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Original Article
Basic Research
Supplementation of Clostridium butyricum Alleviates Vascular Inflammation in Diabetic Mice
Tian Zhou, Shuo Qiu, Liang Zhang, Yangni Li, Jing Zhang, Donghua Shen, Ping Zhao, Lijun Yuan, Lianbi Zhao, Yunyou Duan, Changyang Xing
Diabetes Metab J. 2024;48(3):390-404.   Published online February 2, 2024
DOI: https://doi.org/10.4093/dmj.2023.0109
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AbstractAbstract PDFPubReader   ePub   
Background
Gut microbiota is closely related to the occurrence and development of diabetes and affects the prognosis of diabetic complications, and the underlying mechanisms are only partially understood. We aimed to explore the possible link between the gut microbiota and vascular inflammation of diabetic mice.
Methods
The db/db diabetic and wild-type (WT) mice were used in this study. We profiled gut microbiota and examined the and vascular function in both db/db group and WT group. Gut microbiota was analyzed by 16s rRNA sequencing. Vascular function was examined by ultrasonographic hemodynamics and histological staining. Clostridium butyricum (CB) was orally administered to diabetic mice by intragastric gavage every 2 days for 2 consecutive months. Reactive oxygen species (ROS) and expression of nuclear factor erythroid-derived 2-related factor 2 (Nrf2) and heme oxygenase-1 (HO-1) were detected by fluorescence microscopy. The mRNA expression of inflammatory cytokines was tested by quantitative polymerase chain reaction.
Results
Compared with WT mice, CB abundance was significantly decreased in the gut of db/db mice, together with compromised vascular function and activated inflammation in the arterial tissue. Meanwhile, ROS in the vascular tissue of db/db mice was also significantly increased. Oral administration of CB restored the protective microbiota, and protected the vascular function in the db/db mice via activating the Nrf2/HO-1 pathway.
Conclusion
This study identified the potential link between decreased CB abundance in gut microbiota and vascular inflammation in diabetes. Therapeutic delivery of CB by gut transplantation alleviates the vascular lesions of diabetes mellitus by activating the Nrf2/HO-1 pathway.
Review
Basic Research
Revisiting the Bacterial Phylum Composition in Metabolic Diseases Focused on Host Energy Metabolism
Yeonmi Lee, Hui-Young Lee
Diabetes Metab J. 2020;44(5):658-667.   Published online July 9, 2020
DOI: https://doi.org/10.4093/dmj.2019.0220
  • 9,173 View
  • 133 Download
  • 19 Web of Science
  • 19 Crossref
AbstractAbstract PDFPubReader   ePub   

Over a hundred billion bacteria are found in human intestines. This has emerged as an environmental factor in metabolic diseases, such as obesity and related diseases. The majority of these bacteria belong to two dominant phyla, Bacteroidetes and Firmicutes. Since the ratio of Firmicutes to Bacteroidetes increases in people with obesity and in various animal models, it has been assumed that phylum composition causes the increase in occurrence of metabolic diseases over the past decade. However, this assumption has been challenged by recent studies that have found even an opposite association of phylum composition within metabolic diseases. Moreover, the gut microbiota affects host energy metabolism in various ways including production of metabolites and interaction with host intestinal cells to regulate signaling pathways that affect energy metabolism. However, the direct effect of gut bacteria on host energy intake, such as energy consumption by the bacteria itself and its effects on intestinal energy absorption, has been underestimated. This review aims to discuss whether increased ratio of Firmicutes to Bacteroidetes is associated with the development of metabolic diseases, and whether energy competition between the bacteria and host is a missing part of the mechanism linking gut microbiota to metabolic diseases.

Citations

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    Aishwarya Murali, Varun Giri, Franziska Maria Zickgraf, Philipp Ternes, Hunter James Cameron, Saskia Sperber, Volker Haake, Peter Driemert, Hennicke Kamp, Dorothee Funk-Weyer, Shana J. Sturla, Ivonne M.C.M. Rietjens, Bennard van Ravenzwaay
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  • Short-Term Alternate Feeding between Terrestrially Sourced Oil- and Fish Oil-Based Diets Modulates the Intestinal Microecology of Juvenile Turbot
    Xiuhua Ma, Yaoyao Kong, Houguo Xu, Qingzhu Bi, Mengqing Liang, Kangsen Mai, Yanjiao Zhang
    Biology.2023; 12(5): 650.     CrossRef
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    Zhang Yanan, Ma Lu, Zhang Lu, Huo Jinhai, Wang Weiming
    Frontiers in Nutrition.2023;[Epub]     CrossRef
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    Claudia I. Gamboa-Gómez, Laura J. Barragán-Zúñiga, Fernando Guerrero-Romero, Gerardo Martínez-Aguilar, José Luis Gónzalez, Almendra A. Valenzuela-Ramírez, Juan A. Rojas-Contreras, Monica Anese, Maribel Cervantes Flores, Marilisa Alongi
    Journal of Functional Foods.2023; 111: 105889.     CrossRef
  • Gut Microbiota and Bacterial Translocation in the Pathogenesis of Liver Fibrosis
    Roman Maslennikov, Elena Poluektova, Oxana Zolnikova, Alla Sedova, Anastasia Kurbatova, Yulia Shulpekova, Natyia Dzhakhaya, Svetlana Kardasheva, Maria Nadinskaia, Elena Bueverova, Vladimir Nechaev, Anna Karchevskaya, Vladimir Ivashkin
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  • Eugenol, A Major Component of Clove Oil, Attenuates Adiposity, and Modulates Gut Microbiota in High‐Fat Diet‐Fed Mice
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    Fernanda Pace, Paula I. Watnick
    Trends in Microbiology.2021; 29(9): 849.     CrossRef
  • Heat stress on microbiota composition, barrier integrity, and nutrient transport in gut, production performance, and its amelioration in farm animals
    Amlan Kumar Patra, Indrajit Kar
    Journal of Animal Science and Technology.2021; 63(2): 211.     CrossRef
  • Mechanisms linking gut microbial metabolites to insulin resistance
    Hye Rim Jang, Hui-Young Lee
    World Journal of Diabetes.2021; 12(6): 730.     CrossRef
  • The impact of gut microbiota metabolites on cellular bioenergetics and cardiometabolic health
    Lenka Tomasova, Marian Grman, Karol Ondrias, Marcin Ufnal
    Nutrition & Metabolism.2021;[Epub]     CrossRef
Original Articles
Basic Research
Effects of Microbiota on the Treatment of Obesity with the Natural Product Celastrol in Rats
Weiyue Hu, Lingling Wang, Guizhen Du, Quanquan Guan, Tianyu Dong, Ling Song, Yankai Xia, Xinru Wang
Diabetes Metab J. 2020;44(5):747-763.   Published online May 11, 2020
DOI: https://doi.org/10.4093/dmj.2019.0124
  • 9,513 View
  • 140 Download
  • 16 Web of Science
  • 17 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Obesity has become one of the most serious issues threatening the health of humankind, and we conducted this study to examine whether and how celastrol protects against obesity.

Methods

We fed male Sprague-Dawley rats a high-fat diet and administered celastrol to obese rats for 3 weeks. By recording body weight (BW) and other measures, we identified the effective dose of celastrol for obesity treatment. Feces were collected to perform 16S rRNA sequencing, and hypothalami were extracted for transcriptome sequencing. We then treated leptin knockout rats with celastrol and explored the changes in energy metabolism. Male Institute of Cancer Research (ICR) mice were used to test the acute toxicity of celastrol.

Results

We observed that celastrol reduced BW and promoted energy expenditure at a dose of 500 µg/kg BW but that food intake was not changed after administration. The diversity of the gut microbiota was improved, with an increased ratio of Bacteroidetes to Firmicutes, and the gut microbiota played an important role in the anti-obesity effects of celastrol. Hypothalamic transcriptome analysis showed a significant enrichment of the leptin signaling pathway, and we found that celastrol significantly enhanced energy expenditure, which was mediated by the leptin signaling pathway. Acute lethal toxicity of celastrol was not observed at doses ranging from 0 to 62.5 mg/kg BW.

Conclusion

Our study revealed that celastrol decreased the BW of obese rats by enhancing energy expenditure but not by suppressing food intake and that this effect was mediated by the improvement of the gut microbiota and the activation of the hypothalamic leptin signaling pathway.

Citations

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  • Natural compounds as obesity pharmacotherapies
    Xin‐Yuan Zhao, Ji‐Qiu Wang, G. Gregory Neely, Yan‐Chuan Shi, Qiao‐Ping Wang
    Phytotherapy Research.2024; 38(2): 797.     CrossRef
  • Celastrol functions as an emerging manager of lipid metabolism: Mechanism and therapeutic potential
    Jia Gu, Ya-Ning Shi, Neng Zhu, Hong-Fang Li, Chan-Juan Zhang, Li Qin
    Biomedicine & Pharmacotherapy.2023; 164: 114981.     CrossRef
  • Tripterygium hypoglaucum extract ameliorates adjuvant-induced arthritis in mice through the gut microbiota
    Jianghui HU, Jimin NI, Junping ZHENG, Yanlei GUO, Yong YANG, Cheng YE, Xiongjie SUN, Hui XIA, Yanju LIU, Hongtao LIU
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  • Celastrol: An Update on Its Hepatoprotective Properties and the Linked Molecular Mechanisms
    Mengzhen Li, Faren Xie, Lu Wang, Guoxue Zhu, Lian-Wen Qi, Shujun Jiang
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    Pingping Chen, Bin Wang, Meng Li, Chunxue Cui, Fei Liu, Yonggang Gao
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  • Investigating Celastrol’s Anti-DCM Targets and Mechanisms via Network Pharmacology and Experimental Validation
    Rui Xi, Yongxin Wan, Lihong Yang, Jingying Zhang, Liu Yang, Shuai Yang, Rui Chai, Fengchen Mu, Qiting Sun, Rui Yan, Zhifang Wu, Sijin Li, Zhijun Liao
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    Carlos A. Fuzo, Ronaldo B. Martins, Thais F. C. Fraga‐Silva, Martin K. Amstalden, Thais Canassa De Leo, Juliano P. Souza, Thais M. Lima, Lucia H. Faccioli, Débora Noma Okamoto, Maria Aparecida Juliano, Suzelei C. França, Luiz Juliano, Vania L. D. Bonato,
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Basic Research
Role of Intestinal Microbiota in Metabolism of Voglibose In Vitro and In Vivo
Mahesh Raj Nepal, Mi Jeong Kang, Geon Ho Kim, Dong Ho Cha, Ju-Hyun Kim, Tae Cheon Jeong
Diabetes Metab J. 2020;44(6):908-918.   Published online April 6, 2020
DOI: https://doi.org/10.4093/dmj.2019.0147
  • 5,779 View
  • 114 Download
  • 6 Web of Science
  • 6 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   ePub   
Background

Voglibose, an α-glucosidase inhibitor, inhibits breakdown of complex carbohydrates into simple sugar units in intestine. Studies showed that voglibose metabolism in the liver might be negligible due to its poor intestinal absorption. Numerous microorganisms live in intestine and have several roles in metabolism and detoxification of various xenobiotics. Due to the limited information, the possible metabolism of voglibose by intestinal microbiota was investigated in vitro and in vivo.

Methods

For the in vitro study, different concentrations of voglibose were incubated with intestinal contents, prepared from both vehicle- and antibiotics-treated mice, to determine the decreased amount of voglibose over time by using liquid chromatography-mass spectrometry. Similarly, in vivo pharmacodynamic effect of voglibose was determined following the administration of voglibose and starch in vehicle- and antibiotic-pretreated non-diabetic and diabetic mice, by measuring the modulatory effects of voglibose on blood glucose levels.

Results

The in vitro results indicated that the remaining voglibose could be significantly decreased when incubated with the intestinal contents from normal mice compared to those from antibiotic-treated mice, which had less enzyme activities. The in vivo results showed that the antibiotic pretreatment resulted in reduced metabolism of voglibose. This significantly lowered blood glucose levels in antibiotic-pretreated mice compared to the control animals.

Conclusion

The present results indicate that voglibose would be metabolized by the intestinal microbiota, and that this metabolism might be pharmacodynamically critical in lowering blood glucose levels in mice.

Citations

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  • Pharmacomicrobiomics and type 2 diabetes mellitus: A novel perspective towards possible treatment
    Liyang Jia, Shiqiong Huang, Boyu Sun, Yongguang Shang, Chunsheng Zhu
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Basic Research
Combination of Probiotics and Salvia miltiorrhiza Polysaccharide Alleviates Hepatic Steatosis via Gut Microbiota Modulation and Insulin Resistance Improvement in High Fat-Induced NAFLD Mice
Wei Wang, Ai-Lei Xu, Zheng-Chao Li, Yi Li, Shun-Fu Xu, Hua-Chao Sang, Fachao Zhi
Diabetes Metab J. 2020;44(2):336-348.   Published online December 3, 2019
DOI: https://doi.org/10.4093/dmj.2019.0042
  • 10,901 View
  • 307 Download
  • 64 Web of Science
  • 64 Crossref
AbstractAbstract PDFSupplementary MaterialPubReader   
Background

Nonalcoholic fatty liver disease (NAFLD) increases the risk of hepatocellular carcinoma, which is currently the leading cause of obesity-related cancer deaths in middle-aged men.

Methods

Probiotics with lipid-lowering function were screened from the fecal microbiota of healthy adults. Polysaccharide from different sources was screened for improving insulin resistance. The combination of probiotics and Salvia miltiorrhiza polysaccharide (LBM) was investigated for alleviating hepatic steatosis.

Results

First, Bifidobacterium bifidum V (BbV) and Lactobacillus plantarum X (LpX) were obtained from the fecal microbiota of healthy adults. Second, to improve insulin resistance, a Salvia miltiorrhiza Bunge polysaccharide showing good performance in reducing insulin resistance was obtained. The liver total cholesterol (TC) and total triglyceride (TG) levels and the serum levels of free fatty acid, alanine transaminase, aspartate transaminase, low density lipoprotein cholesterol, TG, and TC can be significantly reduced through supplementation with LpX-BbV (LB) in NAFLD mice. Interestingly, the function of the probiotic LB can be enhanced by S. miltiorrhiza Bunge polysaccharide. Furthermore, the gut microbiota was modulated by LpX-BbV+S. miltiorrhiza Bunge polysaccharide (LBM). The lipopolysaccharide concentration of the LBM group was decreased by 73.6% compared to the NAFLD group. Ultimately, the mRNA concentrations of the proinflammatory cytokines (tumor necrosis factor α, interleukin 1β [IL-1β], and IL-6) decreased with LB and LBM treatment.

Conclusion

The results of this this study indicate that the LBM combination can be used as a therapeutic for ameliorating NAFLD via modulating the gut microbiota and improving insulin resistance.

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Review
Obesity and Metabolic Syndrome
Understanding Bile Acid Signaling in Diabetes: From Pathophysiology to Therapeutic Targets
Jessica M. Ferrell, John Y. L. Chiang
Diabetes Metab J. 2019;43(3):257-272.   Published online June 13, 2019
DOI: https://doi.org/10.4093/dmj.2019.0043
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AbstractAbstract PDFPubReader   

Diabetes and obesity have reached an epidemic status worldwide. Diabetes increases the risk for cardiovascular disease and non-alcoholic fatty liver disease. Primary bile acids are synthesized in hepatocytes and are transformed to secondary bile acids in the intestine by gut bacteria. Bile acids are nutrient sensors and metabolic integrators that regulate lipid, glucose, and energy homeostasis by activating nuclear farnesoid X receptor and membrane Takeda G protein-coupled receptor 5. Bile acids control gut bacteria overgrowth, species population, and protect the integrity of the intestinal barrier. Gut bacteria, in turn, control circulating bile acid composition and pool size. Dysregulation of bile acid homeostasis and dysbiosis causes diabetes and obesity. Targeting bile acid signaling and the gut microbiome have therapeutic potential for treating diabetes, obesity, and non-alcoholic fatty liver disease.

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Diabetes Metab J : Diabetes & Metabolism Journal