scholarly journals EEG Changes Related to Gut Dysbiosis in Diabetes—Review

2021 ◽  
Vol 11 (24) ◽  
pp. 11871
Author(s):  
Roxana Toderean ◽  
Mihai Dimian ◽  
Claudiu Cobuz

Humans are facing a devastating epidemic of metabolic syndrome that is linked to the worldwide dramatic increase in obesity and diabetes. Significant evidence suggests that the intestinal microbiota plays a major role in the pathogenesis of metabolic diseases. Due to the gut–brain axis link, dysbiosis in the gut microbiota have been demonstrated in both metabolic and neurological disease. Increasing evidence suggests that the gut microbiota is very important in maintaining health and changes in its composition may contribute to psychiatric and neurodegenerative disorders. It is also in research that changes in microbiota composition profile due to diabetes are modulated by the vagus nerve. Therefore, it is plausible that disruptions in the gut microbiota may be captured through electroencephalography signaling. Several studies which used standard methods of signal processing have highlighted some changes in electroencephalographic rhythms on patients with diabetes.

2018 ◽  
Vol 2018 ◽  
pp. 1-7 ◽  
Author(s):  
You Lv ◽  
Xue Zhao ◽  
Weiying Guo ◽  
Ying Gao ◽  
Shuo Yang ◽  
...  

Metabolic diseases, especially diabetes mellitus, have become global health issues. The etiology of diabetes mellitus can be attributed to genetic and/or environmental factors. Current evidence suggests the association of gut microbiota with metabolic diseases. However, the effects of glucose-lowering agents on gut microbiota are poorly understood. Several studies revealed that these agents affect the composition and diversity of gut microbiota and consequently improve glucose metabolism and energy balance. Possible underlying mechanisms include affecting gene expression, lowering levels of inflammatory cytokines, and regulating the production of short-chain fatty acids. In addition, gut microbiota may alleviate adverse effects caused by glucose-lowering agents, and this can be especially beneficial in diabetic patients who experience severe gastrointestinal side effects and have to discontinue these agents. In conclusion, gut microbiota may provide a novel viewpoint for the treatment of patients with diabetes mellitus.


Author(s):  
Sidharth P Mishra ◽  
Shalini Jain ◽  
Subhash Taraphder ◽  
Hariom Yadav

Abstract Decade-old studies have demonstrated that microbes living in our gut (microbiota) contribute to both maintaining normal metabolic function and to the pathology of metabolic diseases, such as obesity and diabetes. Emerging evidence suggests that gut microbiota influences the personalized effects of diets and drugs and impact the gut–brain axis and leaky gut inflammation to control metabolic function/diseases. Gut microbiota can be an ideal source of prognostic markers and therapies for metabolic diseases. Here we discuss the emerging concepts in the area of microbiota and metabolic interactions in personalized nutrition, drug response, and disease prognosis.


2015 ◽  
Vol 114 (11) ◽  
pp. 1756-1765 ◽  
Author(s):  
J. M. G. Gomes ◽  
J. A. Costa ◽  
R. C. Alfenas

AbstractEvidence from animal and human studies has associated gut microbiota, increased translocation of lipopolysaccharide (LPS) and reduced intestinal integrity (II) with the inflammatory state that occurs in obesity and type 2 diabetes mellitus (T2DM). Consumption of Ca may favour body weight reduction and glycaemic control, but its influence on II and gut microbiota is not well understood. Considering the impact of metabolic diseases on public health and the role of Ca on the pathophysiology of these diseases, this review critically discusses possible mechanisms by which high-Ca diets could affect gut microbiota and II. Published studies from 1993 to 2015 about this topic were searched and selected from Medline/PubMed, Scielo and Lilacs databases. High-Ca diets seem to favour the growth of lactobacilli, maintain II (especially in the colon), reduce translocation of LPS and regulate tight-junction gene expression. We conclude that dietary Ca might interfere with gut microbiota and II modulations and it can partly explain the effect of Ca on obesity and T2DM control. However, further research is required to define the supplementation period, the dose and the type of Ca supplement (milk or salt) required for more effective results. As Ca interacts with other components of the diet, these interactions must also be considered in future studies. We believe that more complex mechanisms involving extraintestinal disorders (hormones, cytokines and other biomarkers) also need to be studied.


2017 ◽  
Vol 8 (5) ◽  
pp. 705-716 ◽  
Author(s):  
M. Gonai ◽  
A. Shigehisa ◽  
I. Kigawa ◽  
K. Kurasaki ◽  
O. Chonan ◽  
...  

Gut microbiota affects the host’s metabolism, and it is suggested that there are differences in gut microbiota composition between patients with type 2 diabetes and healthy individuals. Additionally, dysbiosis may increase the concentration of lipopolysaccharides (LPS), causing metabolic endotoxemia, which induces impaired glucose tolerance. Several studies have reported relationships between metabolic diseases and the gut microbiota; and prebiotics, such as oligosaccharides, are commonly consumed to regulate gut microbiotas in healthy individuals. Galacto-oligosaccharides (GOS) are a major prebiotic, which specifically increase Bifidobacteriaceae abundance. Recent studies have reported that Bifidobacteriaceae improved metabolic endotoxemia or impaired glucose tolerance. However, there are few studies reporting the effects of GOS on patients with type 2 diabetes. In the current study, we compared clinical parameters, faecal gut microbiota, their associated metabolic products and their components such as LPS, and LPS-binding protein (LBP) produced by the host, between patients with diabetes and healthy controls. We then assessed the effects of GOS on glycaemic control, and gut microbiotas and metabolites in patients with type 2 diabetes in a double-blind controlled manner. LBP levels were significantly higher in patients with diabetes than those of healthy subjects, which was consistent with previous reports. The abundance of Bifidobacteriaceae and the diversity of intestinal microbiota were significantly lower in patients with diabetes than in healthy subjects. Interestingly, Bifidobacteriaceae was markedly restored in patients with diabetes after consumption of GOS, whereas LBP and glucose tolerance did not improve during this short-term trial period. In the present study, we demonstrated that GOS can ameliorate dysbiosis in patients with diabetes, and continuous intake of GOS may be a promising method for managing type 2 diabetes.


2021 ◽  
pp. 1-9
Author(s):  
Kazuo Yamashiro ◽  
Naohide Kurita ◽  
Takao Urabe ◽  
Nobutaka Hattori

<b><i>Background:</i></b> Major advances have been made in stroke treatment and prevention in the past decades. However, the burden of stroke remains high. Identification of novel targets and establishment of effective interventions to improve stroke outcomes are, therefore, needed. Recent research highlights the contribution of the gut microbiota to stroke pathogenesis. <b><i>Summary:</i></b> Compositional and functional alterations of the gut microbiota, termed dysbiosis, are linked to stroke risk factors, such as obesity, metabolic diseases, and atherosclerosis. In acute cerebral ischemia, the gut microbiota plays a key role in bidirectional interactions between the gut and brain, referred to as the microbiota-gut-brain axis. Gut dysbiosis prior to ischemic stroke affects outcomes. Additionally, the brain affects the gut microbiota during acute ischemic brain injury, which in turn impacts outcomes. Interactions between the gut microbiota and stroke pathogenesis are mediated by several factors including bacterial components (e.g., lipopolysaccharide), gut microbiota-related metabolites (e.g., short-chain fatty acids and trimethylamine N-oxide), and the immune and nervous systems. Clinical studies have reported that patients with acute ischemic stroke exhibit gut dysbiosis, which is associated with host metabolism and inflammation, as well as functional outcomes. Modulation of the gut microbiota or its metabolites improves conditions related to stroke pathogenesis, including inflammation, cardiometabolic disease, atherosclerosis, and thrombosis. <b><i>Key Messages:</i></b> Accumulating evidence indicates that the gut microbiota plays a possible role in stroke pathogenesis. Modulation of the gut microbiota may provide a novel therapeutic strategy for the treatment and prevention of stroke.


Author(s):  
Natalia Di Tommaso ◽  
Antonio Gasbarrini ◽  
Francesca Romana Ponziani

The intestinal mucosa provides a selective permeable barrier for nutrient absorption and protection from external factors. It consists of epithelial cells, immune cells and their secretions. The gut microbiota participates in regulating the integrity and function of the intestinal barrier in a homeostatic balance. Pathogens, xenobiotics and food can disrupt the intestinal barrier, promoting systemic inflammation and tissue damage. Genetic and immune factors predispose individuals to gut barrier dysfunction, and changes in the composition and function of the gut microbiota are central to this process. The progressive identification of these changes has led to the development of the concept of ‘leaky gut syndrome’ and ‘gut dysbiosis’, which underlie the relationship between intestinal barrier impairment, metabolic diseases and autoimmunity. Understanding the mechanisms underlying this process is an intriguing subject of research for the diagnosis and treatment of various intestinal and extraintestinal diseases.


2018 ◽  
Vol 98 (1) ◽  
pp. 107-116 ◽  
Author(s):  
X. Jia ◽  
L. Jia ◽  
L. Mo ◽  
S. Yuan ◽  
X. Zheng ◽  
...  

Postmenopausal osteoporosis (PMO) is a risk factor for periodontitis, and current therapeutics against PMO prevent the aggravated alveolar bone loss of periodontitis in estrogen-deficient women. Gut microbiota is recognized as a promising therapeutic target for PMO. Berberine extracted from Chinese medicinal plants has shown its effectiveness in the treatment of metabolic diseases such as obesity and diabetes via regulating gut microbiota. Here, we hypothesize that berberine ameliorates periodontal bone loss by improving the intestinal barriers by regulating gut microbiota under an estrogen-deficient condition. Experimental periodontitis was established in ovariectomized (OVX) rats, and the OVX-periodontitis rats were treated with berberine for 7 wk before sacrifice for analyses. Micro–computed tomography and histologic analyses showed that berberine treatment significantly reduced alveolar bone loss and improved bone metabolism of OVX-periodontitis rats as compared with the vehicle-treated OVX-periodontitis rats. In parallel, berberine-treated OVX-periodontitis rats harbored a higher abundance of butyrate-producing gut microbiota with elevated butyrate generation, as demonstrated by 16S rRNA sequencing and high-performance liquid chromatography analysis. Berberine-treated OVX-periodontitis rats consistently showed improved intestinal barrier integrity and decreased intestinal paracellular permeability with a lower level of serum endotoxin. In parallel, IL-17A-related immune responses were attenuated in berberine-treated OVX-periodontitis rats with a lower serum level of proinflammatory cytokines and reduced IL-17A+ cells in alveolar bone as compared with vehicle-treated OVX-periodontitis rats. Our data indicate that gut microbiota is a potential target for the treatment of estrogen deficiency–aggravated periodontal bone loss, and berberine represents a promising adjuvant therapeutic by modulating gut microbiota.


Diseases ◽  
2019 ◽  
Vol 7 (1) ◽  
pp. 21 ◽  
Author(s):  
Nima Jazani ◽  
Javad Savoj ◽  
Michael Lustgarten ◽  
Wei Lau ◽  
Nosratola Vaziri

Chronic kidney disease (CKD) is a worldwide major health problem. Traditional risk factors for CKD are hypertension, obesity, and diabetes mellitus. Recent studies have identified gut dysbiosis as a novel risk factor for the progression CKD and its complications. Dysbiosis can worsen systemic inflammation, which plays an important role in the progression of CKD and its complications such as cardiovascular diseases. In this review, we discuss the beneficial effects of the normal gut microbiota, and then elaborate on how alterations in the biochemical environment of the gastrointestinal tract in CKD can affect gut microbiota. External factors such as dietary restrictions, medications, and dialysis further promote dysbiosis. We discuss the impact of an altered gut microbiota on neuroendocrine pathways such as the hypothalamus–pituitary–adrenal axis, the production of neurotransmitters and neuroactive compounds, tryptophan metabolism, and the cholinergic anti-inflammatory pathway. Finally, therapeutic strategies including diet modification, intestinal alpha-glucosidase inhibitors, prebiotics, probiotics and synbiotics are reviewed.


2019 ◽  
Vol 9 (1) ◽  
Author(s):  
Yong-feng Bai ◽  
Si-wei Wang ◽  
Xiao-xiao Wang ◽  
Yuan-yuan Weng ◽  
Xue-yu Fan ◽  
...  

Abstract Background Flavonoids are reported to modulate the composition of gut microbiota, which play an important role in preventing obesity and associated metabolic diseases. In this study, we investigated the effect of Total Flavonoids of Quzhou Fructus Aurantii Extract (TFQ) on gut microbial community in mice fed with a high-fat diet (HFD). Methods C57BL/6J mice were fed with either a chow diet or HFD with or without oral gavage of TFQ (300 mg/kg/day) for 12 weeks. Results Our data indicate TFQ significantly reduced obesity, inflammatio,n and liver steatosis. TFQ elevates the expression of tight junction proteins and reduces metabolic endotoxemia. In addition, TFQ treatment reverses HFD-induced gut dysbiosis, as indicated by the reduction of Firmicutes to Bacteroidetes ratio, the increase of genera Akkermansia and Alistipes, and the decrease of genera Dubosiella, Faecalibaculum, and Lactobacillus. Conclusion These findings support a prebiotic role of TFQ as a dietary supplement for the intervention of gut dysbiosis and obesity-related metabolic disorders.


2017 ◽  
Vol 71 (Suppl. 1) ◽  
pp. 17-22 ◽  
Author(s):  
Junko Sato ◽  
Akio Kanazawa ◽  
Hirotaka Watada

Background: A high proportion of type 2 diabetes cases are associated with host genetic and environmental factors. During the past decade, microorganisms that inhabit the gut have emerged as contributors to the pathogenesis of obesity and type 2 diabetes. Therefore, manipulation of the human gut microbiota will provide essential clues regarding new therapeutic targets for diabetes. Summary: Several studies have established the presence of gut dysbiosis in patients with type 2 diabetes mellitus, even though there are some differences among the studies that could be explained by differences in ethnicity, diet, and methodology. Gut dysbiosis affects the quality and quantity of short-chain fatty acids and secondary bile acids that act as signaling molecules in energy, glucose, and lipid metabolism. In addition, gut dysbiosis affect intestinal permeability. In particular, a high-fat diet can lead to changes in the gut microbiota that strongly reduce intestinal permeability due to the malfunction of tight junction proteins, such as occludin and ZO-1 [<citeref rid="ref1">1</citeref>]. The formation of leaky gut results in increased plasma levels of lipopolysaccharide, which activate Toll-like receptor 4 and result in innate and adaptive immune responses [<citeref rid="ref2">2</citeref>]. Key messages: Gut dysbiosis play an important role in the pathogenesis of obesity and diabetes, for example, via chronic low-grade inflammation. Normalizing gut dysbiosis could be a new approach to overcome diseases of insulin resistance, such as diabetes mellitus.


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