Fucoidan ameliorates glucose metabolism by the improvement of intestinal barrier and inflammatory damage in type 2 diabetic rats

Liu, Yaping; Xu, Ze; Huang, Haoming; Xue, Yue; Zhang, Dongdong; Zhang, Yujing; Li, Wenjie; Li, Xing

doi:10.1016/j.ijbiomac.2022.01.102

Cited by 20 publications

(14 citation statements)

References 53 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…The imbalance of intestinal homoeostasis and high GLU production increase intestinal membrane permeability and destroy the intestinal barrier 57 , 58 . The increase in intestinal membrane permeability allows harmful metabolites in the intestine to reach the corresponding target organs through body fluid circulation, causing inflammation and the subsequent development of obesity and diabetes 21 , 59 .…”

Section: Discussionmentioning

confidence: 99%

Gut microbiome dysregulation drives bone damage in broiler tibial dyschondroplasia by disrupting glucose homeostasis

Chen

Zhang

et al. 2023

npj Biofilms Microbiomes

View full text Add to dashboard Cite

Tibial dyschondroplasia (TD) with multiple incentives is a metabolic skeletal disease that occurs in fast-growing broilers. Perturbations in the gut microbiota (GM) have been shown to affect bone homoeostasis, but the mechanisms by which GM modulates bone metabolism in TD broilers remain unknown. Here, using a broiler model of TD, we noted elevated blood glucose (GLU) levels in TD broilers, accompanied by alterations in the pancreatic structure and secretory function and damaged intestinal barrier function. Importantly, faecal microbiota transplantation (FMT) of gut microbes from normal donors rehabilitated the GM and decreased the elevated GLU levels in TD broilers. A high GLU level is a predisposing factor to bone disease, suggesting that GM dysbiosis-mediated hyperglycaemia might be involved in bone regulation. 16S rRNA gene sequencing and short-chain fatty acid analysis revealed that the significantly increased level of the metabolite butyric acid derived from the genera Blautia and Coprococcus regulated GLU levels in TD broilers by binding to GPR109A in the pancreas. Tibial studies showed reduced expression of vascular regulatory factors (including PI3K, AKT and VEFGA) based on transcriptomics analysis and reduced vascular distribution, contributing to nonvascularization of cartilage in the proximal tibial growth plate of TD broilers with elevated GLU levels. Additionally, treatment with the total flavonoids from Rhizoma drynariae further validated the improvement in bone homoeostasis in TD broilers by regulating GLU levels through the regulation of GM to subsequently improve intestinal and pancreatic function. These findings clarify the critical role of GM-mediated changes in GLU levels via the gut–pancreas axis in bone homoeostasis in TD chickens.

show abstract

Section: Discussionmentioning

confidence: 99%

Gut microbiome dysregulation drives bone damage in broiler tibial dyschondroplasia by disrupting glucose homeostasis

Chen

Zhang

et al. 2023

npj Biofilms Microbiomes

View full text Add to dashboard Cite

show abstract

“…Alpha-glucosidase inhibitors (AGIs) are oral antidiabetic drugs that mainly affect the intestine and inhibit the conversion of carbohydrates into monosaccharides to prevent the rapid increase of postprandial blood glucose in T2DM patients [16,19]. Several traditional Chinese medicines that potentially target α-glucosidase, such as Ramulus mori (Sangzhi) alkaloid (SZ-A), Berberine and Fucoidan, ameliorate glucose metabolism not only by preventing the intestinal digestion of carbohydrates but also by playing an important role in maintaining the intestinal homeostasis [16,[20][21][22]. In addition, the inhibition of α-glucosidase induces the secretion of GLP-1 by moving unprocessed nutrients to the terminal part of the gut, where more L-cells are located and there is a prolonged duration of contact with nutrients [23].…”

Section: Discussionmentioning

confidence: 99%

Voglibose Regulates the Secretion of GLP-1 Accompanied by Amelioration of Ileal Inflammatory Damage and Endoplasmic Reticulum Stress in Diabetic KKAy Mice

Liu

et al. 2022

IJMS

View full text Add to dashboard Cite

Voglibose is an α-glycosidase inhibitor that improves postprandial hyperglycemia and increases glucagon-like peptide-1 (GLP-1) secretion in patients with type 2 diabetes. Recently, there has been increasing interest in the anti-inflammatory effects of voglibose on the intestine, but the underlying mechanism is not clear. This study evaluated the effects and mechanisms of voglibose on glycemic control and intestinal inflammation. Type 2 diabetic KKAy mice were treated with voglibose (1 mg/kg) by oral gavage once daily. After 8 weeks, glucose metabolism, levels of short-chain fatty acids (SCFAs), systematic inflammatory factors, intestinal integrity and inflammation were evaluated using hematoxylin and eosin staining, immunohistochemistry, immunofluorescence and Western blot analysis. Voglibose ameliorated glucose metabolism by enhancing basal- and glucose-dependent GLP-1 secretion. Several beneficial SCFAs, such as acetic acid and propionic acid, were increased by voglibose in the fecal sample. Additionally, voglibose notably decreased the proportion of pro-inflammatory macrophages and the expression of nuclear factor kappa B but increased the expression of tight junction proteins in the ileum, thus markedly improving intestinal inflammatory damage and reducing the systematic inflammatory factors. Ileal genomics and protein validation suggested that voglibose attenuated inositol-requiring protein 1α-X-box binding protein 1-mediated endoplasmic reticulum stress (ERS). Together, these results showed that voglibose enhanced the secretion of GLP-1, which contributed to the glycemic control in KKAy mice at least in part by regulating intestinal inflammation and the expression of ERS factors.

show abstract

“…The imbalance of intestinal homeostasis and high glucose production increases intestinal membrane permeability and destroys intestinal barrier. 50,51 The increase of intestinal membrane permeability allows harmful metabolites in the intestine to reach the corresponding target organs through body uid circulation, causing in ammation leading to obesity and diabetes. 16,52 In this study, intestinal tight junction proteins Claudin 1 and Occludin were signi cantly down-regulated in the high-glucose TD broilers, suggesting that the intestinal barrier had been damaged, and the DAO content in plasma had increased, suggesting increased intestinal permeability.…”

Section: Discussionmentioning

confidence: 99%

Gut dysregulation drives bone damage in tibial dyschondroplasia by disrupting glucose homeostasis

Huang

Chen

et al. 2022

Preprint

View full text Add to dashboard Cite

Tibial dyschondroplasia (TD) with multiple incentives is a metabolic skeletal disease that occurs in fast-growing broilers. Perturbations in the gut microbiota (GM) have been shown to affect bone homeostasis and the mechanisms by which GM modulates bone metabolism in TD broilers remain unrevealed. Here, by using a broiler model of TD, we noted elevated blood glucose (GLU) levels in TD broilers, accompanied by altered pancreatic structure and its secretory function, and damaged intestinal barrier function. Importantly, fecal microbiota transplantation (FMT) of gut microbes from normal donors could rehabilitate the GM and depress the elevation of GLU in TD broilers, high GLU level is a predisposing cause of bone disease, suggesting that GM dysbiosis-mediated hyperglycemia might involve in bone regulation. 16s rRNA gene sequencing and short-chain fatty acids analysis revealed that the significantly increased genera Blautia and Coprococcus-derived metabolite butyric acid regulated GLU levels in TD broilers by binding to GPR109A on the pancreas. Tibial studies showed reduced expression of vascular regulatory factors (including PI3K, AKT and VEFGA) based on transcriptional analysis and inhibited vascular distribution contributed to non-vascularization of cartilage in the proximal tibial growth plate in TD broilers with elevated GLU. Additionally, the total flavonoids of Rhizoma drynariae treatment further validated the improvement of bone homeostasis in TD broilers by regulating GLU levels originating from regulating GM and improving intestinal and pancreatic function. These findings clarify the critical role of GM-mediated GLU levels via the gut-pancreas axis in bone homeostasis in TD chickens.

show abstract

Fucoidan ameliorates glucose metabolism by the improvement of intestinal barrier and inflammatory damage in type 2 diabetic rats

Cited by 20 publications

References 53 publications

Gut microbiome dysregulation drives bone damage in broiler tibial dyschondroplasia by disrupting glucose homeostasis

Gut microbiome dysregulation drives bone damage in broiler tibial dyschondroplasia by disrupting glucose homeostasis

Voglibose Regulates the Secretion of GLP-1 Accompanied by Amelioration of Ileal Inflammatory Damage and Endoplasmic Reticulum Stress in Diabetic KKAy Mice

Gut dysregulation drives bone damage in tibial dyschondroplasia by disrupting glucose homeostasis

Contact Info

Product

Resources

About