A mixture of the aqueous extract of Garcinia cambogia, soy peptide and L: -carnitine reduces the accumulation of visceral fat mass in rats rendered obese by a high fat diet.
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ABSTRACT:
SUBMITTER: Kim YJ
PROVIDER: S-EPMC2478482 | biostudies-other | 2008 Feb
REPOSITORIES: biostudies-other
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Project description:Objectives: Lotus leaf is a kind of traditional Chinese medicine. We aimed to explore the effects of lotus leaf aqueous extract (LLAE) on peroxisome proliferative activated receptor γ2 (PPARγ2) expression in preadipocytes and adipocytes and further investigate its effects on high fat diet (HFD)-induced obese rats. Methods: pGL3-Enhancer-PPARγ2 (625 bp)-Luc plasmid, a luciferase reporter gene expression plasmid containing PPARγ2 promoter, was stably transfected into 3T3-L1 preadipocytes. PPARγ2 promoter activities were determined by assaying the luciferase activities. Then PPARγ2 promoter activities in preadipocytes and PPARγ2 mRNA levels in human subcutaneous adipocytes were measured after the administration with LLAE. Additionally, the effects of LLAE on body weight, fat mass, glucose and lipid metabolism and the expression of PPARγ2, insulin receptor substrate 1 and glucose transporter 4 (GLUT4) in visceral adipose tissue (VAT) were measured in HFD-induced obese rats treated with low or high dose [0.5 or 3.0 g crude drug/(kg.d)] LLAE for 6 weeks. Results: Ten μg/ml LLAE significantly increased the luciferase activities in 3T3-L1 cells and the stimulatory action reached 2.51 folds of controls when LLAE was 1000 μg/ml (P < 0.01). After treating 3T3-L1 cells with 100 μg/ml LLAE, the stimulatory role peaked at 32 h where it was 2.58 folds of controls (P < 0.01). Besides, 100 μg/ml LLAE significantly increased PPARγ2 mRNA levels in human adipocytes to 1.91 folds of controls (P < 0.01). In HFD-induced obese rats, administration with both low and high dose LLAE notably reduced visceral fat mass by 45.5 and 58.4%, respectively, and significantly decreased fasting serum insulin levels (P < 0.05). The high dose LLAE also significantly decreased homeostasis model assessment of insulin resistance in obese rats (P < 0.05). Furthermore, the mRNA levels of PPARγ2 and GLUT4 in VAT of obese rats were significantly increased when compared with control rats, and were notably suppressed by LLAE intervention for 6 weeks (P < 0.05). Conclusion: LLAE significantly reduces visceral fat mass and ameliorates insulin resistance in HFD-induced obese rats. These beneficial effects of LLAE may associate with its role in stimulating PPARγ2 expression in preadipocytes and subcutaneous adipocytes and suppressing PPARγ2 and GLUT4 expression in VAT.
| S-EPMC5481353 | biostudies-literature
Project description:The aim of this study was to explore the effects of Garcinia mangostana (mangosteen) and Curcuma longa independently and synergistically in modulating oxidative stress, dyslipidemia, and hyperglycemia commonly observed in high-fat diet-induced obesity in rodent models. Male albino Wistar rats were divided into eight experimental groups, fed on a normal diet or high-fat diet (HFD), then given mangosteen extract (400 mg /kg /day) and/or curcumin (80 mg/kg /day) for 6 weeks. Oxidative stress markers, glucose, and lipid fractions were measured in the sera. Mangosteen pericarp extract (MPE) induced a remarkable decrease in BMI (from 0.86 to 0.81 gm/cm2), while curcuma either alone or in combination was more effective, as treated rats recorded BMIs of 0.78 and 0.79 gm/cm2, respectively. Regarding the antioxidant effects, MPE induced a significant increase of GSH in obese rats (123.86 ± 15.53 μg/ml vs 288.72 ± 121.37 μg/ml). As anti-atherogenic agents MPE demonstrate significant effect recorded higher level of HDL-C in treated animals, but ineefective as anti-dyslipidemic agent. Curcumin was more effective in reducing LDL-C levels in obese rats. Both extracts effectively reduced blood glucose. The present study demonstrated that MPE and curcumin were independently and synergistically effective in treating obesity-induced atherogenesis.
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Project description:Adipose browning leads to increased energy expenditure and reduced adiposity and has, therefore, become an attractive therapeutic strategy for obesity. In this study, we elucidated the effect of green tea aqueous extract (GTAE) on the browning of inguinal white adipose tissue (Ing-WAT) and brown adipose tissue (BAT) in high-fat diet (HFD)-fed mice. The main phytochemical components identified in GTAE through high-performance liquid chromatography (HPLC) included (-)-gallocatechin, (-)-epigallocatechin, (-)-catechin, (-)-epigallocatechin-3-gallate, caffeine, (-)-epicatechin, (-)-gallocatechin gallate, and (-)-epicatechin-3-gallate. Daily supplementation with 1% GTAE for 12 weeks markedly reduced bodyweight gain, systemic inflammation, oxidative stress, and improved insulin resistance. Additionally, histological analysis revealed that dietary supplementation with 1% GTAE reversed HFD-induced adipocyte size and hepatic steatosis. These effects were associated with activation of browning in the Ing-WAT and BAT, which mediate systemic metabolic dysfunction in HFD-fed mice. Taken together, our data support the use of GTAE, a natural product, for the attenuation of obesity through the activation of fat browning.
| S-EPMC8645728 | biostudies-literature
Project description:Cranberry (Vaccinium macrocarpon) consumption has been associated with health beneficial effects. Nonalcoholic fatty liver disease (NAFLD) is a comorbidity of obesity. In the present study, we investigated the effect of a polyphenol-rich cranberry extract (CBE) on hepatic inflammation in high fat (HF)-fed obese C57BL/6J mice. Following dietary treatment with 0.8% CBE for 10 weeks, we observed no change in body weight or visceral fat mass in CBE-supplemented mice compared to HF-fed control mice. We did observe a significant decrease in plasma alanine aminotransferase (31%) and histological severity of NAFLD (33% decrease in area of involvement, 29% decrease in lipid droplet size) compared to HF-fed controls. Hepatic protein levels of tumor necrosis factor ? and C-C chemokine ligand 2 were reduced by 28% and 19%, respectively, following CBE supplementation. CBE significantly decreased hepatic mRNA levels of toll-like receptor 4 (TLR4, 63%) and nuclear factor ?B (NF?B, 24%), as well as a number of genes related to the nucleotide-binding domain, leucine-rich-containing family, pyrin domain-containing 3 inflammasome. In conclusion, CBE reduced NAFLD and hepatic inflammation in HF-fed obese C57BL/6J mice. These effects appear to be related to mitigation of TLR4-NF?B related signaling; however, further studies into the underlying mechanisms of these hepatoprotective effects are needed.
| S-EPMC5228292 | biostudies-literature
Project description:Background: The damage to intestinal barrier function plays an important role in the development of obesity and associated diseases. Soy isoflavones are effective natural active components for controlling obesity and reducing the level of blood lipid. Here, we explored whether these effects of soy isoflavones were associated with the intestinal barrier function. Methods and Results: The obese rat models were established by high fat diet feeding. Then, those obese rats were supplemented with soy isoflavones at different doses for 4 weeks. Our results showed that obesity induced the expressions of pro-inflammatory cytokines, decreased the anti-inflammatory cytokine (IL-10) expression, elevated intestinal permeability, altered gut microbiota and exacerbated oxidative damages in colon. The administration of soy isoflavones reversed these changes in obese rats, presenting as the improvement of intestinal immune function and permeability, attenuation of oxidative damage, increase in the fraction of beneficial bacteria producing short-chain fatty acids and short-chain fatty acid production, and reduction in harmful bacteria. Furthermore, soy isoflavones blocked the expressions of TLR4 and NF-κB in the colons of the obese rats. Conclusions: Soy isoflavones could improve obesity through the attenuation of intestinal oxidative stress, recovery of immune and mucosal barrier, as well as re-balance of intestinal gut microbiota.
| S-EPMC6470843 | biostudies-other
Project description:ObjectiveExcess visceral fat accumulation is associated with the metabolic disturbances of obesity. Differential lipid redistribution through lipoproteins may affect body fat distribution. This is the first study to investigate VLDL-triglyceride (VLDL-TG) storage in visceral fat.Research design and methodsNine upper-body obese (UBO; waist circumference >88 cm) and six lean (waist circumference <80 cm) women scheduled for elective tubal ligation surgery were studied. VLDL-TG storage in visceral, upper-body subcutaneous (UBSQ), and lower-body subcutaneous (LBSQ) fat were measured with [9,10-(3)H]-triolein-labeled VLDL.ResultsVLDL-TG storage in visceral fat accounted for only ~0.8% of VLDL-TG turnover in UBO and lean women, respectively. A significantly larger proportion of VLDL-TG turnover was stored in UBSQ (~5%) and LBSQ (~4%) fat. The VLDL-TG fractional storage was similar in UBO and lean women for all regional depots. VLDL-TG fractional storage and VLDL-TG concentration were correlated in UBO women in UBSQ fat (r = 0.68, P = 0.04), whereas an inverse association was observed for lean women in visceral (r = -0.89, P = 0.02) and LBSQ (r = -0.87, P = 0.02) fat.ConclusionsVLDL-TG storage efficiency is similar in all regional fat depots, and trafficking of VLDL-TG into different adipose tissue depots is similar in UBO and lean women. Postabsorptive VLDL-TG storage is unlikely to be of major importance in the development of preferential upper-body fat distribution in obese women.
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Project description:BackgroundVisceral obesity and related diabetes is reaching epidemic proportions in the United Arab Emirates (UAE). Adiponectin is a hormone that is secreted by adipose tissue and may play an important role in obesity-related morbidity. The aim of this study was to investigate total adiponectin levels in overweight and obese UAE subjects visiting health care facilities for weight management.MethodsAll overweight and obese subjects visiting community health centers were invited to take part in the study. Two hundred and six participants received individualized structured dietary education for weight management. Demographic data, anthropometric measurements and fasting venous blood samples were taken for measurements of total adiponectin and markers of inflammation and nutritional status at baseline and follow up. Multivariate analysis was performed to determine the independent effects of prognostic factors on serum adiponectin levels.ResultsA total of 193 (93%) females with a mean age (±SD) 36 ± 11 years were included in the analysis. During a follow up period of 427 ± 223 days, participants received 13 ± 5 structured dietary education sessions. We observed decreased levels of total adiponectin with increasing quartiles of both waist circumference (WC) and body mass index (BMI). Male gender and history of both gestational and type 2 diabetes were associated with significantly lower total adiponectin levels (p < 0.05). After adjusting for age, gender, BMI and hip circumference, multiple regression analysis revealed a significant and independent association between waist circumference and total adiponectin levels. At follow up visceral fat loss was associated with a significant decrease in inflammatory markers and a non-significant increase in total adiponectin levels.ConclusionIncreased visceral fat in overweight and obese subjects is associated with decreased total adiponectin levels. The health benefits of increasing adiponectin levels using different dietary intervention strategies need to be explored in larger studies.Trial registrationNCT01691365 , registered on 11/09/2012.
| S-EPMC6545728 | biostudies-literature
Project description:BackgroundType 2 diabetes (T2D) and obesity are associated with nonalcoholic fatty liver disease, cardiomyopathy, and cardiovascular mortality. Both show stronger links between ectopic and visceral fat deposition, and an increased cardiometabolic risk compared with subcutaneous fat.ObjectivesThis study investigated whether lean patients (Ln) with T2D exhibit increased ectopic and visceral fat deposition and whether these are linked to cardiac and hepatic changes.MethodsTwenty-seven obese patients (Ob) with T2D, 15 Ln-T2D, and 12 normal-weight control subjects were studied. Subjects underwent cardiac computed tomography, cardiac magnetic resonance imaging (MRI), proton and phosphorus MR spectroscopy, and multiparametric liver MR, including hepatic proton MRS, T1- and T2*-mapping yielding "iron-corrected T1" [cT1].ResultsDiabetes, with or without obesity, was associated with increased myocardial triglyceride content (p = 0.01), increased hepatic triglyceride content (p = 0.04), and impaired myocardial energetics (p = 0.04). Although cardiac structural changes, steatosis, and energetics were similar between the T2D groups, epicardial fat (p = 0.04), hepatic triglyceride (p = 0.01), and insulin resistance (p = 0.03) were higher in Ob-T2D. Epicardial fat, hepatic triglyceride, and insulin resistance correlated negatively with systolic strain and diastolic strain rates, which were only significantly impaired in Ob-T2D (p < 0.001 and p = 0.006, respectively). Fibroinflammatory liver disease (elevated cT1) was only evident in Ob-T2D patients. cT1 correlated with hepatic and epicardial fat (p < 0.001 and p = 0.01, respectively).ConclusionsIrrespective of body mass index, diabetes is related to significant abnormalities in cardiac structure, energetics, and cardiac and hepatic steatosis. Obese patients with T2D show a greater propensity for ectopic and visceral fat deposition.
| S-EPMC4925621 | biostudies-literature
Project description:To investigate the effects of soy protein isolate (SPI) on Wnt/?-catenin signaling in the liver of obese rats, as well as the roles of this pathway in regulating the hepatic fat accumulation.Obese and lean Zucker rats were fed diets containing either casein or SPI as protein source for 17 weeks. Histology and biochemical analysis, real-time PCR, Western blot, immunostaining, short interfering RNA assay were performed for liver samples.Our study showed that fat content was significantly lowered in the liver of SPI-fed obese rats, accompanied by a reduction in hepatocellular vacuolation, compared to the casein-fed control. ?-Catenin protein level in the liver of obese rats was downregulated compared to the lean group, indicating that the obese genotype exhibits an overall reduction in Wnt signaling. Importantly the repression of ?-catenin in the obese rats was alleviated by feeding the SPI diet. siRNA treatment in rat hepatoma cells confirmed that silencing of ?-catenin exacerbated fatty acid-induced fat accumulation, which implicated an important function of Wnt/?-catenin signaling in hepatic fat metabolism.SPI intake restored ?-catenin signaling and alleviated hepatic fat accumulation and liver damage in the obese rats.
| S-EPMC3690171 | biostudies-literature
Project description:BackgroundGarcinia subelliptica Merr. is a multipurpose coastal tree, the potential medicinal effects of which have been studied, including cancer suppression. Here, we present evidence that the ethanol extract of G. subelliptica Merr. (eGSM) induces autophagy in human lung adenocarcinoma cells.MethodsTwo different human lung adenocarcinoma cell lines, A549 and SNU2292, were treated with varying amounts of eGSM. Cytotoxicity elicited by eGSM was assessed by MTT assay and PARP degradation. Autophagy in A549 and SNU2292 was determined by western blotting for AMPK, mTOR, ULK1, and LC3. Genetic deletion of AMPKα in HEK293 cells was carried out by CRISPR.ResultseGSM elicited cytotoxicity, but not apoptosis, in A549 and SNU2292 cells. eGSM increased LC3-II production in both A549 and, more extensively, SNU2292, suggesting that eGSM induces autophagy. In A549, eGSM activated AMPK, an essential autophagy activator, but not suppressed mTOR, an autophagy blocker, suggesting that eGSM induces autophagy by primarily activating the AMPK pathway in A549. By contrast, eGSM suppressed mTOR activity without activating AMPK in SNU2292, suggesting that eGSM induces autophagy by mainly suppressing mTOR in SNU2292. In HEK293 cells lacking AMPKα expression, eGSM increased LC3-II production, confirming that the autophagy induced by eGSM can occur without the AMPK pathway.ConclusionOur findings suggest that eGSM induces autophagy by activating AMPK or suppressing mTOR pathways, depending on cell types.
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