2 kg/m). Outcome measures include menopause status, body composition by dual-energy x-ray absorptiometry (total fat mass [FM], trunk FM, and total fat-free mass), waist circumference, visceral and abdominal subcutaneous fat, fasting glucose and insulin levels, homeostasis model assessment of insulin resistance, plasma lipid levels (triglycerides, total cholesterol, and high- and low-density lipoprotein cholesterol), and resting blood pressure. Repeated-measure analyses revealed significant increases for FM, percentage FM, trunk FM, visceral fat, plasma fasting glucose, and high-density lipoprotein cholesterol (0.05 > P < 0.01) and a significant decrease for plasma glucose levels after follow-up. Those who were in perimenopause or postmenopause by year 3 of the study showed a significant increase in visceral fat (P < 0.01) compared with baseline. Despite some significant changes in the metabolic profile among the menopause statuses, the women did not show any cardiometabolic deterioration by the end of the study. Our results suggest that changes in body composition and fat distribution can occur in nonobese women as they go through the menopausal transition. However, these changes were not accompanied by cardiometabolic deteriorations in the present study.

Obesity, insulin resistance, and the pathway to type 2 diabetes

The increase in obesity in the U.S. and elsewhere can be explained by a variety of factors, as outlined by David Allison and his colleagues. Not only is the fast food diet a factor, but also are changes in ambient temperature, obesity-causing psychoactive molecules, associative sorting, changes in smoking habits, and reduction in sleep. In particular is the increase in visceral fat, which is associated with insulin resistance. We have shown in experimental animals that omentectomy increases insulin sensitivity implicating visceral fat per se as an important factor. We have followed longitudinally changes in organ function and crosstalk in a large animal model, rendered overweight by a high fat, hypercaloric diet. In normal animals, like in normal humans, there is a wide range of adiposity as well as visceral and subcutaneous fat deposition. Feeding fat increases visceral and subcutaneous fat with little change in body weight. Physiologic changes occur with absolutely no change in fasting glucose: most predictive of insulin resistance is relative reduction in metabolic clearance of insulin by liver, and a modest increase in beta cell sensitivity to glucose. The latter changes result in hyperinsulinemia. Change in insulin sensitivity is also predicted by change in liver insulin clearance, implicating metabolic clearance of insulin as the primary factor in development of the insulin resistance syndrome.

Liposuction Induces a Compensatory Increase of Visceral Fat Which Is Effectively Counteracted by Physical Activity: A Randomized Trial

Liposuction is suggested to result in long-term body fat regain that could lead to increased cardiometabolic risk. We hypothesized that physical activity could prevent this effect. Our objective was to investigate the effects of liposuction on body fat distribution and cardiometabolic risk factors in women who were either exercise trained or not after surgery. Thirty-six healthy normal-weight women participated in this 6-month randomized controlled trial at the University of Sao Paulo, Sao Paulo, Brazil. Patients underwent a small-volume abdominal liposuction. Two months after surgery, the subjects were randomly allocated into two groups: trained (TR, n = 18, 4-month exercise program) and nontrained (NT, n = 18). Body fat distribution (assessed by computed tomography) was assessed before the intervention (PRE) and 2 months (POST2), and 6 months (POST6) after surgery. Secondary outcome measures included body composition, metabolic parameters and dietary intake, assessed at PRE, POST2, and POST6, and total energy expenditure, physical capacity, and sc adipocyte size and lipid metabolism-related gene expression, assessed at PRE and POST6. Liposuction was effective in reducing sc abdominal fat (PRE vs. POST2, P = 0.0001). Despite the sustained sc abdominal fat decrement at POST6 (P = 0.0001), the NT group showed a significant 10% increase in visceral fat from PRE to POST6 (P = 0.04; effect size = -0.72) and decreased energy expenditure (P = 0.01; effect size = 0.95) when compared with TR. Dietary intake, adipocyte size, and gene expression were unchanged over time. Abdominal liposuction does not induce regrowth of fat, but it does trigger a compensatory increase of visceral fat, which is effectively counteracted by physical activity.

Testosterone and farnesoid X receptor agonist INT-747 counteract high fat diet-induced bladder alterations in a rabbit model of metabolic syndrome

In the male, metabolic syndrome (MetS) is associated to an increased risk of benign prostatic hyperplasia (BPH) and lower urinary tract symptoms (LUTS). A recently established rabbit model of high fat diet (HFD)-induced MetS showed hypogonadism and the presence of prostate gland alterations, including inflammation, hypoxia and fibrosis. The present study investigated whether HFD-induced MetS might also alter bladder structure and function. Testosterone and the farnesoid X receptor (FXR) agonist INT-747, were evaluated for possible effects on HFD bladder. MetS rabbits develop bladder alterations, including fibrosis (reduced muscle/fiber ratio), hypoxia [2-fold increase as compared to regular diet (RD) group], low-grade inflammation (increased leukocyte infiltration and inflammatory markers) and RhoA/ROCK hyperactivity. Bladder strips from HFD rabbits, pre-contracted with carbachol, showed an overactive response to the selective ROCK inhibitor Y-27632. All these HFD-induced bladder alterations were partially blunted by testosterone and almost completely reverted by INT-747. Both treatments prevented some MetS features (glucose intolerance and visceral fat increase), thus suggesting that their effects on bladder could be ascribed to an improvement of the metabolic and/or hypogonadal state. However, a pathogenetic role for hypogonadism has been ruled out as GnRH analog-induced hypogonadal rabbits, fed a regular diet, did not show any detectable bladder alterations. In addition, INT-747 did not revert the MetS-induced hypogonadal state. FXR mRNA was highly expressed in rabbit bladder and positively associated with visceral fat increase. A direct effect of INT-747 on bladder smooth muscle was further suggested by inhibition of RhoA/ROCK-mediated activity by in vitro experiments on isolated cells. In conclusion, HFD-related MetS features are associated to bladder derangements, which are ameliorated by testosterone or INT-747 administration. INT-747 showed the most marked effects in counteracting MetS-related RhoA/ROCK overactivity, thus opening novel therapeutic opportunities for this drug.

Role of Serotonin from Thought and Anxiety to Weight Gain and Metabolic Syndrome

Studies indicated that targeting localized serotonin 5-HT2C receptors can treat obesity which is consistent with the role in regulating pathways of food intake and body weight that could lead to obesity. The association of diminished serotonergic activity with metabolic syndrome may have implications for the prevention and treatment of the metabolic syndrome. Antipsychotics are 5-HT2C receptors antagonists that can knock down the satiety centers located in ventromedial nucleus in hypothalamus leading to increased weight gain. The potential for weight gain differs among atypical antipsychotics. While ziprasidone and aripiprazole care thought to be weight neutral, dibenzodiazepines like clozapine and olanzapine are implicated in lot of weight gain that can cause obesity and metabolic syndrome. The amount of body weight gain varies with each drug. The difference in weight gains between quetiapine and each of the other atypical medication was significant in our studies (Mean weight gain was least with quetiapine 9.31b and greatest for olanzapine 20.89 lb). Weight gain was also greater with olanzapine than with clozapine. In the literature survey we observed clozapine has been associated with some of the largest bodyweight gains of olanzapine in the long term use and higher weight gain with clozapine seems to be on shorter duration. For many of the metabolic disorders related to weight gain and obesity, scientists have implicated abdominal visceral fat. An increase in visceral fat, in turn, leads to an increased concentration of free fatty acids in the portal vein. An increased free fatty acid concentration may lead to a decrease in hepatic insulin clearance, insulin resistance, hyperinsulinemia, and hypertension. This sequence of events may lead to diabetes, assorted dyslipidemia, and ultimately to coronary artery disease. The purpose of the study was to evaluate the impact of intervention on improving overall cardiovascular adverse effects of antipsychotic therapy. Long-term metabolic complications such as obesity, diabetes, dyslipidemia, hypertension, and ECG changes were of particular interest but the results from our study has not shown any significant change in clinical practice that lead to reduction in cardiovascular risk. During the study period (8/2009 – 11/2009), 118 treatment recommendations were made by pharmacy students and clinical pharmacist preceptor and most were for new lipid and FBG/HgA1C panel for missing lab values or more accurate assessment of patient’s recent status and 82 recommendations were accepted. As appreciated by the result from this study period, the key limiting factor in accurately assessing effectiveness of consultant intervention is that the treatment decision is ultimately made by the patient’s psychiatrist who reviews the recommendation. However the clinical recommendation from the psychopharmacy consultant may still help to increase overall awareness on part of psychiatrists regarding patients’ current cardiovascular risk. Whether it will lead to active intervention will be dependent on other factors. For example, most of the psychopharmacy recommendations are for lipid and A1C/FBG labs as seen during this study period, but even when the recommendation is accepted, the patient may not necessarily require therapeutic intervention as the lab values often do not show any significant changes or are stable-normal. Or in case the recommendation is not accepted, it may be influenced by the therapy/lab cost or availability of other nonpharmacological interventions (e.g. diet/lifestyle modification) more so than the clinical competency of the recommending pharmacist. Other limiting factors of the study include lack of control group for comparison and need for objective monitoring tool for evaluating overall cardiovascular risk of the patients. For this study period, there was significant cardiovascular reduction seen through clinical pharmacy intervention in high-risk patients receiving antipsychotic. More studies are needed to support clinical pharmacist’s role in improving overall cardiovascular risk associated with antipsychotic therapy but in the meanwhile, interdisciplinary monitoring and careplan in regards to high- risk patients should be continued and American diabetic association recommends serum glucose and serum lipids on quarterly basis for the patients who receive atypical antipsychotics (dibenzodiazepine more so) and that is the standard of care. In the future, there may be several changes that can be made to the study protocol for better assessment of effectiveness of clinical pharmacy intervention. First, one may consider increasing the sample size by increasing the duration and thus more patients to increase the power of the study. Second, recommending pharmacist should leave a written progress note for which other psychiatrist/physicians may be able to refer back to rather than verbal recommendations to one attending psychiatrist as done so far. And lastly, one may consider

Variations in adiponectin levels in patients with chronic kidney disease: a prospective study of 12 months

Cardiovascular complications remain the main cause of mortality in patients with chronic kidney disease (CKD). Adiponectin is an adipose tissue-derived protein that carries important cardioprotective properties. We aimed at investigating the determinants of adiponectin levels in CKD patients. This prospective observational study included 98 CKD patients [glomerular filtration rate (GFR) 36.1+-14.4 ml/min, 56.5+-10.4 y, 63% male, 31% diabetics, and body mass index (BMI) 27.1+-5.2 kg/m²]. Evaluation of adiponectin (imunoenzimatic assay), laboratory parameters, nutritional status (subjective global assessment), total body fat (dual x-ray energy absorptiometry), and visceral and subcutaneous abdominal fat (computed tomography) was performed at baseline and after 12 months. Adiponectin correlated with GFR (r = -0.45; p < 0.001), proteinuria (r = 0.21; p = 0.04), BMI (r = -0.33; p < 0.01), and visceral fat (r = -0.49; p < 0.001). In the linear regression analysis, the determinants of adiponectin levels were sex (female β = 3.8; p < 0.01), age (β = 0.14; p = 0.03), GFR (β = -0.15; p < 0.01) and visceral fat (β = -0.04; p < 0.001) (R² = 0.41). After 12 months, a progression of the disease was evidenced by the reduction of GFR (-1.6+-6.3 ml/min; p = 0.01) and increase of proteinuria (0.3+-0.8 g/d; p < 0.01). An accumulation of visceral fat was observed, from 97+-73 cm² to 111+-82 cm² (p < 0.001), with a concomitant reduction of adiponectin concentration, from 27.6+-7.5 mg/l to 22.2+-11.6 mg/l (p < 0.001). Body weight, BMI, total body fat, and subcutaneous abdominal fat remained unchanged. After adjustments for the baseline determinants of adiponectin, the increase in visceral fat was independently associated with overtime decrease in adiponectin levels (β = -0.04; p = 0.025; R² = 0.21). Age, sex, renal function and visceral fat were independently associated with adiponectin levels in nondialyzed CKD patients. However, variation in visceral fat was the only predictor of variation in adiponectin levels over 12 months.

Longitudinal Body Composition Changes Due to Dialysis

Nutritional status remains a powerful predictor of outcome in the dialysis population. High body mass index (BMI) seems protective, but which body compartment (fat or lean mass) confers this protection remains unclear. This was a longitudinal study (n = 60; n = 46 completed) examining changes in body composition in incident peritoneal dialysis (PD) and hemodialysis (HD) patients over 12 months. We measured total body protein (TBP) by in vivo neutron activation, expressed as nitrogen index (NI), and lean body mass (LBM) and total body fat (TBF) by dual-energy x-ray absorptiometry. Visceral and subcutaneous fat areas (SFAs) were determined from computed tomography. Comparisons were made between different BMI groups and dialysis modalities. No significant change was found in TBP, NI, or TBF. The obese group (BMI >30) had an increase in all mean LBM parameters with a significant increase in NI compared with normal-weight and the overweight group. This increase in NI remained significant after multivariate analysis β coefficient (0.08). PD patients had the greatest increase in TBF, with a significant increase in visceral fat (VFA:SFA ratio β coefficient = 0.23). Obese patients showed preservation of TBP compared with normal- and overweight patients, suggesting that energy storage as fat mass is of value in the dialysis population.

Medición volumétrica de grasa visceral abdominal con RM y su relación con elastografía hepática en una población diabética

Background. Increase in visceral fat is associated to the development of fatty liver and liver fibrosis. Hepatic elastography is a novel noninvasive method for assessing liver fibrosis. Objective. To evaluate the relationship between visceral adipose tissue volume (VAT), subcutaneous adi- pose tissue volume (SAT) as measured by Magnetic Resonance Imaging (MRI) and transient elastography (TrE) values using ARFI (Acoustic Radiation Force Impulse) in type 2 Diabetic Mellitus patients (DM2). Methods. We included 20 DM2 patients (mean age: 62 years, range: 55-75, mean weight: 77.8 kg, range: 61.5-97). Patients underwent an MRI study in a Philips Intera 1.5T scanner. MR imaging protocol included a spectral excitation sequence centered on the fat peak. The sequence included 32 cross sections, 7mm thick, from the diaphragmatic cupula to the inferior border of the kidney. VAT was measured by using the semiautomatic Image J software. Each patient underwent a hepatic elastograpy (HE); 10 ARFI measure- ments were performed in the right hepatic lobe. Finally, a statistical analysis was performed by applying Pearson correlation between abdominal fat volumes and ARFI scores Results. Mean VAT was 2472 ± 861 cc, (1173-4020 cc), whilst the mean ARFI was 1.62 ± 0.8 m/s, (0.8- 3.4 m/s). Correlations obtained were r= 0.08 between VAT and ARFI (p=0 .72); 0.13 between SAT and ARFI (p=0.57), and -0.06 between (VAT+SAT) and ARFI (p=0.77). By subdividing the sample universe, we observed that the group with ARFI scores greater than 1.6 m/s (7 patients) had a correlation of 0.63 between VAT and ARFI (p=0.12); of 0.66 between SAT and ARFI (p=0.10), and of 0.94 between VAT+SAT and ARFI (p=0.001). In the subgroup with ARFI values inferior to 1.6 m/s (13 patients), the correlation was of 0.11 between VAT and ARFI (p=0.71); of 0.26 between SAT and ARFI (p=0.38), and of 0.32 between ( VAT+SAT) and ARFI (p=0.28). When adjusted for gender, ARFI scores greater than 1.6m/s (6 patients) in the subgroup of female patients revealed a correlation of 0.79 (p=0.05) between ARFI and VAT, and of 0.92 (p=0.009) for VAT+SAT. Conclusions. In DM2 patients, ARFI values greater than 1.6 m/s seem to be indicative of a good correlation between VAT and VAT+SAT, thus indicating that those with greater liver damage may present increased abdominal fat accumulation. Keywords: Acoustic radiation force impulse, Diabetes Mellitus type 2, Fat assessment, Intra-abdominal fat, Magnetic resonance imaging, Nonalcoholic fatty liver disease, Transient elastography, Visceral adipose tissue.

The association between the ratio of visceral fat to thigh muscle area and metabolic syndrome: the Korean Sarcopenic Obesity Study (KSOS)

A relationship between visceral fat accumulation and metabolic syndrome (MetS) has been established. However, the effect of a relative increase in visceral fat and a decrease in muscle mass on metabolic disorders has not been investigated. The aim of the present study was to examine the association between the ratio of visceral fat to thigh muscle area (VMR) and MetS in Korean adults. STUDY SUBJECT/MEASUREMENTS: A total of 264 age-and gender-matched subjects recruited from the Korean Sarcopenic Obesity Study (KSOS), an ongoing prospective observational cohort study, were categorized into four groups based on their body mass index (BMI) and VMR. We measured visceral fat area and thigh muscle area using computed tomography. Subjects with MetS showed a significantly higher VMR than those without MetS. In both obese and nonobese groups, the subjects with a higher VMR had a higher prevalence of MetS than those in the lower VMR groups. VMR was significantly related to components of the metabolic syndrome, especially in women, and was positively correlated with a number of MetS components in both men and women. In multiple logistic regression analysis, the odds ratio for MetS was 6·72 (highest vs lowest quartile, 95% confidence interval, 1·60-28·14) after an adjustment of potential confounders, including BMI and waist-to-hip ratio. VMR is significantly increased in subjects with MetS and independently associated with MetS. These results suggest that the VMR may be a potential indicator for MetS risk in Korean adults.

Dietary n-3 polyunsaturated fatty acids fail to reduce prostate tumorigenesis in the PB-ErbB-2 x Pten+/- preclinical mouse model

Diet and obesity, and their associated metabolic alterations, are some of the fastest-growing causes of disease and death in America. Findings from epidemiological studies correlating obesity, the sources of dietary fat and prostate cancer (PCa) are conflicting. We have previously shown that 15% of PB-ErbB-2 x pten+/- mice developed PCa and exhibited increased phosphorylated 4E-BP1, but not the key PI3-kinase intermediary phospho-protein, mTOR, when maintained on unrefined mouse chow. We report herein that 100% of animals fed refined, westernized AIN-93-based diets containing corn oil developed PCa by 12 months of age. Increases in visceral fat and mTOR activation in the tumors were also observed. Furthermore, nuclear cyclin E levels were significantly induced by the AIN-93-corn oil-based diets versus chow. Replacing 50% of the corn oil with menhaden oil, with 21% of its triglycerides being n-3 PUFA’s, had no effect on tumorigenesis, fat deposition, cyclin E or mTOR. Phosphorylated BAD levels were similar in the tumors of mice in all three diets. Our data demonstrated that in the context of our preclinical model, components of crude chow, but not dietary n-3 PUFAs, protect against PCa progression. In addition, these data establish phosphorylated mTOR, nuclear cyclin E and visceral fat deposits as possible biomarkers of increased dietary risk for PCa.

Increased visceral adipose tissue mass is associated with increased C-reactive protein in patients with manifest vascular diseases

BackgroundObesity is related to the development of vascular diseases and metabolic complications. Low grade inflammation is a key feature of central obesity, characterized by elevated plasma levels of C-reactive protein (CRP). We hypothesize that visceral adipose tissue contributes to systemic concentrations of CRP. MethodsIn 2410 patients (1729 men and 681 women) with vascular diseases, subcutaneous and visceral fat masses were analyzed with ultrasonography. Metabolic parameters and CRP were measured in a fasting state. The association between fat measurements and plasma CRP was quantified using linear regression analysis. CRP levels were logarithmically transformed. Adjustments were made for age, smoking, type 2 diabetes mellitus, insulin resistance (HOMA-IR) and medication use. ResultsVisceral fat was categorized into quartiles (Q) ranging from 3.2 to 7.8cm in Q1 (reference) to 11.0–19.8cm in Q4 in men and 2.7–6.0cm in Q1 (reference) to 9.0–17.4cm in Q4 in women. β-coefficients gradually increased across the quartiles from 0.07 (0.01–0.13) in Q2 to 0.25 (0.19–0.31) in Q4 in men and 0.17 (0.07–0.26) in Q2 to 0.42 (0.32–0.52) in Q4 in women, indicating 0.25 and 0.42mg/l higher logarithmically transformed (log)CRP levels in Q4 compared to Q1 in respectively men and women. Per standard deviation increase of visceral fat, logCRP levels increased with 0.10mg/l (0.07–0.12) in men and with 0.11 (0.15–0.19) in women. Likewise, in separate analyses waist circumference and body mass index showed a positive, but weaker association with logCRP levels across quartiles (in men: β 0.21 (0.15–0.27) in Q4 for waist circumference and β 0.23 (0.17–0.30) in Q4 for body mass index; in women: β 0.32 (0.22–0.42) in Q4 for waist circumference and β 0.32 (0.22–0.42) in Q4 for body mass index). In men subcutaneous fat was not associated with logCRP (β-coefficients relative to Q1: −0.01 (−0.07 to −0.05), −0.01 (−0.07 to −0.05) and 0.05 (−0.01 to −0.11) in Q2 to Q4 respectively). ConclusionsIn conclusion, visceral fat thickness is the strongest contributor to the systemic CRP concentrations in patients with vascular diseases.

Body Fat Distribution, Waist Circumference and Body Mass Index in Permanent Seed Prostate Brachytherapy

Purpose: Recent studies have shown that obesity is associated with more aggressive prostate cancer variants and a higher prostate specific antigen (PSA) recurrence following prostatectomy. The aim of this study is to analyze the influence of body mass index (BMI) and the distribution of adipose tissue on clinical pretreatment variables and PSA evolution post 125I prostate brachytherapy. Materials and Methods: We studied 59 men with low risk or ‘low tier” intermediate risk (maximum one intermediate risk feature) prostate cancer who had undergone 125I radioactive seed implantation as monotherapy. Inclusion criteria were an absence of hormonal therapy or external beam radiotherapy, a minimum of 8 months of followup and at least 3 followup PSA values. We calculated the BMI (kg/m2), waist circumference and the quotient between visceral and subcutaneous fat (VF/SF) measured on computed tomography at the iliac crest level. To analyze the influence of anthropometric measures on post-brachytherapy PSA evolution, we divided the patients into 2 groups: 1) rapid PSA descent post-brachytherapy to <0.5 ng/mL in the first 12 months following brachytherapy (n = 28); 2) slow PSA descent post-brachytherapy to <0.50 ng/mL and a followup of ≥24 months (n = 23) or a PSA bounce of ≥0.50 ng/mL (n = 6). The influence of those anthropometric measures on pretreatment PSA, prostate volume and number of positive biopsies were calculated using Spearman correlation coefficient. Differences between the 3? post-brachytherapy outcome groups were analyzed using the Pearson chi-square and Fisher's exact test. Relative risk estimate was calculated to measure of the strength of the association between the presence of a factor and the occurrence of an event. All tests were two-tailed. Results: There was an influence of the different anthropometric measures on pretreatment characteristics; there was a positive correlation between VF/SF and the PSA before treatment (r = 0.282, p = 0.029); and waist circumference with the number of positive biopsies (r = 0.374, p = 0.004). VS/SF, BMI and waist circumference were not different between both post-brachytherapy PSA-outcome groups (p≥0.439). The following factors were associated with being in the slow descent group: younger patients (less than the median age of 65 years), p = 0.003, relative risk (RR) 2.256 (95% confidence interval (CI), 1.249-4.073) and prostates smaller than the median 41 cc, p = 0.034, RR 0.550 (95%CI, 0.320-0.944). All patients with a waist circumference of >100 cm were in the rapid descent group. Among the patients with a VF/SF >0.9, 83% were in the slow descent group. Conclusions: In this small pilot study, waist circumference and VF/SF were weakly correlated to pretreatment characteristics. There seems to be a tendency that an increase in visceral fat and waist circumference has an influence on the type of PSA response. Larger studies are needed to determine if anthropomorphic measures have a direct influence on post-brachytherapy PSA response.

The impact of liver fat vs visceral fat in determining categories of prediabetes

Impaired fasting glucose (IFG) and impaired glucose tolerance (IGT) are risk factors for type 2 diabetes and cardiovascular disease; however, their impact on these endpoints differs. Because liver fat and visceral fat are important determinants of glucose and lipid metabolism, we investigated whether these fat compartments and their humoral products, the adipokine adiponectin and the hepatokine fetuin-A, differ in their impact on the glucose categories. In 330 individuals at risk of type 2 diabetes, glucose tolerance status was determined by a 2 h 75 g OGTT. Total-body and visceral fat were precisely quantified by magnetic resonance (MR) tomography and liver fat by (1)H-MR spectroscopy. A total of 210 individuals had normal glucose tolerance (NGT), 41 isolated IFG, 43 isolated IGT and 36 IFG+IGT. Total-body fat was not different (p = 0.51), although a small but continuous increase in visceral fat was found among the categories after adjustment for age and sex (NGT: 3.07 +/- 0.10 kg; IFG: 3.11 +/- 0.21 kg; IGT: 3.61 +/- 0.21 kg; IFG+IGT: 3.84 +/- 0.23 kg [SEs], p = 0.03). A larger difference was found for liver fat (NGT: 4.73 +/- 0.42%; IFG: 5.86 +/- 0.92%; IGT: 8.65 +/- 0.92%; IFG + IGT: 11.11 +/- 1.01%, p < 0.0001). The differences among the categories were small for adiponectin (p = 0.14), but larger for fetuin-A (p = 0.015). Among fat compartments, liver fat (p < 0.0001) and among circulating variables fetuin-A (p = 0.016) were the strongest determinants of the categories. Liver fat, more than visceral fat, strongly increases when glycaemia and glucose tolerance move from NGT to isolated IFG, isolated IGT and IFG+IGT. Because liver-derived circulating fetuin-A determines, although weakly, prediabetes categories, it is worth searching for hepatokines more strongly predicting prediabetes.

Nitric Oxide Plays a Crucial Role in the Development/Progression of Nonalcoholic Steatohepatitis in the Choline‐Deficient, l‐Amino Acid‐Defined Diet‐Fed Rat Model

The pathogenesis of nonalcoholic steatohepatitis (NASH) is still unclear. Recently, the 2-hit hypothesis was proposed, in which nitric oxide production, representing oxidative stress, was proposed as a very important candidate for the second hit. The total study period was 10 weeks. A total of 20 rats were randomly divided into 2 groups. Group 1 was administered the Choline-Deficient, l-Amino Acid-Defined diet to produce a NASH model, and Group 2 as control received the Choline-Sufficient, l-Amino Acid-defined diet. The blood and tissue concentrations of nitrate + nitrite were measured using the Griess reagent and the expression levels of inducible nitric oxide synthase (iNOS) proteins and mRNA was determined by Western blotting. In regard to nitric oxide (NO) and NO metabolites, there were significant differences in the blood (especially portal venous blood) as well as tissue (liver and visceral fat) concentrations between the 2 animal groups; the amounts of NO metabolites in the tissues were much higher in the NASH models. The level of nitrotyrosine was much markedly higher in the NASH models than in the controls. In regard to the tissue expression of iNOS a significant difference between the 2 groups was found in the visceral fat, especially in the mesenterium. Based on these results, we hypothesize that the iNOS expression and NO levels in the visceral fat increase, with increased diffusion of NO and its metabolites into the liver, resulting in increased nitrotyrosine formation in the liver; this, in turn, induces inflammation, apoptosis, and fibrosis in the liver, which are one of the characteristic features of NASH.

Two unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, on inducing metabolic syndrome in Wistar rats and C57BL/6J mice

To establish animal models with diet-induced metabolic disorders similar to human metabolic syndrome, 2 unhealthy dietary habits featuring a high fat content and a sucrose-containing beverage intake, alone or in combination, were tested on Wistar rats and C57BL/6J mice. The 2 dietary habits were, respectively, simulated by feeding a high-fat diet (regimen A) or additionally providing 30% sucrose (wt/vol) in the drinking water (regimen B). Using a 2 × 2 factorial design, 4 groups of animals were fed chow diet plus plain water (group C), high-fat diet (30% [wt/wt] fat) plus plain water (group A), chow diet plus sucrose in drinking water (group B), and high-fat diet plus sucrose in drinking water (group AB) for 26 weeks. In Wistar rats, regimen B caused a significant increase in visceral fat; serum levels of lipids, glucose, insulin, and uric acid; insulin resistance; and blood pressure, whereas regimen A only caused a significant increase in visceral fat and serum insulin levels (P < .05). In contrast, regimen A induced a full array of metabolic syndrome in C57BL/6J mice; but regimen B only caused slight obesity and hyperlipidemia. In both Wistar rats and C57BL/6J mice, there were no additive effects of the 2 regimens, indicated by significant interactions between regimens A and B on the metabolic indexes measured. These results show that, in terms of inducing metabolic syndrome, Wistar rats are more responsive to sucrose water regimen, whereas C57BL/6J mice are more responsive to the high-fat diet regimen.

Age and Sex Differences in Fat Distribution in Non-Obese Japanese Children

To assess fat distribution in non-obese Japanese children and adolescents. 130 non-obese Japanese children (73 boys and 57 girls) from Kikugawa, Hamamatsu were included. The visceral fat area (VFA) and subcutaneous fat area (SFA) were measured by computed tomography (CT) and calculated (in cm(2)). Subjects were divided into three groups based on age: group A (6-10 years), group B (11-15 years), and group C (16-20 years). Girls had more subcutaneous fat than boys in groups B and C (P<0.01). Boys had an age-dependent increase in visceral fat, but girls did not. In group C (16-20 years), boys had more visceral fat than girls (P<0.01). In non-obese Japanese children, there are significant differences in visceral and subcutaneous fat amounts by age and sex. VFA seems to accumulate more in boys than in girls, and SFA is more prevalent in girls than boys.

Exercise, abdominal obesity, skeletal muscle, and metabolic risk: evidence for a dose response.

The obese are at increased risk for cardiovascular disease and type 2 diabetes. However, some who are obese have no metabolic abnormalities. So, it is not adipose tissue per se, but perhaps where it is located that is important for determining metabolic consequences. Regular exercise is known to reduce risk for metabolic disease through numerous mechanisms. The purpose of this report is to highlight some of the efficacy-based data on the effects of exercise (and also a sedentary lifestyle) on abdominal obesity, visceral fat, and metabolic risk. We also discuss how impaired fatty acid oxidation (FAO) in skeletal muscle may be related to both insulin resistance and a contributor to weight gain. In summary, it is evident that exercise in sufficient amounts can lead to substantial decreases in body weight, total body fat, and visceral fat. Additionally, evidence now supports the conclusion that there is a dose-response relationship between exercise amount and these changes, i.e., more exercise leads to additional benefits. Additionally, there are a number of important cardiometabolic risk factors that were most favorably effected by moderate-intensity compared to vigorous-intensity exercise. Unfortunately, it is also apparent that in sedentary middle-aged men and women, short periods of physical inactivity lead to significant weight gain, substantial increases in visceral fat, and further metabolic deterioration. Finally, favorable modulation of mitochondrial oxidative capacity in skeletal muscle by exercise training may reduce a block for complete oxidation of fatty acids in muscle and thereby relieve a block to effective insulin signaling.