scholarly journals Effectiveness of Bioactive Food Components in Experimental Colon Carcinogenesis

2009 ◽  
Vol 78 (4) ◽  
pp. 661-666 ◽  
Author(s):  
Emília Hijová ◽  
Anna Chmelárová ◽  
Alojz Bomba

The aim of the present study was the evaluation of possible protective effects of selected bioactive food components in experimental N,N-dimethylhydrazine (DMH)-induced colon carcinogenesis. Wistar albino rats (n = 92) were fed a high fat diet or conventional laboratory diet. Two weeks after the beginning of the trial, DMH injections were given to six groups of rats at the dose of 20 mg/kg b.w. twice weekly. The activity of bacterial enzymes in faeces and serum bile acid concentrations were determined. High fat diet, DMH injections, and their combination significantly increased the activies of β-galactosidase, β-glucuronidase, and α-glucosidase (p < 0.001) compared to the control group of rats. Treatment with the prebiotic inulin, Hyppocastani extractum siccum and Lini oleum virginale significantly decreased the activity of β-galactosidase, β-glucuronidase, and α-glucosidase (p < 0.001), as well as the bile acid concentration compared to the group at the highest risk. The protective effects of selected bioactive food components in experimentally induced colon carcinogenesis allow for their possible use in cancer prevention or treatment.

Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1353
Author(s):  
Ji Hyun Kim ◽  
Sanghyun Lee ◽  
Eun Ju Cho

Obesity increases risk of Alzheimer’s Disease (AD). A high fat diet (HFD) can lead to amyloidosis and amyloid beta (Aβ) accumulation, which are hallmarks of AD. In this study, protective effects of the ethyl acetate fraction of Acer okamotoanum (EAO) and isoquercitrin were evaluated on obesity and amyloidosis in the HFD- and Aβ-induced mouse model. To induce obesity and AD by HFD and Aβ, mice were provided with HFD for 10 weeks and were intracerebroventricularly injected with Aβ25–35. For four weeks, 100 and 10 mg/kg/day of EAO and isoquercitrin, respectively, were administered orally. Administration of EAO and isoquercitrin significantly decreased body weight in HFD and Aβ-injected mice. Additionally, EAO- and isoquercitrin-administered groups attenuated abnormal adipokines release via a decrease in leptin and an increase in adiponectin levels compared with the control group. Furthermore, HFD and Aβ-injected mice had damaged liver tissues, but EAO- and isoquercitrin-administered groups attenuated liver damage. Moreover, administration of EAO and isoquercitrin groups down-regulated amyloidosis-related proteins in the brain such as β-secretase, presenilin (PS)-1 and PS-2 compared with HFD and Aβ-injected mice. This study indicated that EAO and isoquercitrin attenuated HFD and Aβ-induced obesity and amyloidosis, suggesting that they could be effective in preventing and treating both obesity and AD.


2019 ◽  
Vol 17 (2) ◽  
pp. 89 ◽  
Author(s):  
Saeed Mirzaee ◽  
Mohammad Ehsan Bayatpoor ◽  
Shima Shahyad ◽  
Mohammad Taghi Mohammadi ◽  
Zahra Bahari

Background: Male hypogonadism is associated with type II diabetes mellitus due totesticular dysfunction. Medicinal plants have received considerable attention for themanagement of diabetes and its complications.Objective: The aim of present study was to evaluate the anti-diabetic and protectiveinfluence of Crocin on testopathy in diabetic rats.Materials and Methods: In this experimental study, type II of diabetes mellitus wasinduced by high-fat diet and low dose of streptozotocin. Male Wistar rats (8 weeks,150–200 gr, 18 rats; n= 6 per group) were divided into a control group (standarddiet), diabetic group (streptozotocin+high-fat diet), and treatment group (High-fatdiet+streptozotocin+Crocin at 20 mg/kg/day, i.p. for 60 days). After 60 days, animalswere euthanized, testis and epididymis were dissected, and weights of testes andsperm count were analyzed. Hematoxylin-eosin-stained was done for histopathologicalexamination. Blood samples were collected for the assessment of serum glucose andcholesterol.Results: High-fat diet and streptozotocin significantly increased the serum glucoseand cholesterol levels as compared to the control group (p≤ 0. 001). Moreover, therewas a significant decrease in the weight of right (p= 0.008) and left testes (p≤ 0. 001)and also the total sperm count (p= 0.023) in the diabetic group compared with thecontrol


Author(s):  
Hui-Li Lin ◽  
Pei-Wen Cheng ◽  
Yi-Chen Tu ◽  
Bor-Chun Yeh ◽  
Bin-Nan Wu ◽  
...  

Abstract Objectives Eugenosedin-A (Eu-A), an adrenergic and serotonergic antagonist, is known to have anti-metabolic syndrome effects. In this study, we evaluated its protective effects against diabetes mellitus (DM) in spontaneous hypertensive rats (SHR) and compared it with two anti-diabetes medications, glibenclamide (Gli) and pioglitazone (Pio). Methods We divided 10-week-old SHRs into five groups: a control group fed a normal diet; an untreated DM group induced by injecting the SHRs with STZ/NA and feeding them a high-fat diet (HFD); and three treated groups (after giving STZ/NA and HFD) gavage given with Eu-A, Gli or Pio (5 mg/kg per day) for 4 weeks. Key findings The untreated DM group weighed less and had hyperglycaemia, hypoinsulinemia and hyperlipidemia. They were also found to have aberrant glucose-dependent insulin pathways, glucose metabolism and lipid synthesis proteins, while the controls did not. Eu-A, Gli and Pio ameliorated the above biochemical parameters in the treatment groups. Eu-A and Pio, but not Gli, improved hypertension and tachycardia. Conclusions Taken together, Eu-A ameliorated DM, hypertension and tachycardia by improving glucose, lipid homeostasis and anti-adrenergic, serotonergic activities. We concluded that Eu-A could be used in the development of an effective agent for controlling DM and its complications.


2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Jian Li ◽  
Zezhou Liu ◽  
Mingxing Guo ◽  
Kejia Xu ◽  
Miao Jiang ◽  
...  

Objective. Berberine has been used to treat nonalcoholic steatohepatitis (NASH), which has been addressed in many studies. In this study, we investigated the molecular pharmacology mechanisms of berberine using metabolomic techniques.Methods. Sprague-Dawley rats were randomly divided into three groups (10 rats in each group): (i) normal control group; (ii) high-fat diet- (HFD-) induced NASH model group; and (iii) HFD berberine-treated group (i.d. 200 mg/kg). The handling procedure lasted eight weeks. Then, UPLC-Q-TOF/MS techniques coupled with histopathology and biochemical analyses were adopted to explore the mechanisms of berberine on the protective effects against NASH.Key Findings. (i) According to conventional test results, berberine treatment plays a fighting role in HFD-induced NASH due to its beneficial effects against insulin resistance, inflammation, and lipid metabolism. (ii) Based on UPLC-Q-TOF/MS techniques, metabolic profiles that involved sphingomyelin (SM), phosphatidylcholine (PC), lysophosphatidylcholine (LysoPC), 13-hydroperoxy-9, 11-octadecadienoic acid (13-HpODE), eicosatrienoic acid, docosatrienoic acid, and eicosenoic acid could provide potential metabolic biomarkers to address the pharmacological mechanisms of berberine.Conclusions. The parts of molecular pharmacological mechanisms of berberine for NASH treatment are related to the regulation of metabolic disruption involving phospholipid and unsaturated fatty acids in rats with NASH.


Background and Aims: Non-alcoholic fatty liver disease (NAFLD) is associated with such symptoms as steatosis, fibrosis, and liver cirrhosis. Kelussia has attracted assiduous attention due to its protective effects on the liver. The PNPLA3 gene is mainly expressed in the liver and plays a major role in the degradation rate of hepatic triglycerides. Therefore, the present study aimed to assess the effect of Kelussia extract on PNPLA3 gene expression in rats with fatty liver and healthy rats. Materials and Methods: This experimental study was conducted on 24 male Wistar rats in the control group (no treatment), obese group (which received a high-fat diet), treatment group 1 (which received a high-fat diet with Kelussia extract 400 mg/kg) and treatment group 2 (a high-fat diet with Kelussia extract 800 mg/kg) for six weeks. Blood samples were taken from rats and the factors of (LDL, HDL, Cholesterol, Triglyceride, and fasting sugar) were measured. After sampling the rat liver, the effect of Kelussia on PNPLA3 gene expression was investigated using the Real-time reverse transcription-polymerase chain reaction (RT-PCR) technique and analyzed in SPSS software (version 22). Results: Based on the results, Kelussia extract at a dose of 800 mg/kg resulted in a more dramatic decrease in PNPLA3 gene expression in rats with fatty liver, compared to a dose of 400 mg /kg, and this reduction was statistically significant, compared to the fatty liver group (P<0.05). The results of biochemical tests confirmed liver improvement in the rats treated with Kelussia extract at a dose of 800 mg/kg. Conclusion: It can be said that Kelussia had a beneficial effect on the reduction of blood lipids; moreover, it reduces the accumulation of triglycerides in the liver and improves the tissue structure of the liver by reducing the expression of PNPLA3 gene; therefore, with more studies, it can be considered a supplement to reduce blood lipids.


2016 ◽  
Vol 310 (6) ◽  
pp. G367-G375 ◽  
Author(s):  
Yasuki Higashimura ◽  
Yuji Naito ◽  
Tomohisa Takagi ◽  
Kazuhiko Uchiyama ◽  
Katsura Mizushima ◽  
...  

High-fat diet (HFD)-induced alteration in the gut microbial composition, known as dysbiosis, is increasingly recognized as a major risk factor for various diseases, including colon cancer. This report describes a comprehensive investigation of the effect of agaro-oligosaccharides (AGO) on HFD-induced gut dysbiosis, including alterations in short-chain fatty acid contents and bile acid metabolism in mice. C57BL/6N mice were fed a control diet or HFD, with or without AGO. Terminal restriction fragment-length polymorphism (T-RFLP) analysis produced their fecal microbiota profiles. Profiles of cecal organic acids and serum bile acids were determined, respectively, using HPLC and liquid chromatography-tandem mass spectrometry systems. T-RFLP analyses showed that an HFD changed the gut microbiota significantly. Changes in the microbiota composition induced by an HFD were characterized by a decrease in the order Lactobacillales and by an increase in the Clostridium subcluster XIVa. These changes of the microbiota community generated by HFD treatment were suppressed by AGO supplementation. As supported by the data of the proportion of Lactobacillales order, the concentration of lactic acid increased in the HFD + AGO group. Data from the serum bile acid profile showed that the level of deoxycholic acid, a carcinogenic secondary bile acid produced by gut bacteria, was increased in HFD-receiving mice. The upregulation tended to be suppressed by AGO supplementation. Finally, results show that AGO supplementation suppressed the azoxymethane-induced generation of aberrant crypt foci in the colon derived from HFD-treated mice. Our results suggest that oral intake of AGO prevents HFD-induced gut dysbiosis, thereby inhibiting colon carcinogenesis.


Gut ◽  
2017 ◽  
Vol 67 (10) ◽  
pp. 1881-1891 ◽  
Author(s):  
Na Jiao ◽  
Susan S Baker ◽  
Adrian Chapa-Rodriguez ◽  
Wensheng Liu ◽  
Colleen A Nugent ◽  
...  

ObjectiveBile acids are regulators of lipid and glucose metabolism, and modulate inflammation in the liver and other tissues. Primary bile acids such as cholic acid and chenodeoxycholic acid (CDCA) are produced in the liver, and converted into secondary bile acids such as deoxycholic acid (DCA) and lithocholic acid by gut microbiota. Here we investigated the possible roles of bile acids in non-alcoholic fatty liver disease (NAFLD) pathogenesis and the impact of the gut microbiome on bile acid signalling in NAFLD.DesignSerum bile acid levels and fibroblast growth factor 19 (FGF19), liver gene expression profiles and gut microbiome compositions were determined in patients with NAFLD, high-fat diet-fed rats and their controls.ResultsSerum concentrations of primary and secondary bile acids were increased in patients with NAFLD. In per cent, the farnesoid X receptor (FXR) antagonistic DCA was increased, while the agonistic CDCA was decreased in NAFLD. Increased mRNA expression for cytochrome P450 7A1, Na+-taurocholate cotransporting polypeptide and paraoxonase 1, no change in mRNA expression for small heterodimer partner and bile salt export pump, and reduced serum FGF19 were evidence of impaired FXR and fibroblast growth factor receptor 4 (FGFR4)-mediated signalling in NAFLD. Taurine and glycine metabolising bacteria were increased in the gut of patients with NAFLD, reflecting increased secondary bile acid production. Similar changes in liver gene expression and the gut microbiome were observed in high-fat diet-fed rats.ConclusionsThe serum bile acid profile, the hepatic gene expression pattern and the gut microbiome composition consistently support an elevated bile acid production in NAFLD. The increased proportion of FXR antagonistic bile acid explains, at least in part, the suppression of hepatic FXR-mediated and FGFR4-mediated signalling. Our study suggests that future NAFLD intervention may target the components of FXR signalling, including the bile acid converting gut microbiome.


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.


2015 ◽  
Vol 2015 ◽  
pp. 1-7 ◽  
Author(s):  
Warinda Susutlertpanya ◽  
Duangporn Werawatganon ◽  
Prasong Siriviriyakul ◽  
Naruemon Klaikeaw

Nonalcoholic steatohepatitis (NASH) has become a global chronic liver disease, but no effective medicine has been proven to cure it. This study investigated the protective effects of genistein, a phytoestrogen, on NASH and examined whether it has any effect on hepatic PPARγ. Male Sprague-Dawley rats were divided into four groups: control group fed ad libitum with standard rat diet, NASH group fed ad libitum with high-fat diet to induce NASH and NASH + Gen8 group and NASH + Gen16 group fed with high-fat diet plus intragastric administration of 8 or 16 mg/kg genistein once daily. After 6 weeks, liver samples were collected to determine MDA, TNF-α, PPARγ, and histopathology. The findings were that levels of hepatic MDA and TNF-αincreased in NASH group, but 16 mg/kg genistein reduced these levels significantly. Downregulation of hepatic PPARγwas observed in NASH group, but genistein significantly upregulated the expression of PPARγin both NASH + Gen groups. The histological appearance of liver in NASH group presented pathological features of steatohepatitis which were diminished in both NASH + Gen groups. The results suggest that genistein attenuates the liver histopathology of NASH with upregulation of hepatic PPARγ, reduction of oxidative stress, and inhibition of inflammatory cytokine.


Nutrients ◽  
2021 ◽  
Vol 13 (8) ◽  
pp. 2501
Author(s):  
Maihemuti Mijiti ◽  
Ryosuke Mori ◽  
Bingyu Huang ◽  
Kenichiro Tsukamoto ◽  
Keisuke Kiriyama ◽  
...  

Dietary protamine can ameliorate hyperlipidemia; however, the protamine-derived active peptide and its hypolipidemic mechanism of action are unclear. Here, we report the discovery of a novel anti-obesity and hypocholesterolemic peptide, RPR (Arg-Pro-Arg), derived from protamine in mice fed a high-fat diet for 50 days. Serum cholesterol levels were significantly lower in the protamine and RPR groups than in the control group. White adipose tissue weight was significantly decreased in the protamine and RPR groups. The fecal excretion of cholesterol and bile acid was significantly higher in the protamine and RPR groups than in the control group. We also observed a significant decrease in the expression of hepatic SCD1, SREBP1, and adipocyte FAS mRNA, and significantly increased expression of hepatic PPARα and adipocyte PPARγ1 mRNA in the protamine group. These findings demonstrate that the anti-obesity effects of protamine are linked to the upregulation of adipocyte PPARγ1 and hepatic PPARα and the downregulation of hepatic SCD1 via SREBP1 and adipocyte FAS. RPR derived from protamine has a crucial role in the anti-obesity action of protamine by evaluating the effective dose of adipose tissue weight loss.


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