scholarly journals Anthocyanins from black wolfberry (Lycium ruthenicum Murr.) prevent inflammation and increase fecal fatty acid in diet-induced obese rats

RSC Advances ◽  
2017 ◽  
Vol 7 (75) ◽  
pp. 47848-47853 ◽  
Author(s):  
Jinjin Yin ◽  
Tao Wu

This study aimed to determine whether black wolfberry (Lycium ruthenicumMurr.) anthocyanin (BWA) consumption can alleviate oxidative stress and reduce inflammation in high-fat diet-induced obese male Sprague-Dawley rats.

2021 ◽  
Author(s):  
Minchun Zhang ◽  
Jie Chen ◽  
Minglan Yang ◽  
Cheng Qian ◽  
Yu Liu ◽  
...  

Abstract Background: Artificial sweeteners (AS) are widely used as sugar substitutes to reduce calorie intake. However, high doses of AS induced glucose tolerance by modulating gut microbiota. The objective of this study was to investigate the effects of lower doses of sucralose on fecal microbiota in obesity. Methods: Eight weeks after high-fat diet, the male Sprague Dawley rats were randomly divided into four groups (n=24) and administrated by a daily gavage of 2ml normal saline (CON), 0.54mM sucralose (N054), 0.78mM sucralose (N078) and 324mM sucrose (S324) respectively. After four weeks, fecal samples were obtained and used in 16S ribosomal RNA gene sequencing. Results: The richness and diversity of fecal microbiota did not change by these sucralose and sucrose dosage. Both 0.54mM (0.43mg) and 0.78mM (0.62mg) tended to reduce the beneficial bacteria, Lactobacillaceae and Akkermansiaceae. The relative abundance of family Acidaminoccaceae and its genus Phascolarctobacteriam were increased with 0.54mM sucralose. In functional prediction, 0.54mM sucralose increased profiles of carbohydrate metabolism, whereas 0.78 mM sucralose enhanced that of amino acids metabolism. Conclusions: The lower doses of sucralose altered the compositions and the metabolic functions of fecal microbiota. The benefits of sucralose and its recommended dose for obese patients should be reassessed comprehensively.


2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
C. Neves ◽  
T. Rodrigues ◽  
J. Sereno ◽  
C. Simões ◽  
J. Castelhano ◽  
...  

Nonalcoholic fatty liver disease (NAFLD) is caused by excessive liver lipid accumulation, but insulin resistance is specifically associated with impaired lipid saturation, oxidation, and storage (esterification), besides increased de novo lipogenesis. We hypothesized that dietary glycotoxins could impair hepatic lipid metabolism in obesity contributing to lipotoxicity-driven insulin resistance and thus to the onset of nonalcoholic steatohepatitis (NASH). In diet-induced obese rats with methylglyoxal-induced glycation, magnetic resonance spectroscopy, mass spectrometry, and gas chromatography were used to assess liver composition in fatty acyl chains and phospholipids. High-fat diet-induced obesity increased liver lipid fraction and suppressed de novo lipogenesis but did not change fatty acid esterification and saturation or insulin sensitivity. Despite a similar increase in total lipid fraction when supplementing the high-fat diet with dietary glycotoxins, impairment in the suppression of de novo lipogenesis and decreased fatty acid unsaturation and esterification were observed. Moreover, glycotoxins also decreased polyunsaturated cardiolipins and caused oxidative stress, portal inflammation, and insulin resistance in high-fat diet-induced obese rats. Dietary glycated products do not change total lipid levels in the liver of obese rats but dramatically modify the lipidemic profile, leading to oxidative stress, hepatic lipotoxicity, and insulin resistance in obesity and thus contribute to the onset of NASH.


2014 ◽  
Vol 112 (4) ◽  
pp. 477-485 ◽  
Author(s):  
Xiaowei Sun ◽  
Rennan Feng ◽  
Yanchuan Li ◽  
Song Lin ◽  
Wei Zhang ◽  
...  

Obesity is considered to be accompanied by a chronic low-grade inflammatory state that contributes to the occurrence of many chronic diseases. Our previous study has demonstrated that histidine supplementation significantly ameliorates inflammation and oxidative stress in obese women. However, the in vivo potential mechanisms are not known. The present study was conducted to investigate the mechanisms underlying the effects of histidine on inflammation in a high-fat diet (HFD)-induced female obese rat model. An obese model was established in female Sprague–Dawley rats by HFD feeding for 8 weeks and followed by histidine supplementation for another 4 weeks. The results revealed that HFD-increased body weight and HFD-lowered serum histidine concentrations were significantly reversed by histidine supplementation (P< 0·05). In addition, the serum concentrations of TNF-α, IL-6, C-reactive protein (CRP) and malondialdehyde were significantly reduced and those of superoxide dismutase (SOD) were significantly increased by histidine supplementation when compared with those in obese rats (P< 0·05). Correspondingly, the mRNA expressions of TNF-α, IL-6 and CRP in the adipose tissue were significantly down-regulated and that of CuZnSOD was significantly up-regulated by histidine supplementation (P< 0·05). Histidine supplementation significantly reduced the HFD-induced translocation of NF-κB p65 into the nucleus (P= 0·032) by reducing the phosphorylation of the inhibitor of κBα in the adipose tissue. The results also revealed that the expression of adiponectin was markedly increased both in the serum and in the adipose tissue after histidine supplementation, accompanied by the activation of PPARγ (P= 0·021). These findings indicate that histidine is an effective candidate for ameliorating inflammation and oxidative stress in obese individuals via the NF-κB- and PPARγ-involved pathways.


2021 ◽  
Vol 8 ◽  
Author(s):  
Minchun Zhang ◽  
Jie Chen ◽  
Minglan Yang ◽  
Cheng Qian ◽  
Yu Liu ◽  
...  

Artificial sweeteners (AS) have been widely used as sugar substitutes to reduce calorie intake. However, it was reported that high doses of AS induced glucose intolerance via modulating gut microbiota. The objective of this study was to investigate the effects of lower doses of sucralose on fecal microbiota in obesity. Eight weeks after high-fat diet (HFD), the male Sprague Dawley rats were randomly divided into four groups (6 in each group) and administrated by a daily gavage of 2 ml normal saline (CON), 0.54 mM sucralose (N054), 0.78 mM sucralose (N078), and 324 mM sucrose (S324), respectively. After 4 weeks, fecal samples were obtained and analyzed by 16S ribosomal RNA gene sequencing. The richness and diversity of fecal microbiota were not changed by sucralose or sucrose. Both 0.54 mM (0.43 mg) and 0.78 mM (0.62 mg) sucralose tended to reduce the beneficial bacteria, Lactobacillaceae and Akkermansiaceae. The relative abundance of family Acidaminoccaceae and its genus Phascolarctobacteriam were increased after 0.54 mM sucralose. In functional prediction, 0.54 mM sucralose increased profiles of carbohydrate metabolism, whereas 0.78 mM sucralose enhanced those of amino acid metabolism. The lower doses of sucralose might alter the compositions of fecal microbiota. The effects of sucralose in different dosages should be considered in the future study.


2020 ◽  
Vol 18 (2) ◽  
Author(s):  
Othman ZA ◽  
Wan ghazali WS ◽  
Noordin L ◽  
Omar N ◽  
Mohd. Yusof NA ◽  
...  

Introduction: Orlistat is a widely used drug in treating obesity as it promotes weight reduction. The aim of this study was to determine the protective effects of orlistat (10 mg/kg/day) on cardiovascular parameters and oxidative stress biomarkers in high-fat diet (HFD)-induced obese rats. Methods: Twenty-four male rats Sprague Dawley rats were divided into three groups and fed with normal diet (N), HFD and HFD with orlistat (HFD+O). Orlistat was administered daily by oral gavage and after six weeks, all rats were sacrificed. Results: Administration of orlistat along with HFD (HFD+O) has brought significant decreases in Lee obesity index and LDL level compared to HFD group. Activities of cardiac superoxide dismutase (SOD), glutathione peroxidase (GPx) and catalase (CAT) were significantly higher, whereas level of oxidised LDL was significantly lower in HFD+O group compared to HFD group. HFD group had significantly higher necrotic patch area in myocardium while minimal histological changes were seen in HFD+O group. Conclusion: This study may suggest that administration of orlistat at 10 mg/kg/day for 6 weeks may have protective effects against the changes on Lee obesity index, lipid profiles, cardiac oxidative stress biomarkers and histology of myocardium in HFD-induced obese rats possibly through its hypolipidaemic and antioxidant actions.


2017 ◽  
Vol 41 (2) ◽  
pp. 598-608 ◽  
Author(s):  
Xiangrong Cui ◽  
Chunlan Long ◽  
Jing Zhu ◽  
Jie Tian

Background: Statins can reduce reproductive damage induced by obesity or high-fat diet (HFD), but the specific regulatory mechanisms are largely unknown. Since mTOR/p70s6k sinaling promotes spermatogonia proliferation and spermatogenesis, we hypothesized that this pathway will be involved in the protective effects of statin in HFD-induced reproductive dysfunction. Methods: Male Sprague Dawley rats (3 weeks old) were randomly divided into a control group (standard diet), HFD group, and a fluvastatin group (HFD + fluvastatin at 6mg/kg, once daily by oral gavage). After 8 weeks, body weight was obtain and rats were sacrificed. Weights of the testes, gross morphology, sperm parameters, circulating levels of sex hormones, lipid levels, and tissue mTOR, p-P70s6k were measured. Another set of male rats were treated with rapamycin or vehicle. Flow cytometry was used to detect the spermatogonia marker c-kit and cell cycle. p-P70s6k expression was analyzed by Western blot. Results: HFD not only results in rat obesity but also leads to spermatogenetic damage and fluvastatin was able to partially block the effects of HFD. Fluvastatin also partially reversed the suppression of mTOR and p-p70s6k expresson. Conclusion: Our data suggest that fluvastatin has protective effects on reproductive function in obese male rats most probably through enhanced signaling of mTOR.


1957 ◽  
Vol 191 (2) ◽  
pp. 371-376 ◽  
Author(s):  
Paul D. Altland ◽  
Olaf Mickelsen ◽  
Benjamin Highman

Osborne-Mendel rats became obese when fed a high fat diet for 6–15 months. Obese rats and stock-fed rats were exposed 6 1/2 hours a day, 5 days a week to 18,000 or 25,000 feet simulated altitude for from 4 to 6 months. Both groups of rats developed the same degree of polycythemia and had the same mortality rate. The obese rats lost more weight from altitude exposure and also showed a slightly higher incidence of cardiovalvular thickening and cardiac vegetations, particularly among those that died. The mean heart weight of unexposed obese rats was 50% greater than that of stock-fed rats; the heart weights of both groups increased about 70% following 191 days of exposure. In acute altitude tests at 33,500 feet simulated altitude, both Osborne-Mendel and Sprague-Dawley rats on the high-fat diet, irrespective of the degree of obesity, died within 86 minutes. Sixty per cent of the stock-fed rats survived for a longer period. Some of the heaviest Osborne-Mendel rats on the high-fat diet died within 3 minutes at this altitude. Preoxygenation prevented these early deaths, but neither preoxygenation nor a slow rate of ascent (500 ft/min) had any effect on the high mortality of rats on a high-fat diet exposed to altitude.


2018 ◽  
Vol 5 ◽  
Author(s):  
Alexis Panny Y. S. Chung ◽  
Sunil Gurtu ◽  
Srikumar Chakravarthi ◽  
Mohanambal Moorthy ◽  
Uma D. Palanisamy

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