The antidiabetic effects of <i>Bifidobacterium longum subsp. longum</i> BL21 through regulating gut microbiota structure in type 2 diabetic mice

Hao, Junyu; Zhang, Yongli; Wu, Tao; Li, Rui; Sui, Wenjie; Zhu, Jianguo; Fang, Shuguang; Geng, Jie‐Ting; Zhang, Min

doi:10.1039/d2fo01109c

Cited by 17 publications

(23 citation statements)

References 46 publications

(70 reference statements)

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“…To explore the effects of CDs on glucose metabolism and gut microbiota, we established a mouse model of chronic CD exposure and added a probiotic supplementation group for comparison. Accumulating evidence reveals that several intestinal bacteria are beneficial for improving T2DM, such as Bifidobacterium , Lactobacillus , Bacillus , Streptococcus thermophilus , and Akkermansia , which can be used as probiotics. − In this study, VSL#3 was selected for probiotic supplementation, which has been extensively studied and tested in animal models of intestinal inflammation and contains a high concentration (450 billion colonies/sachet) mixture of viable, lyophilized Bifidobacterium , Lactobacillus , and Bacillus thermophilus . , Mice treated with CDs are shown in Figure a. After 14 weeks of CD exposure, the mice showed high fasting glucose levels (Figure b), unchanged fasting weight (Figure c), and impaired glucose tolerance (Figure d and e), indicating disturbed glucose homeostasis.…”

Section: Resultsmentioning

confidence: 99%

Foodborne Carbon Dot Exposure Induces Insulin Resistance through Gut Microbiota Dysbiosis and Damaged Intestinal Mucus Layer

Zhang

Fan

et al. 2023

ACS Nano

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Foodborne carbon dots (CDs), an emerging food nanocontaminant, are an increasing risk factor for metabolic toxicity in mammals. Here, we report that chronic CD exposure induced glucose metabolism disorders via disruption of the gut−liver axis in mice. 16s rRNA analysis demonstrated that CD exposure decreased the abundance of beneficial bacteria (Bacteroides, Coprococcus, and S24-7) and increased the abundance of harmful bacteria (Proteobacteria, Oscillospira, Desulfovibrionaceae, and Ruminococcaceae), as well as increased the Firmicutes/Bacteroidetes ratio. Mechanistically, the increased pro-inflammatory bacteria release the endotoxin lipopolysaccharide, which induces an intestinal inflammation and disruption of the intestinal mucus layer, activating systemic inflammation and inducing hepatic insulin resistance in mice via the TLR4/NFκB/MAPK signaling pathway. Furthermore, these changes were almost completely reversed by probiotics. Fecal microbiota transplantation from CD-exposed mice induced glucose intolerance, damaged liver function, intestinal mucus layer injury, hepatic inflammation, and insulin resistance in the recipient mice. However, microbiota-depleted mice exposed to CDs had normal levels of these biomarkers consistent with microbiota-depleted control mice, which revealed that gut microbiota dysbiosis contributes to CDinduced inflammation-mediated insulin resistance. Together, our findings revealed that gut microbiota dysbiosis contributes to CD-induced inflammation-mediated insulin resistance and attempted to elucidate the specific underlying mechanism. Furthermore, we emphasized the importance of assessing the hazards associated with foodborne CDs.

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Section: Resultsmentioning

confidence: 99%

Foodborne Carbon Dot Exposure Induces Insulin Resistance through Gut Microbiota Dysbiosis and Damaged Intestinal Mucus Layer

Zhang

Fan

et al. 2023

ACS Nano

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“…The supplementary probiotics in the PPDP study were provided by Bifico (Approval number: S10950032), an over-the-counter capsule consisting of live combined Bifidobacterium longum, Lactobacillus acidophilus and Enterococcus faecalis. It has been reported that Bifidobacterium longum supplementation can attenuate hyperglycemia, improve the antioxidant capacity of the liver, repair intestinal barrier injury, and reduce inflammation in diabetic mice (15). Lactobacillus acidophilus was also reported that can alleviate T2DM by regulating hepatic glucose, lipid metabolism and gut microbiota in mice (16).…”

Section: Discussionmentioning

confidence: 99%

Probiotics intervention in preventing conversion of impaired glucose tolerance to diabetes: The PPDP follow-on study

Yan

Hu²,

Tian³

et al. 2023

Front. Endocrinol.

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ObjectivesThe purpose of this study was to assess the incidence of type 2 diabetes mellitus (T2DM) after 6 years in patients with IGT who received early probiotic intervention in the Probiotics Prevention Diabetes Program (PPDP) trial.Methods77 patients with IGT in the PPDP trial were randomized to either probiotic or placebo. After the completion of the trial, 39 non-T2DM patients were invited to follow up glucose metabolism after the next 4 years. The incidence of T2DM in each group was assessed using Kaplan-Meier analysis. The 16S rDNA sequencing technology was used to analyze gut microbiota’s structural composition and abundance changes between the groups.ResultsThe cumulative incidence of T2DM was 59.1% with probiotic treatment versus 54.5% with placebo within 6 years, there was no significant difference in the risk of developing T2DM between the two groups (P=0.674).ConclusionsSupplemental probiotic therapy does not reduce the risk of IGT conversion to T2DM.Clinical Trial Registrationhttps://www.chictr.org.cn/showproj.aspx?proj=5543, identifier ChiCTR-TRC-13004024.

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“…These changes were reversed when HE pups were fostered by NC dams. According to published studies, a drop in Alloprevotella ( Wang J. et al, 2020 ; Wu et al, 2021 ; Zhang et al, 2021 ; Zhao et al, 2021 ; Hao et al, 2022 ; Liu et al, 2022 ) and an increase in Blautia ( Zhao et al, 2021 ; Bao et al, 2022 ) and Tyzzerella ( Li et al, 2022 ) are found in animal models of in insulin resistance or glucose intolerance. On the other hand, antidiabetic medications and bioactive compounds modulate the gut microbial community of diabetic mouse model, characterized by increased Alistipes ( Hu et al, 2019 ; Jeong et al, 2021 ; Li et al, 2021 ; Wu R. et al, 2022 ) and decreased Anaerotruncus ( Yong et al, 2022 ), Oscillibacter ( Lin et al, 2022 ; Wang et al, 2022 ), Allobaculum ( Jia et al, 2017 ; Shen et al, 2021 ; Xu et al, 2021 ; Ma et al, 2022 ), Acetatifactor ( Wu Y. et al, 2022 ) and Turicibacter ( Zhao et al, 2021 ).…”

Section: Discussionmentioning

confidence: 99%

Surrogate fostering of mice prevents prenatal estradiol-induced insulin resistance via modulation of the microbiota-gut-brain axis

Zhou

Sun

2023

Front. Microbiol.

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IntroductionPrenatal and early postnatal development are known to influence future health. We previously reported that prenatal high estradiol (HE) exposure induces insulin resistance in male mice by disrupting hypothalamus development. Because a foster dam can modify a pup’s gut microbiota and affect its health later in life, we explored whether surrogate fostering could also influence glucose metabolism in HE offspring and examined mechanisms that might be involved.MethodsWe performed a surrogate fostering experiment in mice and examined the relationship between the metabolic markers associated to insulin resistance and the composition of the gut microbiota.ResultsHE pups raised by HE foster dams (HE-HE) developed insulin resistance, but HE pups fostered by negative control dams (NC-HE) did not. The gut microbiota composition of HE-HE mice differed from that of NC mice raised by NC foster dams (NC-NC), whereas the composition in NC-HE mice was similar to that of NC-NC mice. Compared with NC-NC mice, HE-HE mice had decreased levels of fecal short-chain fatty acids and serum intestinal hormones, increased food intake, and increased hypothalamic neuropeptide Y expression. In contrast, none of these indices differed between NC-HE and NC-NC mice. Spearman correlation analysis revealed a significant correlation between the altered gut microbiota composition and the insulin resistance-related metabolic indicators, indicating involvement of the microbiota-gut-brain axis.DiscussionOur findings suggest that alterations in the early growth environment may prevent fetal-programmed glucose metabolic disorder via modulation of the microbiota-gut-brain axis. These findings offer direction for development of translational solutions for adult diseases associated with aberrant microbial communities in early life.

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The antidiabetic effects of Bifidobacterium longum subsp. longum BL21 through regulating gut microbiota structure in type 2 diabetic mice

Abstract: Bifidobacterium longum subsp. longum BL21 (BL21) possess hypoglycemic activity, but its anti-diabetic mechanism has rarely been illustrated. In the present work, the effect of BL21 on type 2 diabetes mellitus...

Cited by 17 publications

References 46 publications

Foodborne Carbon Dot Exposure Induces Insulin Resistance through Gut Microbiota Dysbiosis and Damaged Intestinal Mucus Layer

Foodborne Carbon Dot Exposure Induces Insulin Resistance through Gut Microbiota Dysbiosis and Damaged Intestinal Mucus Layer

Probiotics intervention in preventing conversion of impaired glucose tolerance to diabetes: The PPDP follow-on study

Surrogate fostering of mice prevents prenatal estradiol-induced insulin resistance via modulation of the microbiota-gut-brain axis

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