Visceral Adipose Tissue Weight Research Articles

Chronic High Dose Zinc Supplementation Induces Visceral Adipose Tissue Hypertrophy without Altering Body Weight in Mice.

The trace element zinc plays an important role in human life. Zinc deficiency impairs growth, reproduction, metabolism and immunity in both human and animals. Thus, zinc supplementation is recommended in daily life. However, the effect of long-term chronic zinc supplementation on adipose homeostasis has not been well elucidated. In the current study, mice were supplemented with zinc sulfate in the drinking water for 20 weeks. The results suggested that chronic zinc supplementation impaired systemic glucose clearance after exogenous insulin or glucose challenges, as compared to the control mice. Further study revealed that chronic zinc supplementation made no difference to body weight, but increased visceral adipose tissue weight and adipocyte size. In addition, gene expression of leptin and IL6 in the visceral adipose tissue of zinc-supplemented mice were higher than those of control mice. Moreover, serum level of leptin of the zinc-supplemented mice was twice as high as that of the control mice. Besides, phosphorylation level of AKT T308 was attenuated in the perirenal adipose tissue of zinc-supplemented mice. In comparison, the expression of macrophage marker genes and lipogenic genes were not affected by chronic zinc supplementation, but the protein levels of FAS and SCD1 decreased or tended to decrease in the perirenal adipose tissue of zinc-supplemented mice, as compared to the control mice. Our findings suggest that chronic high dose zinc supplementation induces visceral adipose tissue hypertrophy and impairs AKT signaling in perirenal adipose tissue.

Acacetin from Traditionally Used Saussurea involucrata Kar. et Kir. Suppressed Adipogenesis in 3T3-L1 Adipocytes and Attenuated Lipid Accumulation in Obese Mice.

Acacetin, a flavone that can be isolated from the Saussurea involucrata plant, has anti-tumor and anti-inflammatory properties that ameliorate airway hyperresponsiveness in asthmatic mice. This study investigated whether acacetin has anti-adipogenic effects in 3T3-L1 adipocytes and whether it regulates the inflammatory response in adipocytes and macrophages. It also investigated whether acacetin ameliorates lipid accumulation in high-fat diet- (HFD) induced obese mice. Differentiated 3T3-L1 cells were treated with acacetin. The glycerol levels in the culture medium were measured, and the expression of proteins and genes involved in adipogenesis and lipolysis were assayed by Western blot and real-time PCR, respectively. Inflammatory cytokine signaling pathway activity was assessed in macrophages that were treated with acacetin and cultured with differentiated medium from 3T3-L1 cells. Intraperitoneal injections of acacetin were administered to HFD-induced obese mice twice a week for 10 weeks. Acacetin significantly increased the levels of glycerol in the culture medium and significantly inhibited lipid accumulation in adipocytes. Acacetin reduced the expression of adipogenesis-related transcription factors, including the expression of the CCAAT/enhancer-binding protein; it also increased sirtuin 1 expression and AMPK phosphorylation in adipocytes. In macrophages cultured with differentiated media from 3T3-L1 adipocytes, acacetin reduced the levels of inflammatory mediators and the activity of the mitogen-activated protein kinase and NF-κB pathways. In obese mice, acacetin reduced both body weight and visceral adipose tissue weight. These results demonstrate that acacetin inhibited adipogenesis in adipocytes and in obese mice. Acacetin also reduced the inflammatory response of macrophages that were stimulated with differentiated media from 3T3-L1 cells.

Anti-obesity effect of robusta fermented with Leuconostoc mesenteroides in high-fat diet-induced obese mice.

Robusta beans cultivated with Monascus ruber (RMR) were successively fermented with Leuconostoc mesenteroides (LM) and the antiobesity effects were examined. To produce an obese mouse model to investigate the hypolipidemic effects, ICR mice were fed the same high-fat diet for 6 weeks. Treatment groups were given 10 or 20% RMR-LM. Body weight changes in the 20% RMR-LM group were lower compared with those in the control group. Visceral adipose tissue weight and adipose size were significantly lower in the 20% RMR-LM group compared with those in the control group. Significant improvement in glucose tolerance was observed in the 10 and 20% RMR-LM groups compared with the control group. The 20% RMR-LM group exhibited a significant reduction in serum glucose concentration. Hepatic mRNA levels of sterol regulatory element-binding protein 1, fas cell surface death receptor, and peroxisome proliferator-activated receptor γ, which are associated with lipid, and fatty acid metabolism, in the 20% RMR-LM group were significantly lower compared with those in the control group. The results of the present study demonstrated that 20% RMR-LM may be used to prevent obesity, and ameliorate diabetes and lipid metabolism imbalances.

Abstract 441: Macrophage CD40 in Atherosclerosis, Obesity and Multiple Sclerosis

Introduction: The co-stimulatory dyad CD40-CD40L plays a central role in fine-tuning immune reactions in atherosclerosis, obesity-induced inflammation and multiple sclerosis (MS). Inhibition of CD40 in atherosclerosis and experimental autoimmune encephalomyelitis (EAE) ameliorates disease outcome, whereas CD40-deficiency in a diet induced obesity (DIO) model worsens insulin resistance and induces excessive adipose tissue inflammation. Although inhibition of CD40 has powerful effects, we do not know which CD40 expressing cell-type is responsible for the amelioration/aggravation of disease. As myeloid CD40 is known to play a role in leukocyte trafficking, which is important in atherosclerosis, obesity and neuro-inflammation, we hypothesize that myeloid CD40 is important in these disease modalities. Methods: To investigate the role of myeloid CD40 in atherosclerosis, obesity and EAE we have generated macrophage specific LysM-CD40flfl - (ApoE-/-), and dendritic cell/adipose tissue macrophage specific CD11C-CD40flfl). Atherosclerosis was induced by aging the LysM-CD40flfl - ApoE-/- mice until 30 weeks. EAE was induced in LysM-CD40flfl mice by subjecting them to myelin oligodendrocyte glycoprotein peptide (MOG35-55), and LysM-CD40flfl and CD11c-CD40flfl mice were subjected to a 60% high fat diet for 18 wks. Results: LysM-CD40flfl - ApoE-/- mice showed a significant reduction in atherosclerotic plaque area, with a reduced macrophage accumulation. Loss of macrophage CD40 in EAE results in a significant decrease in the neurological symptoms of EAE, and a majority of the LysM-CD40flfl mice were fully protected against EAE. LysM-CD40flfl mice subjected to DIO showed an increase in macrophage accumulation in the visceral adipose tissue, but did not affect adipose tissue mass, insulin tolerance, or plasma triglyceride concentrations. The CD11CcreCD40flfl mice exhibited a decrease in visceral adipose tissue weight, an increased lipid content in the liver and slightly decreases leukocyte numbers and pro-inflammatory gene expression in the adipose tissue. Conclusions: Macrophage CD40 is an important driver of atherosclerosis and EAE. Macrophage CD40 is protective in obesity-induced inflammation, but is probably not the key player.

PPAR-γ agonist ameliorates liver pathology accompanied by increasing regulatory B and T cells in high-fat-diet mice.

Peroxisome proliferator-activated receptor (PPAR)-γ plays critical roles in human metabolic disorders. However, the mechanism remains incompletely understood. Regulatory cells contribute to these metabolic improvements; therefore, whether PPAR-γ agonist regulates regulatory cells was investigated. C57BL/6J mice received a normal or high-fat diet (HFD) with or without pioglitazone treatment. Mice were sacrificed for detecting the metabolic parameters. Lymphocytes from spleen and visceral adipose tissue (VAT) were collected and analyzed for ST2+ Tregs and Bregs by flow cytometry. IL-10 in the liver or VAT was detected by immunofluorescence and ELISA. Correlation analysis between IL-10 and liver weight or serum total cholesterol was made by Pearson correlation analysis. Pioglitazone increased VAT weight but reduced serum total cholesterol, hepatic steatosis, and cholesterol crystallization formation. Pioglitazone treatment enhanced ST2+ Tregs and Bregs in the VAT and spleen of HFD-fed mice (all P < 0.05). Pioglitazone treatment increased IL-10 in the livers or VAT of HFD-fed mice (all P < 0.05). The expression of IL-10 in the liver was significantly negatively correlated with liver weight or serum total cholesterol in pioglitazone-treated HFD-fed mice (r2 = 0.74, P < 0.05; r2 = 0.58, P < 0.05). PPAR-γ signaling plays a critical role in the regulation of metabolic disorders through promoting regulatory cell response.

Development of a new diet-induced obesity (DIO) model using Wistar lean rats.

Obesity is an increasingly severe socioeconomic health issue worldwide. Rodents with diet-induced obesity (DIO) are widely used as models of obesity. The main aim of this study was to establish a DIO model using Wistar lean (+/+ or +/−) rats by feeding a high-fat diet (45 kcal% fat) to dams during the latter term of gestation and the lactation period. A second aim was to examine the effect of post-weaning nutrition independently of maternal nutrition. Some pups (group D) were fed the same high-fat diet after weaning, while others (group C) were fed a chow diet after weaning. In the control groups, the dams were fed only the chow diet and the pups were fed either the chow diet (group A) or high-fat diet (group B) after weaning. Between 16–21 weeks of age, group D showed the heaviest body weight and visceral adipose tissue weight among groups, in addition to glucose intolerance and high concentrations of glucose and cholesterol in plasma. Group B showed mild obesity with dysfunctions in glucose and lipid metabolism. Interestingly, group C showed mild obesity and impaired glucose tolerance, similar to the phenotype of group B. In summary, the high-fat diet challenge of dams during gestation and lactation caused an increase in adipose tissue weight and abnormalities of glucose and lipid metabolism in their adult offspring. Our results suggest the importance of both maternal and post-weaning nutrition for DIO production and provide useful DIO models.

Adipocyte-specific Hypoxia-inducible gene 2 promotes fat deposition and diet-induced insulin resistance

ObjectiveAdipose tissue relies on lipid droplet (LD) proteins in its role as a lipid-storing endocrine organ that controls whole body metabolism. Hypoxia-inducible Gene 2 (Hig2) is a recently identified LD-associated protein in hepatocytes that promotes hepatic lipid storage, but its role in the adipocyte had not been investigated. Here we tested the hypothesis that Hig2 localization to LDs in adipocytes promotes adipose tissue lipid deposition and systemic glucose homeostasis. MethodWhite and brown adipocyte-deficient (Hig2fl/fl × Adiponection cre+) and selective brown/beige adipocyte-deficient (Hig2fl/fl × Ucp1 cre+) mice were generated to investigate the role of Hig2 in adipose depots. Additionally, we used multiple housing temperatures to investigate the role of active brown/beige adipocytes in this process. ResultsHig2 localized to LDs in SGBS cells, a human adipocyte cell strain. Mice with adipocyte-specific Hig2 deficiency in all adipose depots demonstrated reduced visceral adipose tissue weight and increased glucose tolerance. This metabolic effect could be attributed to brown/beige adipocyte-specific Hig2 deficiency since Hig2fl/fl × Ucp1 cre+ mice displayed the same phenotype. Furthermore, when adipocyte-deficient Hig2 mice were moved to thermoneutral conditions in which non-shivering thermogenesis is deactivated, these improvements were abrogated and glucose intolerance ensued. Adipocyte-specific Hig2 deficient animals displayed no detectable changes in adipocyte lipolysis or energy expenditure, suggesting that Hig2 may not mediate these metabolic effects by restraining lipolysis in adipocytes. ConclusionsWe conclude that Hig2 localizes to LDs in adipocytes, promoting adipose tissue lipid deposition and that its selective deficiency in active brown/beige adipose tissue mediates improved glucose tolerance at 23 °C. Reversal of this phenotype at thermoneutrality in the absence of detectable changes in energy expenditure, adipose mass, or liver triglyceride suggests that Hig2 deficiency triggers a deleterious endocrine or neuroendocrine pathway emanating from brown/beige fat cells.

Fruit vinegars attenuate cardiac injury via anti-inflammatory and anti-adiposity actions in high-fat diet-induced obese rats

Context: Fruit vinegars (FVs) are used in Mediterranean folk medicine for their hypolipidemic and weight-reducing properties.Objective: To investigate the preventive effects of three types of FV, commonly available in Algeria, namely prickly pear [Opuntia ficus-indica (L.) Mill (Cectaceae)], pomegranate [Punica granatum L. (Punicaceae)], and apple [Malus domestica Borkh. (Rosaceae)], against obesity-induced cardiomyopathy and its underlying mechanisms.Materials and methods: Seventy-two male Wistar rats were equally divided into 12 groups. The first group served as normal control (distilled water, 7 mL/kg bw), and the remaining groups were respectively treated with distilled water (7 mL/kg bw), acetic acid (0.5% w/v, 7 mL/kg bw) and vinegars of pomegranate, apple or prickly pear (at doses of 3.5, 7 and 14 mL/kg bw, acetic acid content as mentioned above) along with a high-fat diet (HFD). The effects of the oral administration of FV for 18 weeks on the body and visceral adipose tissue (VAT) weights, plasma inflammatory and cardiac enzymes biomarkers, and in heart tissue were evaluated.Results: Vinegars treatments significantly (p < .05) attenuated the HFD-induced increase in bw (0.2–0.5-fold) and VAT mass (0.7–1.8-fold), as well as increase in plasma levels of CRP (0.1–0.3-fold), fibrinogen (0.2–0.3-fold), leptin (1.7–3.7-fold), TNF-α (0.1–0.6-fold), AST (0.9–1.4-fold), CK-MB (0.3–1.4-fold) and LDH (2.7–6.7-fold). Moreover, vinegar treatments preserved myocardial architecture and attenuated cardiac fibrosis.Discussion and conclusion: These findings suggest that pomegranate, apple and prickly pear vinegars may prevent HFD-induced obesity and obesity-related cardiac complications, and that this prevention may result from the potent anti-inflammatory and anti-adiposity properties of these vinegars.

Phlorizin Supplementation Attenuates Obesity, Inflammation, and Hyperglycemia in Diet-Induced Obese Mice Fed a High-Fat Diet.

Obesity, along with its related complications, is a serious health problem worldwide. Many studies reported the anti-diabetic effect of phlorizin, while little is known about its anti-obesity effect. We investigated the beneficial effects of phlorizin on obesity and its complications, including diabetes and inflammation in obese animal. Male C57BL/6J mice were divided into three groups and fed their respective experimental diets for 16 weeks: a normal diet (ND, 5% fat, w/w), high-fat diet (HFD, 20% fat, w/w), or HFD supplemented with phlorizin (PH, 0.02%, w/w). The findings revealed that the PH group had significantly decreased visceral and total white adipose tissue (WAT) weights, and adipocyte size compared to the HFD. Plasma and hepatic lipids profiles also improved in the PH group. The decreased levels of hepatic lipids in PH were associated with decreased activities of enzymes involved in hepatic lipogenesis, cholesterol synthesis and esterification. The PH also suppressed plasma pro-inflammatory adipokines levels such as leptin, adipsin, tumor necrosis factor-α, monocyte chemoattractant protein-1, interferon-γ, and interleukin-6, and prevented HFD-induced collagen accumulation in the liver and WAT. Furthermore, the PH supplementation also decreased plasma glucose, insulin, glucagon, and homeostasis model assessment of insulin resistance levels. In conclusion, phlorizin is beneficial for preventing diet-induced obesity, hepatic steatosis, inflammation, and fibrosis, as well as insulin resistance.

Targeting TRPV1 for Body Weight Control using TRPV1(-/-) Mice and Electroacupuncture.

Obesity is a global social medical problem resulting in morbidity as high as 20–30%. Here we investigated whether the manipulation of TRPV1 can control mice body weight through electroacupuncture (EA). The results demonstrated that body weight increased with time in the control group (108.19 ± 1.31%, n = 7). The increase of mice body weight was significantly less in the EA group (104.41 ± 0.76%, p < 0.05, compared with the control group, n = 7) but not in the sham EA group (109.1 ± 0.63%, p < 0.05, compared with EA group, n = 7). EA did not decrease the gain of body weight in TRPV1 knock mice (107.94 ± 0.41% and 107.79 ± 1.04% for TRPV1−/− and TRPV1−/− with EA, respectively, p > 0.05). The visceral white adipose tissue (WAT) weight was lower in the EA group at 4 weeks after manipulation. Moreover, the protein levels of TRPV1, pPKA, pPKC, and pERK were increased in the dorsal root ganglion (DRG) and spinal cord (SC) after EA treatment but not in the sham EA and TRPV1−/− mice. This study suggests that targeting TRPV1 is beneficial in controlling body weight and TRPV1-associated mechanisms in mice.

Low intensity exercise prevents disturbances in rat cardiac insulin signaling and endothelial nitric oxide synthase induced by high fructose diet

Increase in fructose consumption together with decrease in physical activity contributes to the development of metabolic syndrome and consequently cardiovascular diseases. The current study examined the preventive role of exercise on defects in cardiac insulin signaling and function of endothelial nitric oxide synthase (eNOS) in fructose fed rats. Male Wistar rats were divided into control, sedentary fructose (received 10% fructose for 9 weeks) and exercise fructose (additionally exposed to low intensity exercise) groups. Concentration of triglycerides, glucose, insulin and visceral adipose tissue weight were determined to estimate metabolic syndrome development. Expression and/or phosphorylation of cardiac insulin receptor (IR), insulin receptor substrate 1 (IRS1), tyrosine-specific protein phosphatase 1B (PTP1B), Akt, extracellular signal-regulated protein kinases 1 and 2 (ERK1/2) and eNOS were evaluated. Fructose overload increased visceral adipose tissue, insulin concentration and homeostasis model assessment index. Exercise managed to decrease visceral adiposity and insulin level and to increase insulin sensitivity. Fructose diet increased level of cardiac PTP1B and pIRS1 (Ser307), while levels of IR and ERK1/2, as well as pIRS1 (Tyr 632), pAkt (Ser473, Thr308) and pERK1/2 were decreased. These disturbances were accompanied by reduced phosphorylation of eNOS at Ser1177. Exercise managed to prevent most of the disturbances in insulin signaling caused by fructose diet (except phosphorylation of IRS1 at Tyr 632 and phosphorylation and protein expression of ERK1/2) and consequently restored function of eNOS. Low intensity exercise could be considered as efficient treatment of cardiac insulin resistance induced by fructose diet.

Effects of metformin on serum visfatin and visfatin expression in visceral adipose tissue of type 2 diabetic rats

Objective To investigate the effects of metformin on serum visfatin and the level of visfatin mRNA in visceral adipose tissue of type 2 diabetic rats. Methods Forty Wistar rats were randomly assigned into normal diet group (NC) and diabetic group. The rats in the diabetic group were fed with high glucose and high fat diet, and then injected with streptozotocin (STZ). The diabetic rats were divided into diabetic control (DC), metformin (MET), and insulin-treatment (INS) groups. Eight weeks later, body weight (BW), visceral adipose tissue weight, and biochemical indicators were assessed. Homeostasis model assessment of insulin resistance (HOMA-IR) and Lee index were calculated. The serum visfatin levels were detected by enzyme-linked immunoassay (EIA), and the visfatin mRNA levels of visceral adipose tissues were detected by real time polymerase chain reaction (PCR). Results Compared to group DC, the visfatin levels of serum and visceral adipose tissue mRNA were lower in INS group, but did not have significant difference (P>0.05); the visfatin levels of serum and visceral adipose tissue mRNA in MET group were significantly lower (P< 0.01). Conclusions Metformin can reduce the visfatin levels of serum and visceral adipose tissue mRNA, and improve the insulin resistance in type 2 diabetic rats. Key words: Metformin/PD; Diabetes mellitus, type 2/DT/ME; Nicotinamide phosphoribosyltransferase/ME; Adipose tissue/ME

Visceral fat is better related to impaired glucose metabolism than body mass index after kidney transplantation.

The role of visceral adipose tissue (VAT) in post-transplant hyperglycaemia is not known. We evaluated 167 patients without diabetes 8-10 weeks after kidney transplantation, performing oral glucose tolerance tests and measuring VAT content from dual-energy X-ray absorptiometry scans. Median VAT weight in normal glucose tolerance patients was 0.9 kg, impaired fasting glucose patients 1.0 kg, impaired glucose tolerance patients 1.3 kg and patients with post-transplant diabetes (PTDM) 2.1 kg (P = 0.004, indicating a difference between groups). Percentage VAT of total body fat was associated with fasting (R(2) = 0.094, P < 0.001) and 2-h glucose concentration (R(2) = 0.062, P = 0.001), while BMI was only associated with 2-h glucose concentration (R(2) = 0.029, P = 0.028). An association between BMI and 2-h glucose concentration was lost in adjusted models, as opposed to the associations between VAT as percentage of total body fat and glucose concentrations (R(2) = 0.132, P < 0.001 and R(2) = 0.097, P = 0.001, respectively for fasting and 2-h glucose concentration). In conclusion, VAT is more closely related to impaired glucose metabolism than BMI after kidney transplantation. The association with central obesity should encourage additional studies on lifestyle interventions to prevent PTDM.

OC-106 Activation of the bile acid receptor, farnesoid-x receptor, may reduce ileal inflammatory cytokine expression in an animal model of diet-induced obesity

<h3>Introduction</h3> A high fat (HF)/high sugar (HS), Western diet has been implicated in the pathogenesis of IBD.¹The BA receptor, farnesoid-x receptor (FXR), is central to the crosstalk between the host and its microbiota.²FXR has an immuno-modulatory role in the GI tract.^3,4We hypothesised that disruption to BA signalling, induced by a HF/HS diet associated dysbiosis, is a mechanism linking diet to the development of IBD. The aim of this study was to investigate the effect of HF/HS feeding and FXR agonism on ileal inflammation in a mouse model of obesity. <h3>Method</h3> Animal husbandry was performed under licence from the Home Office (as per ASPA 1986). C3H/He mice (n = 44) were fed standard chow or HF/HS chow (trans-fats, with fructose corn syrup). At 24 weeks, feed was supplemented with an FXR agonist (5 mg/kg or 1 mg/kg of feed) or control. At 42 weeks, body weight and visceral adipose tissue (VAT) weight was recorded and the ileum was dissected. The expression of TNFα, IFNγ and IL-6 was measured by RT-PCR (ΔΔCt method). FXR and its downstream targets, SHP and IBABP, were measured to assay for FXR activity. <i>T-</i>tests, regression analysis and Pearson correlation were calculated using Prism version 6.0e. P values were 2-tailed, a P value of &lt;0.05 was considered significant. <h3>Results</h3> Mice fed a HF/HS diet were significantly heavier, with more VAT than mice on the control diet (mean weight of 49.9 g versus mean weight of 41.6 g, p &lt; 0.01). There was a positive correlation between the amount of VAT and the ileal expression of TNFα and IFNγ (y = 1.32*X p = 0.05, y = 1.24*X p = 0.02 respectively). The FXR agonist significantly increased the expression of IBABP (fold increase of 2.0, p = 0.01). In HF/HS fed mice, supplementation with 1 mg/kg FXR agonist attenuated the increase in ileal expression of all cytokines assayed, although the observed trend failed to reach significance. <h3>Conclusion</h3> Animals fed a western lifestyle diet express more ileal inflammatory cytokine. There is a trend to suggest that supplementation with an FXR agonist reduces diet induced cytokine expression. By mediating dietary risk, FXR may be a potential therapeutic target in IBD, particularly to reduce relapses in patients with known disease. <h3>Disclosure of interest</h3> None Declared. <h3>References</h3> Ananthakrishnan AN. Gastroenterol Hepatol. 2013;9(6) Swann JR, Want EJ, <i>et al</i>. PNAS 2011;108(1) Vavassori P, Mencarelli A, <i>et al</i>. J Immunol. 2009;183 Gadaleta RM, van Erpecum KJ, <i>et al</i>. Gut 2011;60

Impact of high-fat diet and voluntary running on body weight and endothelial function in LDL receptor knockout mice

ObjectiveObesity and physical inactivity are important cardiovascular risk factors. Regular physical exercise has been shown to mediate beneficial effects in the prevention of cardiovascular diseases. However, the impact of physical exercise on endothelial function in proatherosclerotic low-density lipoprotein receptor deficient (LDLR−/−) mice has not been studied so far. MethodsSix-week-old male LDLR−/− mice were fed a standard diet or a high-fat diet (39 kcal% fat diet) for 20 weeks. The impact of high-fat diet and voluntary running on body weight and amount of white adipose tissue was monitored. Basal tone and endothelial function was investigated in aortic rings using a Mulvany myograph. ResultsLDLR−/− mice on high-fat diet had increased cumulative food energy intake, but also higher physical activity compared to mice on control diet. Body weight and amount of visceral and retroperitoneal white adipose tissue of LDLR−/− mice were significantly increased by high-fat diet and partially reduced by voluntary running. Endothelial function in aortae of LDLR−/− mice was impaired after 20 weeks on standard and high-fat diet and could not be improved by voluntary running. Basal tone showed a trend to be increased by high-fat diet. ConclusionVoluntary running reduced body weight and amount of white adipose tissue in LDLR−/− mice. Endothelial dysfunction in LDLR−/− mice could not be improved by voluntary running. In a clinical context, physical exercise alone might not have an influence on functional parameters and LDL-C levels in patients with familial hypercholesterolemia. However, physical activity in these patients may be in general beneficial and should be performed.

고지방 식이로 유도된 비만 마우스에서 대두 부산물인 순물과 침지수의 항비만 효과

Here we study the anti-obesity effects of by-product from soybean on mouse fed high fat diet. The body weight gain, visceral and subcutaneous adipose tissue weight, liver and epididymal adipose tissue weight in freeze-dried soybean-soaking-water (SSW) powder fed group showed lower level than those in high fat diet (HFD) group by determining with weight measuring and histological methods. Also, histological analyses of the liver and fat tissues of SSW grouped mice revealed significantly less number of lipid droplets formation and smaller size of adipocytes compared to the HFD group. Moreover, the levels of total serum cholesterol, LDL-cholesterol and the atherogenic index were decreased in the SSW groups. Especially, in SSW group, the levels of phosphorylation of two lipid oxidation enzymes, adenosine monophosphate-activated protein kinase (AMPK) and acetyl-CoA carboxylasse (ACC) were elevated hence that may activate fatty acid oxidation. But AST and ALT levels were not changed in blood. By micro-CT analysis of abdomen, SSW groups significantly showed a tendency to decrease visceral and subcutaneous fats as well as fat-deposited areas compared to HFD group. Taken together, we suggest that soybean soaking water has a function in ameliorating obesity through inhibiting lipid synthesis as well as stimulating fatty acid oxidation.

Gum arabic down-regulate PPAR-γ and SCD mRNA expression in mice

Abstract Introduction Gum arabic is a complex polysaccharide used in the food industry as a thickener and stabilizer. It reduced plasma cholesterol level in animals and humans, and it has prebiotic, anticarcinogenic and anti-oxidant effect with a protective role against hepatic and cardiac toxicities. Aim To study the impact of gum arabic on body weight, adipose tissue weight, lipid profiles and expression of some gene control lipid metabolism. Material and methods 20 female CD-1 mice at 5 weeks age were divided into two groups, one served as control and the second received 10% of gum arabic in drinking water for 6 weeks. Liver and visceral adipose tissue and serum were collected from all groups. Total cholesterol, triglyceride, HDL-c and LDL-c were assayed using kits, and the expression of lipid metabolic enzyme gene was detected by RT-PCR. Results and discussion The results showed that gum arabic significantly decreased body weight ( P P P P P Conclusions The results conclude that gum arabic can reduce body weight and visceral adipose tissue weight, and down-regulated PPAR-γ and SCD gene expression.

Conjugated linoleic acid reduces visceral and ectopic lipid accumulation and insulin resistance in chronic severe hypertriacylglycerolemia

ObjectiveThe metabolic health effects of conjugated linoleic acid (CLA), which is one of the principal polyunsaturated fatty acids, are controversial and still not fully accepted. The aim of this study was to examine the effects of CLA on adiposity, ectopic lipid accumulation, and insulin-resistant states in a metabolic syndrome model of non-obese hereditary rats with hypertriacylglycerolmia (HHTg). MethodsGroups of adult male HHTg rats were fed a high-carbohydrate diet (70% sucrose) with a 2% mixture of CLA isomers, or with the same amount of sunflower oil (control group) for 2 mo. ResultsCLA supplementation decreased body weight gain (P < 0.05) and visceral adipose tissue weight (P < 0.01), and distinctively reduced serum triacylglycerols (P < 0.01) and triacylglycerol accumulation in the liver, heart, muscle, and aorta. CLA-treated rats exhibited increased insulin sensitivity in the adipose (P < 0.01), a higher release of fatty acids (P < 0.001), and increased adiponectin secretion (P < 0.01).In the skeletal muscle, CLA supplementation was associated with increased glucose oxidation (P < 0.01) and an elevated anti-inflammatory index (P < 0.05), according to phospholipid fatty acid composition. In the liver, CLA reduced the oxidized form of glutathione and elevated the activity of glutathione-dependent antioxidant enzymes. ConclusionResults suggest that CLA supplementation may protect against HHTg-induced dyslipidemia, ectopic lipid deposition, and insulin resistance. Increased glucose oxidation in the skeletal muscle as well as adiponectin secretion may play a role in the mechanism of the CLA action. Results suggest that CLA could reduce the negative consequences of HHTg and metabolic syndrome.

D‐Xylose suppresses adipogenesis and lipid abnormalities in high‐fat diet‐induced obese mice

Obesity is one of the global epidemic problems and major risk factors for many metabolic diseases. D‐Xylose has been used as an alternative sweetener due to its low absorption rate in the gut. The present study investigated the effect of D‐xylose on adipogenesis and lipid abnormalities in high‐fat diet (HFD)‐induced obese mice. Male C57BL/6 mice were fed a HFD for 4 months with or without 5% D‐xylose (Xylo 5) or 10% D‐xylose (Xylo 10) mixed with sucrose. Although there were no significant difference in body and liver weight among the groups, fasting blood glucose level, subcutaneous and visceral adipose tissue weight, and serum blood markers, including total cholesterol and LDL cholesterol levels were significantly decreased in both of D‐xylose supplemented groups. Furthermore, D‐xylose supplementation down‐regulated expression of adipogenesis‐related genes, such as C/EBPα, FAS, and SREBP‐1C in visceral adipose tissues. Histopathologically, Supplementation withXylo 5 or Xylo 10 resulted in improvement of HFD‐induced fat accumulation in the liver. In conclusion, these results suggested that D‐xylose is beneficial for the alleviation of adipogenesis and dyslipidemia in obese mice.

Effects of resveratrol on lipid metabolism in muscle and adipose tissues: A reevaluation in a pig model

The body fat-lowering effect and mechanisms of action of resveratrol (0, 300, 600 mg resveratrol/kg diet) was evaluated in a pig model. Resveratrol improved serum lipid profiles, and decreased visceral adipose tissue weight and serum leptin level. In adipose tissue, peroxisome proliferator activated receptor γ (PPARγ) and fatty acid synthase (FAS) mRNA levels, and FAS and lipoprotein lipase (LPL) activities were decreased by resveratrol, while hormone sensitive lipase (HSL), adipose triglyceride lipase (ATGL) and carnitine palmitoyl transferase-1(CPT-1) mRNA levels, and HSL and CPT-1 activities were increased. In muscle tissue, PPARγ, FAS, acetyl-CoA carboxylase (ACC) and LPL mRNA levels and FAS and ACC activities were decreased by resveratrol, while HSL mRNA levels and CPT-1 activity were increased. Moreover, compared with the control group, LPL activity was decreased, and CPT-1 mRNA levels and HSL activity were increased in the 600 mg resveratrol/kg diet group. This study provides the very first evidence in a pig model that resveratrol could improve serum lipid profiles and decrease body fat deposition, which might be mediated by a reduction in fatty acid uptake and de novo lipogenesis, as well as an increase in fat mobilization and fatty acid oxidation in muscle and adipose tissues.