Punicalagin alleviates renal injury via the gut-kidney axis in high-fat diet-induced diabetic mice

Pyracantha fortuneana fruit extract (PFE) exhibits beneficial effects on IBF in association with the modulation of glycolipid digestion and gut microbiota in HFD-fed obese rats.

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Intake of Flavonoids from Astragalus Membranaceus Ameliorated Brain Impairment in Diabetic Mice Via Modulating Brain-Gut Axis

10.21203/rs.3.rs-1127751/v1 ◽

2021 ◽

Author(s):

Li Xuling ◽

Junling Gu ◽

Zhe Wang ◽

Jing Lin ◽

Tingting Zhao ◽

...

Keyword(s):

Gut Microbiota ◽

Brain Damage ◽

High Fat Diet ◽

Fasting Blood Glucose ◽

Synaptic Function ◽

Astragalus Membranaceus ◽

Immunological Methods ◽

Diabetic Mice ◽

High Fat

Abstract Background: Brain impairment is one of a major complication of diabetes. Dietary flavonoids have been recommended to prevent brain damage. Astragalus membranaceus is a herbal medicine commonly used to relieve the complications of diabetes. Flavonoids is one of the major ingredients of Astragalus membranaceus, but its function and mechanism on diabetic encepholopathy is still unknown.Methods: Type 2 diabetes mellitus (T2DM) model was induced by high fat diet and STZ in C57BL/6J mice, and BEnd.3 and HT22 cell lines were applied in the in vitro study. Quality of flavonoids was evaluated by LC-MS/MS. Differential expressed proteins in the hippocampus were evaluated by proteomics; influence of the flavonoids on composition of gut microbiota was analyzed by metagenomics. Mechanism of the flavonoids on diabetic encepholopathy was analyzed by Q-PCR, Western Blot, and multi-immunological methods et al. Results: We found that flavonoids from Astragalus membranaceus (TFA) significantly ameliorated brain damage by modulating gut-microbiota-brain axis: TFA oral administration decreased fasting blood glucose and food intake, repaired blood brain barrier, protected hippocampus synaptic function; improved hippocampus mitochondrial biosynthesis and energy metabolism; and enriched the intestinal microbiome in high fat diet/STZ-induced diabetic mice. In the in vitro study, we found TFA increased viability of HT22 cells and preserved gut barrier integrity in CaCO2 monocellular layer, and PGC1α/AMPK pathway participated in this process. Conclusion: Our findings demonstrated that flavonoids from Astragalus Membranaceus ameliorated brain impairment via gut-brain axis. Our present study provided an alternative solution on preventing and treating diabetic cognition impairment.

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Linggui Zhugan Formula Improves Glucose and Lipid Levels and Alters Gut Microbiota in High-Fat Diet-Induced Diabetic Mice

Frontiers in Physiology ◽

10.3389/fphys.2019.00918 ◽

2019 ◽

Vol 10 ◽

Cited By ~ 9

Author(s):

Rui Wu ◽

Dandan Zhao ◽

Ran An ◽

Zhufeng Wang ◽

Yuxiu Li ◽

...

Keyword(s):

Gut Microbiota ◽

High Fat Diet ◽

Diabetic Mice ◽

Lipid Levels ◽

High Fat

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Beneficial Effects of Potentilla discolor Bunge Water Extract on Inflammatory Cytokines Release and Gut Microbiota in High-Fat Diet and Streptozotocin-Induced Type 2 Diabetic Mice

Nutrients ◽

10.3390/nu11030670 ◽

2019 ◽

Vol 11 (3) ◽

pp. 670 ◽

Cited By ~ 20

Author(s):

Lihua Han ◽

Tiange Li ◽

Min Du ◽

Rui Chang ◽

Biyuan Zhan ◽

...

Keyword(s):

Gut Microbiota ◽

Inflammatory Cytokines ◽

High Fat Diet ◽

Intestinal Inflammation ◽

Water Extract ◽

Perennial Herb ◽

Diabetic Mice ◽

High Fat ◽

Type 2 Diabetic

Potentilla discolor Bunge (PDB), a perennial herb, has been used as a traditional Chinese medicine in the therapy of many diseases. The aim of the current study was to investigate the effect of PDB water extract on systemic inflammation and gut microbiota in type 2 diabetic (T2D) mice induced by high-fat diet (HFD) and streptozotocin (STZ) injection. C57BL/6J mice were randomly divided into a normal diet (ND) group, T2D group, and PDB group (diabetic mice treated with PDB water extract at a dose of 400 mg/kg body weight). Results showed that PDB significantly decreased the levels of lipopolysaccharide (LPS) and pro-inflammatory cytokines in serum. Further investigation showed that PDB significantly reduced the ratio of Firmicutes/Bacteroidetes and the relative abundance of Proteobacteria in fecal samples of diabetic mice. In addition, PDB notably alleviated intestinal inflammation as evidenced by decreased expression of toll-like receptor 4 (TLR4), myeloid differentiation factor 88 (MyD88), nuclear factor-κB (NF-κB), and inflammatory cytokines. PDB also reversed the decreased expression of intestinal mucosal tight junction proteins including Claudin3, ZO-1, and Occludin. Meanwhile, the levels of fecal acetic acid and butyric acid and their specific receptors including G-protein-coupled receptor (GPR) 41 and 43 expression in the colon were also increased after PDB treatment. Our results indicated that PDB might serve as a potential functional ingredient against diabetes and related inflammation.

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Glucosamine Ameliorates Symptoms of High-Fat Diet-Fed Mice by Reversing Imbalanced Gut Microbiota

Frontiers in Pharmacology ◽

10.3389/fphar.2021.694107 ◽

2021 ◽

Vol 12 ◽

Author(s):

Xubing Yuan ◽

Junping Zheng ◽

Lishi Ren ◽

Siming Jiao ◽

Cui Feng ◽

...

Keyword(s):

Gut Microbiota ◽

High Fat Diet ◽

Inflammatory Responses ◽

Fasting Blood Glucose ◽

Intestinal Barrier ◽

Intestinal Bacteria ◽

High Fat ◽

Lipid Metabolism Disorder ◽

Metabolism Disorder ◽

Rdna Sequencing

Glucosamine (GlcN) is used as a supplement for arthritis and joint pain and has been proved to have effects on inflammation, cancer, and cardiovascular diseases. However, there are limited studies on the regulatory mechanism of GlcN against glucose and lipid metabolism disorder. In this study, we treated high-fat diet (HFD)-induced diabetic mice with GlcN (1 mg/ml, in drinking water) for five months. The results show that GlcN significantly reduced the fasting blood glucose of HFD-fed mice and improved glucose tolerance. The feces of intestinal contents in mice were analyzed using 16s rDNA sequencing. It was indicated that GlcN reversed the imbalanced gut microbiota in HFD-fed mice. Based on the PICRUSt assay, the signaling pathways of glucolipid metabolism and biosynthesis were changed in mice with HFD feeding. By quantitative real-time PCR (qPCR) and hematoxylin and eosin (H&E) staining, it was demonstrated that GlcN not only inhibited the inflammatory responses of colon and white adipose tissues, but also improved the intestinal barrier damage of HFD-fed mice. Finally, the correlation analysis suggests the most significantly changed intestinal bacteria were positively or negatively related to the occurrence of inflammation in the colon and fat tissues of HFD-fed mice. In summary, our studies provide a theoretical basis for the potential application of GlcN to glucolipid metabolism disorder through the regulation of gut microbiota.

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Improvement of Colonic Immune Function with Soy Isoflavones in High-Fat Diet-Induced Obese Rats

Molecules ◽

10.3390/molecules24061139 ◽

2019 ◽

Vol 24 (6) ◽

pp. 1139 ◽

Cited By ~ 10

Author(s):

Qihui Luo ◽

Dongjing Cheng ◽

Chao Huang ◽

Yifan Li ◽

Chengjie Lao ◽

...

Keyword(s):

Gut Microbiota ◽

Immune Function ◽

Barrier Function ◽

High Fat Diet ◽

Intestinal Barrier ◽

Soy Isoflavones ◽

Short Chain ◽

Intestinal Barrier Function ◽

High Fat ◽

Obese Rats

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.

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Abstract 084: Activation Of Trpv1-expressing Renal Sensory Nerves With N-oleoyldopamine Attenuates High Fat Diet-induced Impairment In Renal Function

Hypertension ◽

10.1161/hyp.64.suppl_1.084 ◽

2014 ◽

Vol 64 (suppl_1) ◽

Author(s):

Shuang-Quan Yu ◽

Donna H Wang

Keyword(s):

Renal Function ◽

Renal Injury ◽

High Fat Diet ◽

Sympathetic Nerve Activity ◽

Intrathecal Injection ◽

Renal Nerves ◽

High Fat ◽

Nerve Activity ◽

Renal Sympathetic Nerve Activity ◽

Renal Sympathetic

Renal injury occurs in obesity. Accumulating evidence indicates that activation of the transient receptor potential vanilloid 1 (TRPV1) protects tissues from injury albeit the mechanisms are largely unknown. We test the hypothesis that high fat diet (HFD) intake impairs afferent renal nerves expressing TRPV1 channels, leading to increased renal sympathetic nerve activity (RSNA), decreased renal function, and hypertension, and that chronic activation of TRPV1 positive afferent renal nerves attenuates HFD-induced impairment. N-oleoyldopamine (OLDA, 1 ng/kg, daily), a selective TRPV1 agonist, was administrated intrathecally (T8-L3) via a indwelled catheter to chronically activate TRPV1 positive afferent renal nerves in rats fed a HFD or normal fat diet (Con) for 8 weeks. HFD decreased renal TRPV1 expression and afferent renal nerve activity (ARNA, Con: 133±8, Con+OLDA: 127±15, HFD: 84±5, HFD+OLDA: 115±7, p<0.05) in response to intra-pelvis perfusion of capsaicin (4 μM, 3 min, 20 ml/min), a selective TRPV1 agonist, which were prevented by OLDA. HFD increased RSNA responses to intrathecal injection of muscimol (3 nmol/kg), a GABA-A receptor agonist, and urinary norepinephrine levels, which were prevented by OLDA. HFD decreased creatinine clearance and increased urinary albumin levels, which were prevented by OLDA (Creatinine clearance, Con: 0.52±0.09, Con+OLDA: 0.54±0.12, HFD: 0.24±0.04, HFD+OLDA: 0.40±0.06 ml/min/100 gbwt, p<0.05). HFD increased levels of collagen deposition, connective tissue growth factor (CTGF), and matrix metalloproteinase-2 (MMP-2) in the kidney, which were prevented by OLDA. HFD increased systolic blood pressure by the week of 6 after HFD, which was prevented by OLDA. Thus, HFD impairs TRPV1-positive afferent renal nerves, increases renal sympathetic nerve activity, and leads to renal injury and hypertension. Segment-specific intrathecal injection of OLDA protects against HFD-induced impairment in afferent renal nerves and prevents HFD-induced renal injury and hypertension. Our data illustrate that preservation of TRPV1 positive afferent renal nerves may be a therapeutic strategy in preventing obesity- or type 2 diabetes-induced renal injury and hypertension.

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