Gut microbiome in type 1 diabetes: A comprehensive review

Zheng, Peilin; Li, Zhixia; Zhang, Zhou

doi:10.1002/dmrr.3043

Cited by 167 publications

(146 citation statements)

References 105 publications

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“…Moreover, different artemether derivatives were used in various mouse models or cells, which may lead to different conclusions. Second, Chinese traditional medicine, such as berberine, has been shown to be potent in modulating gut microbiota (45,46). Artemether and its derivatives might have differential roles in the changes of gut microbiota.…”

Section: Discussionmentioning

confidence: 99%

Artesunate prevents type 1 diabetes in NOD mice mainly by inducing protective IL‐4—producing T cells and regulatory T cells

Shi

Liu

et al. 2019

FASEB j.

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Type 1 diabetes (T1D) is an autoimmune disease characterized by the immune‐mediated destruction of insulin‐producing β cells. Recent studies showed that in addition to malaria, artemisinin and its derivative, artesunate (AS), could alleviate several autoimmune diseases. However, whether AS has a role in the prevention or treatment of T1D is still unknown. Therefore, in this study we administrated AS or DMSO in the drinking water of nonobese diabetic (NOD) mice, a mouse model of T1D. We found that AS administration significantly prevented the incidence of T1D. The frequency of IL‐4—producing CD4+ single‐positive T cells and CD8+ T cells was significantly elevated, and IFN‐γ—producing T cells were reduced in the spleen and pancreatic lymph nodes. In the pancreas, the skewing to IL‐4—producing T cells was also observed. In addition, more regulatory T cells were found in the pancreas. mRNA levels of proinflammatory cytokines, including TNF‐α and IL‐6, were decreased. In addition, AS administration promoted the functional maturity of β cells in vitro. Our findings demonstrate that AS administration can prevent T1D in NOD mice mainly by reducing autoimmune T cells and increasing protective T cells. Our data constitute the first functional study of AS in T1D, which may provide a new rationale for future translational studies.—Li, Z., Shi, X., Liu, J., Shao, F., Huang, G., Zhou, Z., Zheng, P. Artesunate prevents type 1 diabetes in NOD mice mainly by inducing protective IL‐4—producing T cells and regulatory T cells. FASEB J. 33, 8241–8248 (2019). http://www.fasebj.org

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Section: Discussionmentioning

confidence: 99%

Artesunate prevents type 1 diabetes in NOD mice mainly by inducing protective IL‐4—producing T cells and regulatory T cells

Shi

Liu

et al. 2019

FASEB j.

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“…6 Linkage analysis and genome-wide association studies have identified more than 50 type 1 diabetes mellitus susceptibility genes. 7 Environmental factors also play a role in type 1 diabetes mellitus susceptibility. Viruses or environmental toxins may enhance the progression of type 1 diabetes mellitus by inducing insulitis, an inflammatory infiltrate in the islets of Langerhans found in the pancreas, or by activating the immune system through molecular mimicry of islet autoantigens.…”

Section: E Ti Ology and Epidemi Ology Of Diabe Te Smentioning

confidence: 99%

“…Viruses or environmental toxins may enhance the progression of type 1 diabetes mellitus by inducing insulitis, an inflammatory infiltrate in the islets of Langerhans found in the pancreas, or by activating the immune system through molecular mimicry of islet autoantigens. 7 Use of antibiotics has also been implicated in the pathogenesis of type 1 diabetes mellitus but their role is still controversial. The etiology of type 2 diabetes mellitus is intricate and related to risk factors such as age, genetics, race, and ethnicity, as well as environmental factors such as diet, physical activity, and smoking.…”

Section: E Ti Ology and Epidemi Ology Of Diabe Te Smentioning

confidence: 99%

The impact of diabetes on periodontal diseases

Graves

Ding

Yang

2019

Periodontology 2000

221

172

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The susceptibility and severity of periodontal diseases is made more severe by diabetes, with the impact on the disease process inversely proportional to the level of glycemic control. Although type 1 diabetes mellitus and type 2 diabetes mellitus have different etiologies, and their impact on bone is not identical, they share many of the same complications. Studies in animals and humans agree that both forms of diabetes increase inflammatory events in periodontal tissue, impair new bone formation, and increase expression of RANKL in response to bacterial challenge. High levels of glucose, reactive oxygen species, and advanced glycation end‐products are found in the periodontium of diabetic individuals and lead to increased activation of nuclear factor‐kappa B and expression of inflammatory cytokines such as tumor necrosis factor and interleukin‐1. Studies in animals, moreover, suggest that there are multiple cell types in periodontal tissues that are affected by diabetes, including leukocytes, vascular cells, mesenchymal stem cells, periodontal ligament fibroblasts, osteoblasts, and osteocytes. The etiology of periodontal disease involves the host response to bacterial challenge that is affected by diabetes, which increases the expression of RANKL and reduces coupled bone formation. In addition, the inflammatory response also modifies the oral microbiota to render it more pathogenic, as demonstrated by increased inflammation and bone loss in animals where bacteria are transferred from diabetic donors to germ‐free hosts compared with transfer from normoglycemic donors. This approach has the advantage of not relying upon limited knowledge of the specific bacterial taxa to determine pathogenicity, and examines the overall impact of the microbiota rather than the presumed pathogenicity of a few bacterial groups. Thus, animal studies have provided new insights into pathogenic mechanisms that identify cause‐and‐effect relationships that are difficult to perform in human studies.

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“…Furthermore, intraperitoneal injection of 1,25(OH) 2 D 3 (5 ng/g body weight) for 1 month attenuated metabolic endotoxemia (as evidenced by lower plasma lipopolysaccharides (LPS)) and improved intestinal tight junction integrity, as well as Paneth cell defence in HFD + VDD‐fed mice . An elegant review by Zheng and colleagues showed that evidence is accumulating for a role of vitamin D in improved beta cell function in type 1 diabetes (T1D), possibly via effects on the microbiome . Nevertheless, the underlying mechanisms still need further investigations.…”

Section: Role Of Vitamin D In Gutmentioning

confidence: 99%

Vitamin D deficiency in the aetiology of obesity‐related insulin resistance

Pramono

Jocken

Blaak

2019

Diabetes Metabolism Res

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The obese insulin-resistant state is often associated with low circulating concentration of vitamin D 25-hydroxyvitamin D 3 [25(OH)D 3 ]. Fat sequestration of vitamin D in the expanded obese adipose tissue mass has been pointed out as a plausible explanation for this circulating vitamin D deficiency. However, the putative mechanisms behind this hypovitaminosis D remain to be elucidated. The presence of vitamin D receptor and vitamin D-metabolizing enzymes in insulin-sensitive organs suggests that vitamin D may be involved in glucose and lipid metabolism and may be related to insulin sensitivity. Indeed, mainly in vitro studies support a role of vitamin D in regulating glucose and lipid metabolism in several insulin-sensitive tissues including adipose tissue, skeletal muscle, liver, as well as pancreatic insulin secretion. A potential role of vitamin D in gut barrier function and metabolism has also been suggested. This review summarizes recent knowledge on vitamin D deficiency in the aetiology of obesity-related insulin resistance and discusses potential underlying mechanisms. Finally, the role of vitamin D supplementation on insulin sensitivity and glycaemic control is discussed.

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Gut microbiome in type 1 diabetes: A comprehensive review

Cited by 167 publications

References 105 publications

Artesunate prevents type 1 diabetes in NOD mice mainly by inducing protective IL‐4—producing T cells and regulatory T cells

Artesunate prevents type 1 diabetes in NOD mice mainly by inducing protective IL‐4—producing T cells and regulatory T cells

The impact of diabetes on periodontal diseases

Vitamin D deficiency in the aetiology of obesity‐related insulin resistance

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