scholarly journals P0997BLUEBERRY JUICE IMPROVED THE METABOLIC PROFILE IN A PREDIABETIC RAT MODEL INDUCED BY A HYPERCALORIC DIET WITHOUT RENOPROTECTION

2020 ◽  
Vol 35 (Supplement_3) ◽  
Author(s):  
André Alves ◽  
Inês Preguiça ◽  
Adelaide Barbosa ◽  
Pedro Vieira ◽  
Diana Martins ◽  
...  

Abstract Background and Aims Blueberries (BB), due to their enriched content in polyphenolics and in other compounds with potential cytoprotective properties, have been associated with beneficial effects in distinct cardiometabolic conditions. The goal of this study was to evaluate the metabolic and renal effects of long-term blueberry juice (BJ) treatment in a rat model of prediabetes induced by a hypercaloric diet. Method Prediabetes was developed in adult male Wistar rats through the ingestion of high-sucrose (35% HSu) and high-fat (60% HF) diets during 23 wks (HSuHF animals, n=16). After 9 weeks, half of the former rats received BJ orally (25g/kg BW, HSuHF+BJ group). Control animals (n=8) received standard diet during the entire protocol. Glycemic, lipidic and insulinemic profiles were evaluated throughout the protocol, as well as gut microbiota composition, gut barrier permeability, endotoxemia (LPS) and inflammation (hs-CRP). Renal function was assessed by using serum and urinary measures of creatinine, uric acid and blood urea nitrogen and calculating the glomerular filtration rate (GFR). Histological characterization of the kidney was performed by H&E and lipid deposition by Oil Red O staining and quantification of triglycerides. Serum and renal tissue inflammatory markers were evaluated by Elisa (hs-CRP) and by RT-qPCR and/or WB (IL-6, TNF-α, iNOS, MMP2, TLR-4 and RAGE). The study was approved by the local animal welfare body (Ref: 9-2018). Values are presented as means ± S.E.M. and possible differences evaluated by ANOVA/post-hoc tests. Results While no major changes between groups were found for gut microbiota, gut barrier and endotoxemia/inflammation, BJ treatment was able to ameliorate hypercaloric diet-induced glucose intolerance, insulin insensitivity and plasma hypertriglyceridemia. In addition, in the HSuHF+BJ rats there was a trend to alleviate the reduction of GFR found in the HSuHF animals, as well as some early glomerular lesions, including mesangial expansion and basal membrane thickening. However, this nutraceutical intervention was unable to halt or slow down glomerular crescent-like lesions, renal lipidosis and the overexpression of renal IL-6 found in the HSuHF-treated animals. Conclusion Despite the metabolic improvement viewed by the amelioration of glucose intolerance, insulin insensitivity and hypertriglyceridemia, in this rat model of prediabetes a nutraceutical intervention with BJ presented very modest renoprotective effects. Acknowledgements: FEDER, COMPETE and FCT (CENTRO-01-0145-FEDER-000012-HealthyAging2020, UID/NEU/04539/2013, UID/NEU/04539/2019, POCI-01-0145-FEDER-007440, POCI-01-0145-FEDER-031712, PTDC/SAU-NUT/31712/2017 and SFRH/BD/109017/2015), as well as COAPE and MIRTILUSA.

2020 ◽  
Vol 2020 ◽  
pp. 1-19
Author(s):  
Jing Li ◽  
Jinfeng Han ◽  
Juan Lv ◽  
Shiji Wang ◽  
Lai Qu ◽  
...  

Objective. Severe acute pancreatitis (SAP) is a serious and life-threatening disease associated with multiple organ failure and a high mortality rate and is accompanied by distinct oxidative stress and inflammatory responses. Saikosaponin A has strong antioxidant properties and can affect the composition of gut microbiota. We sought to determine the effects of Saikosaponin A interventions on SAP by investigating the changes of gut microbiota and related antioxidant signaling. Methods. A SAP model was established in Sprague-Dawley (SD) rats through the injection of sodium taurocholate into the biliopancreatic duct and confirmed by elevated levels of serum lipase and amylase. The model was fed a standard diet either with saline solution or with Saikosaponin A. Fecal microbiota transplantation (FMT) from Saikosaponin A-induced rats into the rat model was performed to test the effects of gut microbiota. The composition of gut microbiota was analyzed by using 16S rRNA gene sequencing. We measured apoptotic status, inflammatory biomarkers, and Keap1-Nrf2-ARE ((Kelch-like ECH-associated protein 1) nuclear factor erythroid 2-related factor 2-antioxidant response element) antioxidant signaling. Results. Saikosaponin A intervention attenuated SAP lesions and reduced the levels of serum amylase and lipase, oxidative stress, and inflammatory responses by reducing pathological scores and affecting the serum level of oxidative and inflammatory factors. Meanwhile, the expression of Keap1-Nrf2-ARE was increased. Saikosaponin A intervention improved microbiota composition by increasing the relative abundance of Lactobacillus and Prevotella species. FMT resulted in similar results as those caused by the Saikosaponin A intervention, suggesting Saikosaponin A may exert its function via the improvement of gut microbiota composition. Conclusions. Saikosaponin A-induced gut microbiota changes attenuate SAP progression in the rat model and may be a potential natural drug for adjuvant treatment of SAP. Further work is needed to clear up the points.


2017 ◽  
Vol 8 (5) ◽  
pp. 823-831 ◽  
Author(s):  
R. Crescenzo ◽  
A. Mazzoli ◽  
R. Cancelliere ◽  
A. Bucci ◽  
G. Naclerio ◽  
...  

A well-established rat model of diet-induced metabolic syndrome was used to evaluate the effects of the oral administration of spores or cells of HU16, a carotenoid-producing strain of Bacillus indicus. Symptoms of metabolic syndrome were induced in 90-days old, male Sprague-Dawley rats maintained for eight weeks on a high-fat diet, as previously reported. Parallel groups of animals under the same diet regimen also received a daily dose of 1×1010 cells or spores of B. indicus HU16. Cells of strain HU16 were able to reduce symptoms of metabolic syndrome, plasma markers of inflammation and oxidative markers in plasma and liver to levels similar to those observed in rats under a standard diet. HU16 cells did not affect obesity markers or the accumulation of triglycerides in the liver of treated animals. Denaturing gradient gel electrophoresis analysis showed that the oral administration of HU16 cells did not significantly affect the gut microbiota of high fat-fed rats, suggesting that the observed beneficial effects are not due to a reshaping of the gut microbiota but rather to metabolites produced by HU16 cells.


2021 ◽  
Vol 31 (Supplement_2) ◽  
Author(s):  
S Nunes ◽  
S Viana ◽  
I Preguiça ◽  
A Alves ◽  
R Fernandes ◽  
...  

Abstract Background We previously described protective effects of blueberry juice (BJ) against hepatic steatosis evolution in a hypercaloric diet-induced rat model of prediabetes; however, the underlying mechanisms, are still scarcely explored. Herein, we aim to elucidate the molecular pathways underpinning BJ hepatoprotection on the dysmetabolism evolution in a rat model of prediabetes. Methods A rat model of evolutive prediabetes [Male Wistar rats, 8 weeks old] was developed by ingestion of a high-sucrose (HSu, 35%) diet for 9 weeks (W9), supplemented with a high-fat diet (HF, 60%) for further 14 weeks (HSuHF, W23), vs control with standard diet. Half of the animals (n = 10/group) daily received BJ (25g/Kg BW, orally) between W9 and W23. Along with metabolic characterization, BJ effects on serum and hepatic metabolic surrogates were elucidated using a 1H NMR based metabolomic approach. Moreover, the liver expression of genes (RT-PCR) involved in insulin signaling, lipid metabolism, inflammatory response and mitochondrial respiration was also explored. Values are means ± S.E.M (ANOVA followed by post-hoc tests). Results HSuHF+BJ rats restored hepatic levels of betaine and tend to recover the depletion of glutathione content found in HSuHF animals’ livers. Moreover, BJ positively affected the hepatic mRNA expression of key enzymes and mediators involved in fatty acid oxidation, insulin signalling, inflammatory response, as well as mitochondrial respiratory chain-related genes, which were all downregulated (P < 0.05) in HSuHF animals’ livers. Conclusions Altogether, these molecular findings contribute to explain the mechanisms by which BJ elicits protection against hepatic steatosis and mitochondrial dysfunction induced by hypercaloric diets in the frame of prediabetes evolution.


Nutrients ◽  
2021 ◽  
Vol 13 (12) ◽  
pp. 4192
Author(s):  
Sara Nunes ◽  
Sofia D. Viana ◽  
Inês Preguiça ◽  
André Alves ◽  
Rosa Fernandes ◽  
...  

The paramount importance of a healthy diet in the prevention of type 2 diabetes is now well recognized. Blueberries (BBs) have been described as attractive functional fruits for this purpose. This study aimed to elucidate the cellular and molecular mechanisms pertaining to the protective impact of blueberry juice (BJ) on prediabetes. Using a hypercaloric diet-induced prediabetic rat model, we evaluated the effects of BJ on glucose, insulin, and lipid profiles; gut microbiota composition; intestinal barrier integrity; and metabolic endotoxemia, as well as on hepatic metabolic surrogates, including several related to mitochondria bioenergetics. BJ supplementation for 14 weeks counteracted diet-evoked metabolic deregulation, improving glucose tolerance, insulin sensitivity, and hypertriglyceridemia, along with systemic and hepatic antioxidant properties, without a significant impact on the gut microbiota composition and related mechanisms. In addition, BJ treatment effectively alleviated hepatic steatosis and mitochondrial dysfunction observed in the prediabetic animals, as suggested by the amelioration of bioenergetics parameters and key targets of inflammation, insulin signaling, ketogenesis, and fatty acids oxidation. In conclusion, the beneficial metabolic impact of BJ in prediabetes may be mainly explained by the rescue of hepatic mitochondrial bioenergetics. These findings pave the way to support the use of BJ in prediabetes to prevent diabetes and its complications.


2021 ◽  
Author(s):  
Aoxiang Zhuge ◽  
Shengjie Li ◽  
Yin Yuan ◽  
Bo Li ◽  
Lanjuan Li

L. salivarius LI01 and B. longum TC01 synergize in liver injury via altering gut microbiota and protecting gut barrier.


Nanoscale ◽  
2021 ◽  
Author(s):  
Jiyan Qiao ◽  
Rui Chen ◽  
Mengjie Wang ◽  
Ru Bai ◽  
Xuejing Cui ◽  
...  

Exposure to micro/nanoplastics (M/NPLs) deteriorates the intestinal barrier by disturbing the bacterial composition in the gut.


2019 ◽  
Vol 52 ◽  
pp. 516-528 ◽  
Author(s):  
Baoming Tian ◽  
Jianhua Zhao ◽  
Wei An ◽  
Jiawei Zhang ◽  
Xin Cao ◽  
...  

2021 ◽  
Vol 11 (1) ◽  
Author(s):  
Yue Hu ◽  
Fang Chen ◽  
Haiyong Ye ◽  
Bin Lu

AbstractStress is one of the major causes of irritable bowel syndrome (IBS), which is well-known for perturbing the microbiome and exacerbating IBS-associated symptoms. However, changes in the gut microbiome and metabolome in response to colorectal distention (CRD), combined with restraint stress (RS) administration, remains unclear. In this study, CRD and RS stress were used to construct an IBS rat model. The 16S rRNA gene sequencing was used to characterize the microbiota in ileocecal contents. UHPLC-QTOF-MS/MS assay was used to characterize the metabolome of gut microbiota. As a result, significant gut microbial dysbiosis was observed in stress-induced IBS rats, with the obvious enrichment of three and depletion of 11 bacterial taxa in IBS rats, when compared with those in the control group (q < 0.05). Meanwhile, distinct changes in the fecal metabolic phenotype of stress-induced IBS rats were also found, including five increased and 19 decreased metabolites. Furthermore, phenylalanine, tyrosine and tryptophan biosynthesis were the main metabolic pathways induced by IBS stress. Moreover, the altered gut microbiota had a strong correlation with the changes in metabolism of stress-induced IBS rats. Prevotella bacteria are correlated with the metabolism of 1-Naphthol and Arg.Thr. In conclusion, the gut microbiome, metabolome and their interaction were altered. This may be critical for the development of stress-induced IBS.


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