Reduced Body Adiposity Research Articles

Does caffeine ingestion before a short-term sprint interval training promote body fat loss?

We investigated the effect of caffeine ingestion combined with a 2-wk sprint interval training (SIT) on training-induced reductions in body adiposity. Twenty physically-active men ingested either 5 mg/kg of cellulose as a placebo (PLA, n=10) or 5 mg/kg of caffeine (CAF, n=10) 60 min before each SIT session (13×30 s sprint/15 s of rest). Body mass and skinfold thickness were measured pre- and post-training. Energy expenditure was measured at rest, during exercise, and 45 min after exercise in the first SIT session. Body fat was similar between PLA and CAF groups at pre-training (P>0.05). However, there was a significant decrease in body fat after training in the CAF group (−5.9±4.2%, P<0.05) but not in PLA (1.5±8.0%, P>0.05). There was no difference in energy expenditure at rest and during exercise between PLA and CAF groups (P>0.05), but the post-exercise energy expenditure was 18.3±21.4% greater in the CAF than in the PLA group (P<0.05). In conclusion, caffeine ingestion before SIT sessions induced a body fat loss that may be associated with higher post-exercise energy expenditure.

Repeated Transcranial Direct Current Stimulation Induces Behavioral, Metabolic and Neurochemical Effects in Rats on High-Calorie Diet.

Due to its high prevalence, obesity is considered an epidemic, which stimulated research on non-invasive methods to reduce excess body fat. Transcranial direct current stimulation (tDCS) is a non-invasive technique used to modulate the activity of cerebral cortex, which has already found increasing interest in medicine as a promising methodology. The aim of this study was to analyze the impact of tDCS on feeding behavior, metabolic abnormalities and neurotransmitters in certain brain areas involved in appetite control of obese rats. The male Wistar rats were divided into five subgroups depending on consumed diet effect (lean, obese) and tDCS type (anodal, cathodal, sham, and no stimulation). Two 10-min daily sessions of tDCS for 8 consecutive days of the study were applied. Rats subjected to active tDCS (anodal right or cathodal left of the prefrontal cortex) had reduced appetite and showed lesser body weight gain than the animals subjected to sham procedure or those receiving no stimulation at all. Furthermore, tDCS contributed to reduction of epididymal fat pads and to a decrease in blood concentration of leptin. Neurochemical examination revealed that tDCS modulated serotonin pathways of the reward-related brain areas and contributed to a significant decrease in the density of D2 but not D1 dopamine receptors in the dorsal striatum, recorded 5 h after the last stimulation. No significant effect of tDCS on dopamine and it's metabolites in examined brain regions was observed. It seems that the hypothalamus was not affected by tDCS application as no changes in measured neurotransmitters were detected at any examined time point. However, these results do not exclude the possibility of the delayed response of the monoamines in the examined brain areas to tDCS application. Altogether, these findings imply that repeated tDCS of the prefrontal cortex may change feeding behavior of obese rats. Either right anodal or left cathodal tDCS were sufficient to decrease food intake, to reduce body adiposity and to normalize other metabolic anomalies. These beneficial effects can be at least partially explained by changes in serotoninergic and in lesser extent dopaminergic system activity within some brain areas belonging to reward system.

Voluntary running of defined distances reduces body adiposity and its associated inflammation in C57BL/6 mice fed a high-fat diet.

This study investigated the effect of voluntary running of defined distances on body adiposity in male C57BL/6 mice fed a high-fat diet. Mice were assigned to 6 groups and fed a standard AIN93G diet (sedentary) or a modified high-fat AIN93G diet (sedentary; unrestricted running; or 75%, 50%, or 25% of unrestricted running) for 12 weeks. The average running distance was 8.3, 6.3, 4.2, and 2.1 km/day for the unrestricted, 75%, 50%, and 25% of unrestricted runners, respectively. Body adiposity was 46% higher in sedentary mice when fed the high-fat diet instead of the standard diet. Running decreased adiposity in mice fed the high-fat diet in a dose-dependent manner but with no significant difference between sedentary mice and those running 2.1 km/day. In sedentary mice, the high-fat instead of the standard diet increased insulin resistance, hepatic triacylglycerides, and adipose and plasma concentrations of leptin and monocyte chemotactic protein-1 (MCP-1). Running reduced these variables in a dose-dependent manner. Adipose adiponectin was lowest in sedentary mice fed the high-fat diet; running raised adiponectin in both adipose tissue and plasma. Running 8.3 and 6.3 km/day had the greatest, but similar, effects on the aforementioned variables. Running 2.1 km/day did not affect these variables except, when compared with sedentariness, it significantly decreased MCP-1. The findings showed that running 6.3 kg/day was optimal for reducing adiposity and associated inflammation that was increased in mice by feeding a high-fat diet. The findings suggest that voluntary running of defined distances may counteract the obesogenic effects of a high-fat diet.

Effects of voluntary running with defined distances on body adiposity and its associated inflammation in mice fed a high‐fat diet

Sedentary lifestyle contributes to obesity. This study examined the effect of quantitative voluntary running on body adiposity and its associated inflammation in mice fed a high‐fat diet. Male C57BL/6 mice were assigned into six groups and fed the AIN93G (sedentary) or a high‐fat diet (sedentary, unrestricted running, or with 25%, 50%, or 75% restriction in running activity) for 12 weeks. The average daily running distance was 8.3, 6.3, 4.2, and 2.1 km for the unrestricted, 25%, 50%, and 75% restricted runners, respectively. The high‐fat diet increased body fat mass by 46% compared to the AIN93G diet in sedentary mice. Running reduced the fat mass in a dose dependent manner; there was no difference between sedentariness and running at 2.1 km/d. The high‐fat diet significantly increased blood glucose, plasma insulin, HOMA‐IR, and plasma and adipose concentrations of leptin and monocyte chemotactic protein‐1 (MCP‐1) in sedentary mice. Running, despite continued consumption of the high‐diet, reduced these variables in dose‐dependent manners. Running at 8.3 (unrestricted) and 6.3 km/d (25% restricted) had the greatest but similar reductions in, whereas running at 2.1 km/d did not affect (except MCP‐1), these measurements. Running, regardless of daily distance, significantly reduced MCP‐1 in both plasma and adipose tissues. In conclusion, voluntary running at 6.3 km/d is optimal to reduce body adiposity and its associated inflammation and metabolic disturbance in C57BL/6 mice. Results that running at 2.1 km/d reduced MCP‐1 without affecting body fat mass show the benefits of moderate amount of exercise in improving low‐grade inflammation. It suggests that different mechanisms, rather than reducing body adiposity, are responsible for this improvement.Support or Funding InformationThe U.S. Department of Agriculture, ARS, research project 5450‐51000‐045‐00D.

Growth Hormone Control of Hepatic Lipid Metabolism.

In humans, low levels of growth hormone (GH) and its mediator, IGF-1, associate with hepatic lipid accumulation. In mice, congenital liver-specific ablation of the GH receptor (GHR) results in reductions in circulating IGF-1 and hepatic steatosis, associated with systemic insulin resistance. Due to the intricate relationship between GH and IGF-1, the relative contribution of each hormone to the development of hepatic steatosis is unclear. Our goal was to dissect the mechanisms by which hepatic GH resistance leads to steatosis and overall insulin resistance, independent of IGF-1. We have generated a combined mouse model with liver-specific ablation of GHR in which we restored liver IGF-1 expression via the hepatic IGF-1 transgene. We found that liver GHR ablation leads to increases in lipid uptake, de novo lipogenesis, hyperinsulinemia, and hyperglycemia accompanied with severe insulin resistance and increased body adiposity and serum lipids. Restoration of IGF-1 improved overall insulin sensitivity and lipid profile in serum and reduced body adiposity, but was insufficient to protect against steatosis-induced hepatic inflammation or oxidative stress. We conclude that the impaired metabolism in states of GH resistance results from direct actions of GH on lipid uptake and de novo lipogenesis, whereas its actions on extrahepatic tissues are mediated by IGF-1.

Dietary energy restriction reduces high-fat diet-enhanced metastasis of Lewis lung carcinoma in mice.

The objective of this study was to determine whether a reduction in energy intake ameliorated the high-fat diet-enhanced spontaneous metastasis of Lewis lung carcinoma in mice. Male C57BL/6 mice were fed the AIN93G diet, a high-fat diet or a high-fat diet with a 5% restriction of the intake. Energy restriction reduced body adiposity and body weight, but maintained growth similar to mice fed the AIN93G diet. The high-fat diet significantly increased the number and size (cross-sectional area and volume) of metastases formed in lungs. Restricted feeding reduced the number of metastases by 23%, metastatic cross-sectional area by 32% and volume by 45% compared to the high-fat diet. The high-fat diet elevated plasma concentrations of proinflammatory cytokines (monocyte chemotactic protein-1, plasminogen activator inhibitor-1, leptin), angiogenic factors (vascular endothelial growth factor, tissue inhibitor of metalloproteinase-1) and insulin. Restricted feeding significantly reduced the high-fat diet-induced elevations in plasma concentrations of proinflammatory cytokines, angiogenic factors and insulin. These results demonstrated that a reduction in diet intake by 5% reduced high-fat diet-enhanced metastasis, which may be associated with the mitigation of adiposity and down-regulation of cancer-promoting proinflammatory cytokines and angiogenic factors.

Supplementation with two probiotic strains, Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, reduced body adiposity and Lp-PLA2 activity in overweight subjects

The effect of consumption of two probiotic strains, Lactobacillus curvatus HY7601 and Lactobacillus plantarum KY1032, on weight loss, body adiposity and lipoprotein-associated phospholipase A2 (Lp-PLA2) activities in overweight subjects was examined. After 12-week probiotic treatment, the probiotic group presented reductions in body weight (−0.65 ± 0.23 kg), body fat percentage (−0.57 ± 0.19%) and body fat mass (−616 ± 161 g) measured using DEXA, and L1 subcutaneous fat area (−2.68 ± 1.31 cm2) measured using CT, compared to baseline. The probiotic group exhibited greater reductions in oxidized low density lipoprotein (ox-LDL) (P < 0.001) and Lp-PLA2 (P < 0.001) and a greater increase in low density lipoprotein (LDL) particle size (P = 0.001) than the placebo. The change (△, difference from baseline) in total fat mass correlated with △ Lp-PLA2 (r = 0.480, P < 0.001), which correlated with △ ox-LDL (r = 0.537, P < 0.001). Probiotic-induced weight loss was associated with reductions in fat mass, which correlated with the changes in Lp-PLA2 activities (ClinicalTrials.gov: NCT02492698).

Inhibition of MMP-13 prevents diet-induced obesity in mice and suppresses adipogenesis in 3T3-L1 preadipocytes.

Adipose tissue remodeling by the matrix metalloproteases (MMPs) is critical for tissue hypertrophy and obesity. MMP-13 is an important protein that is highly expressed in adipose tissue but whose potential role in adipose tissue expansion is poorly characterized. We investigated the effect of pharmacological inhibition of MMP-13 with a selective inhibitor, CP-544439, on adipose tissue mass in mice on a high fat diet, and determined the effect of the inhibitor during in vitro adipocyte differentiation of 3T3-L1 cells. CP-544439 was administered for 6 weeks to mice on a high fat diet. Body adiposity and glucose tolerance was determined. Differentiating 3T3-L1 adipocytes were also treated with the inhibitor for a maximum of 8 days and adipogenesis assessed. Treatment of mice with the inhibitor resulted in reduction in body adiposity and improvement in glucose clearance. Histological examination of epididymal adipose showed reduced adipocyte hypertrophy accompanied by increased staining for collagen in the inhibitor treated mice. Treatment of differentiating 3T3-L1 cells with the inhibitor resulted in reduced adipocyte differentiation. Knockdown of MMP-13 using small interfering RNA in differentiating 3T3-L1 cells reduced adipocyte differentiation indicated by reduced expression of PPARγ. These results suggest that MMP-13 may play a major role in adipose development and its inhibition could be a potential strategy to prevent obesity.

Emphasis of Yoga in the Management of Diabetes

Objectives: For years, exercise has been considered a cornerstone of diabetes management, along with diet and medication. Growing evidence supports the beneficial effects of yoga in physical and mental health through down regulation of the hypothalamic–pituitary–adrenal (HPA) axis and the sympathetic nervous system (SNS). The purpose of this article is to provide a scholarly review of the literature of research studies comparing the effects of yoga and exercise in diabetes patients. Methods: This review focuses on published research articles indexed in the PubMed, MEDLINE, Google Scholar, Science Direct and Scopus. Search criteria included research articles written in English with the key words “yoga”, “diabetes mellitus (DM)”, “Type 1 DM”, “Type 2 DM”, “Exercise”. Only clinical or human studies published in English language were included. Exclusion criteria included articles that were not written in English. Conclusion: Exercise can improve glucose uptake by improving insulin sensitivity and reducing body adiposity in both patients of type 1 and type 2 DM. Yoga is an ancient discipline designed to bring balance and health to the physical, mental, emotional, and spiritual dimensions of the individual. Yoga may be an attractive alternate to traditional aerobic exercises and strength training program, as it requires only a little space and needs no equipment and literally devoid of side effects, mainly focusing on relaxation of mind and body. It provides a less strenuous and more pleasurable exercise experience to an individual. Yoga can help the person feel better, both improving the physical fitness and elevating the mood. Numerous studies have shown positive benefits of yoga in the management of diabetes with good impact on glycemic control , lipid profile and cardiovascular status. Further it can alleviate stress. Yoga can be considered as a good alternate for exercise therapy.

Abstract 461: Effects Of Energy Restriction On Sleep Apnea, Blood Pressure, Sympathetic Activity, Oxidative Stress, Inflammatory Biomarkers, Endothelial Function And Metabolic Profile In Obese Patients With Obstructive Sleep Apnea

Introduction: Weight loss is one of the treatment options for obstructive sleep apnea (OSA) in patients with excess body adiposity. However, the effects of moderate energy restriction on OSA are not known. Objective: To evaluate the effects of moderate energy restriction on severity of OSA, blood pressure (BP), sympathetic activity, oxidative stress, inflammation, body adiposity, metabolic profile and endothelial function in obese patients with OSA. Methods: A 16-week randomized clinical trial, involving 21 obese subjects aged 20-55y with apnea/hipopnea index (AHI) ≥ 5 events/h. Subjects were randomized in 2 groups: 11 in energy restriction group (ERG) and 10 in control group (CG). ERG was instructed to follow an energy-restricted diet (-800 kcal/day) and CG was advised not to change food intake. At the beginning and at the end of the study, participants underwent evaluation of: OSA with Watch- PAT200® including the determination of OSA severity parameters, body adiposity, BP, plasma catecholamines, c-reactive protein (CRP), adiponectin, malondialdehyde, metabolism of glucose, lipid profile and endothelial function (Endo PAT 2000®). Results: ERG, compared to CG, presented significantly greater reduction in body weight (-5.6±1.8 vs. 0.4±1.2kg, p&lt;0.001) and in all parameters of body adiposity; AHI (-7.2±2.8 vs. 0.1±1.9 events/h, p=0.04); number of O2 desaturation &gt;4% (-33.7±15.6 vs. 1.8±7.9, p=0.04); plasma adrenaline (-12.7±3.0 vs. -1.3±3.9pg/mL, p=0.04); and significantly greater increase in minimum O2 saturation (4.6±1.6 vs. -0.6±1.4%, p=0.03). ERG showed greater decrease, however without statistical significance, in systolic BP (-4.2±1.9 vs. 2.3±1.4mmHg, p=0.05), insulin (-5.1±1.9 vs. -0.7±1.3μU/mL, p=0.07) and HOMA-IR (-1.2±0.5 vs. -0.08±0.3, p=0.09). During the study period, changes in body adiposity presented significant correlation with changes in parameters of OSA severity, BP, insulin, HOMA-IR, norepinephrine and adiponectin. Changes in parameters of OSA severity presented significant association with changes in CRP. Conclusions: This study suggests that in obese patients with OSA moderate energy restriction is able to reduce body adiposity, parameters of OSA severity and sympathetic nervous system activity.

KSRP ablation enhances brown fat gene program in white adipose tissue through reduced miR-150 expression.

Brown adipose tissue oxidizes chemical energy for heat generation and energy expenditure. Promoting brown-like transformation in white adipose tissue (WAT) is a promising strategy for combating obesity. Here, we find that targeted deletion of KH-type splicing regulatory protein (KSRP), an RNA-binding protein that regulates gene expression at multiple levels, causes a reduction in body adiposity. The expression of brown fat–selective genes is increased in subcutaneous/inguinal WAT (iWAT) of Ksrp−/− mice because of the elevated expression of PR domain containing 16 and peroxisome proliferator–activated receptor gamma coactivator 1α, which are key regulators promoting the brown fat gene program. The expression of microRNA (miR)-150 in iWAT is decreased due to impaired primary miR-150 processing in the absence of KSRP. We show that miR-150 directly targets and represses Prdm16 and Ppargc1a, and that forced expression of miR-150 attenuates the elevated expression of brown fat genes caused by KSRP deletion. This study reveals the in vivo function of KSRP in controlling brown-like transformation of iWAT through post-transcriptional regulation of miR-150 expression.

Effect of MMP‐13 inhibition on adipose tissue development

Adipocyte hypertrophy and hyperplasia are supported by several physiological processes including extracellular matrix remodeling. MMPs are enzymes that orchestrate the remodeling process. MMPs regulate the relaxation of adipocyte and preadipocyte microenvironment in favor of hyperplasia and hypetrophy. We determined the effect of matrix metalloprotease 13 (MMP‐13) inhibition on adipose tissue development. In the first study we examined the effect of MMP‐13 inhibition with a MMP‐13 inhibitor, CP‐544439, on mouse adipose tissue development. Administration of CP‐544439, a selective MMP‐13 inhibitor, to mice on high fat diet resulted in reduction of body adiposity. Histology of epididymal adipose tissue showed reduced adipocyte hypertrophy and increased collagen staining by CP‐544439. In 3T3‐L1 adipocytes, PPARγwas markedly suppressed in inhibitor‐treated cells compared to control. Knockdown of MMP‐13 reduced the expression of PPARγ, suggesting that reduction of MMP‐13 activity either by pharmacological inhibition or siRNA deletion results in the reduction of adipocyte differentiation. Therefore, inhibition of MMP‐13 activity may be a strategy to prevent obesity.

Association between dietary phytochemical index and 3-year changes in weight, waist circumference and body adiposity index in adults: Tehran Lipid and Glucose study

BackgroundHigh intakes of phytochemical-rich foods have favorable effects on the prevention of chronic diseases. In this study we assessed the dietary phytochemical index (PI) in relation to 3-year change in weight, waist circumference (WC), body adiposity index (BAI) among Tehranian adults.MethodsThis longitudinal study was conducted in the framework of Tehran Lipid and Glucose Study, between 2006–2008 and 2009–2011, on 1938 adults, aged 19–70 y. The usual intake of participants was measured at baseline using a validated semi-quantitative food frequency questionnaire and dietary PI was calculated. Anthropometric measures were assessed both at baseline and 3 years later. Multiple regression models were used to estimate mean difference changes in anthropometrics associated with various dietary PI.ResultsThe mean age of participants was 40.4 ± 13.0 y, at baseline, respectively. Mean weight gain was 1.49 ± 5.06 kg (1.65 ± 5.3 kg in men and 1.34 ± 4.9 kg in women) during 3-year period. After adjustment for potential confounding variables including age at baseline, sex, BMI, educational levels, smoking, physical activity, total energy intake, dietary intake of carbohydrate, fat and protein, dietary intakes of whole grains in the highest quartile category of PI were inversely associated with 3-year changes in weight and WC (P for trend <0.05). Dietary intake of fruits in the highest quartile was also associated with lower weight gain during the study period (P for trend <0.05). There was significant inverse association between the highest quartile category of dietary PI with the 3-year changes in weight and BAI (P for trend <0.05).ConclusionHigher dietary PI could have favorable effects on prevention of weight gain and reduction of body adiposity in adults.

TCF7L2 genetic variants modulate the effect of dietary fat intake on changes in body composition during a weight-loss intervention

TCF7L2 gene variants have been associated with increased risk of type 2 diabetes and higher adiposity. Observational studies and short-term trials have suggested that macronutrients may modify these effects. However, to our knowledge, this has yet to be verified in long-term interventions. In a long-term intervention setting, we investigated the effects of TCF7L2 polymorphisms rs7903146 and rs12255372 and dietary total fat on changes in body composition and subsequent glycemic control. Data were analyzed for 591 participants in the Preventing Overweight Using Novel Dietary Strategies (Pounds Lost) trial, which is a 2-y weight-loss randomized clinical trial of diets that differed in macronutrient proportions. Adjusted means for changes in body composition at 6 and 24 mo were obtained for gene main effects and interactions with a low-fat diet (20% from energy) compared with a high-fat diet (40% from energy). Interactions with protein and carbohydrate intakes were also tested. Predicted changes in glycemic control from changes in adiposity were determined by genotype and diet type. Significant interactions were observed for rs12255372 TT (risk genotype) and fat intake for changes in BMI, total fat mass, and trunk fat mass (all P/q < 0.05) at 6 mo, with nonsignificant larger decreases for TT carriers on a low-fat diet. No significant associations were observed at 24 mo or for other macronutrients. Changes in body composition for TT carriers predicted reductions in plasma glucose and insulin only on the low-fat diet. Individuals with the TCF7L2 rs12255372 risk genotype may reduce body adiposity by consuming a diet lower in total fat. These reductions may induce better glycemic control for such individuals predisposed to type 2 diabetes. The Pounds Lost trial was registered at clinicaltrials.gov as NCT00072995.

Unsaturated Fatty Acids Revert Diet-Induced Hypothalamic Inflammation in Obesity

BackgroundIn experimental models, hypothalamic inflammation is an early and determining factor in the installation and progression of obesity. Pharmacological and gene-based approaches have proven efficient in restraining inflammation and correcting the obese phenotypes. However, the role of nutrients in the modulation of hypothalamic inflammation is unknown.Methodology/Principal FindingsHere we show that, in a mouse model of diet-induced obesity, partial substitution of the fatty acid component of the diet by flax seed oil (rich in C18:3) or olive oil (rich in C18:1) corrects hypothalamic inflammation, hypothalamic and whole body insulin resistance, and body adiposity. In addition, upon icv injection in obese rats, both ω3 and ω9 pure fatty acids reduce spontaneous food intake and body mass gain. These effects are accompanied by the reversal of functional and molecular hypothalamic resistance to leptin/insulin and increased POMC and CART expressions. In addition, both, ω3 and ω9 fatty acids inhibit the AMPK/ACC pathway and increase CPT1 and SCD1 expression in the hypothalamus. Finally, acute hypothalamic injection of ω3 and ω9 fatty acids activate signal transduction through the recently identified GPR120 unsaturated fatty acid receptor.Conclusions/SignificanceUnsaturated fatty acids can act either as nutrients or directly in the hypothalamus, reverting diet-induced inflammation and reducing body adiposity. These data show that, in addition to pharmacological and genetic approaches, nutrients can also be attractive candidates for controlling hypothalamic inflammation in obesity.

Taurine enhances the anorexigenic effects of insulin in the hypothalamus of rats

Taurine is known to modulate a number of metabolic parameters such as insulin secretion and action and blood cholesterol levels. Recent data have suggested that taurine can also reduce body adiposity in C. elegans and in rodents. Since body adiposity is mostly regulated by insulin-responsive hypothalamic neurons involved in the control of feeding and thermogenesis, we hypothesized that some of the activity of taurine in the control of body fat would be exerted through a direct action in the hypothalamus. Here, we show that the intracerebroventricular injection of an acute dose of taurine reduces food intake and locomotor activity, and activates signal transduction through the Akt/FOXO1, JAK2/STAT3 and mTOR/AMPK/ACC signaling pathways. These effects are accompanied by the modulation of expression of NPY. In addition, taurine can enhance the anorexigenic action of insulin. Thus, the aminoacid, taurine, exerts a potent anorexigenic action in the hypothalamus and enhances the effect of insulin on the control of food intake.

Asociación entre tejido graso abdominal y riesgo de morbilidad: efectos positivos del ejercicio físico en la reducción de esta tendencia

Introduction: The consequences related to the accumulation of abdominal fat above healthy levels create a considerable organic damage. Among the physiological consequences we can highlight heart diseases, hypertension, type-2 diabetes, obesity and metabolic syndrome, which drastically reduce life expectancy and quality. Evidence shows that health improvement is correlated to greater levels of physical activity. However, physical exercise can create oxidative damage on organs and muscular tissue, more relevant in subjects with a high percentage of abdominal fat. This piece of work determines which are the fundamental variables of the exercise program in order to optimize its advantages while minimizing oxidative stress. Main purpose: To know the key variables in the accumulation of abdominal fat above healthy levels, and the role of exercise in prevention and improvement of such issue. Specific purposes: 1) to identify the key variables in an exercise program aimed at reducing abdominal fat; 2) to understand the relationship between abdominal fat, health and exercise; 3) to review the latest research related to physical exercise and its effect on abdominal adipose tissue. Methodology: A search and identification of original and reviewed articles will be carried out in indexed impact journals within the main databases. Discussion: Regular physical exercise, most notably aerobic one, reduces body adipose tissue deposits in general, and abdominal ones in particular, both in obese and overweight subjects.

Positive effects of physical exercise on reducing the relationship between subcutaneous abdominal fat and morbility risk

The consequences related to the accumulation of abdominal fat above healthy levels create a considerable organic damage. Among the physiological consequences we can highlight heart diseases, hypertension, type-2 diabetes, obesity and metabolic syndrome, which drastically reduce life expectancy and quality. Evidence shows that health improvement is correlated to greater levels of physical activity. However, physical exercise can create oxidative damage on organs and muscular tissue, more relevant in subjects with a high percentage of abdominal fat. This piece of work determines which are the fundamental variables of the exercise program in order to optimize its advantages while minimizing oxidative stress. To know the key variables in the accumulation of abdominal fat above healthy levels, and the role of exercise in prevention and improvement of such issue. SPECIFIC PURPOSES: 1) to identify the key variables in an exercise program aimed at reducing abdominal fat; 2) to understand the relationship between abdominal fat, health and exercise; 3) to review the latest research related to physical exercise and its effect on abdominal adipose tissue. A search and identification of original and reviewed articles will be carried out in indexed impact journals within the main databases. Regular physical exercise, most notably aerobic one, reduces body adipose tissue deposits in general, and abdominal ones in particular, both in obese and overweight subjects.

Beta-Carotene Reduces Body Adiposity of Mice via BCMO1

Evidence from cell culture studies indicates that β-carotene-(BC)-derived apocarotenoid signaling molecules can modulate the activities of nuclear receptors that regulate many aspects of adipocyte physiology. Two BC metabolizing enzymes, the BC-15,15′-oxygenase (Bcmo1) and the BC-9′,10′-oxygenase (Bcdo2) are expressed in adipocytes. Bcmo1 catalyzes the conversion of BC into retinaldehyde and Bcdo2 into β-10′-apocarotenal and β-ionone. Here we analyzed the impact of BC on body adiposity of mice. To genetically dissect the roles of Bcmo1 and Bcdo2 in this process, we used wild-type and Bcmo1 -/- mice for this study. In wild-type mice, BC was converted into retinoids. In contrast, Bcmo1-/- mice showed increased expression of Bcdo2 in adipocytes and β-10′-apocarotenol accumulated as the major BC derivative. In wild-type mice, BC significantly reduced body adiposity (by 28%), leptinemia and adipocyte size. Genome wide microarray analysis of inguinal white adipose tissue revealed a generalized decrease of mRNA expression of peroxisome proliferator-activated receptor γ (PPARγ) target genes. Consistently, the expression of this key transcription factor for lipogenesis was significantly reduced both on the mRNA and protein levels. Despite β-10′-apocarotenoid production, this effect of BC was absent in Bcmo1-/- mice, demonstrating that it was dependent on the Bcmo1-mediated production of retinoids. Our study evidences an important role of BC for the control of body adiposity in mice and identifies Bcmo1 as critical molecular player for the regulation of PPARγ activity in adipocytes

Innervation of skeletal muscle by leptin receptor-containing neurons

In addition to suppressing food intake, leptin reduces body adiposity by altering metabolism within peripheral tissues such as adipose tissue and muscle. Recent work indicates that leptin action within the brain is sufficient to promote glucose uptake and increase fat oxidation within skeletal muscle, and that these effects are dependent on the sympathetic nervous system. To identify neuronal circuits through which leptin impacts skeletal muscle metabolism, we used LepRb-GFP reporter mice in combination with muscle-specific injection of an mRFP-expressing pseudorabies virus (PRV), which acts as a transsynaptic retrograde tracer. Consistent with previous observations in the rat, muscle-specific PRV injection lead to labeling within multiple areas of the hypothalamus and brainstem. However, the only areas in which PRV and LepRb colocalization was detected were within the brainstem nucleus of the solitary tract (NTS) and the hypothalamic retrochiasmatic area. Within the NTS 28.5 ± 9.4% of PRV-positive neurons contained LepRb-GFP, while in the RCH 37 ± 1.7% of PRV neurons also contained LepRb. In summary, these data clearly implicate the NTS and RCH as key sites through which brain leptin impacts skeletal muscle, and as such provide an anatomical framework within which to interpret physiological data indicating that leptin acts in the brain to influence metabolism within skeletal muscle.