scholarly journals Gut Microbiota: A Key Regulator in the Effects of Environmental Hazards on Modulates Insulin Resistance

2022 ◽  
Vol 11 ◽  
Author(s):  
Ruixue Huang
Keyword(s):  
Insulin Resistance ◽  
Environmental Factors ◽  
Gut Microbiota ◽  
Health Effect ◽  
Critical Role ◽  
Environmental Hazards ◽  
Baseline Drift ◽  
Short Period ◽  
Drift Theory

Insulin resistance is a hallmark of Alzheimer’s disease (AD), type II diabetes (T2D), and Parkinson’s disease (PD). Emerging evidence indicates that these disorders are typically characterized by alterations in the gut microbiota composition, diversity, and their metabolites. Currently, it is understood that environmental hazards including ionizing radiation, toxic heavy metals, pesticides, particle matter, and polycyclic aromatic hydrocarbons are capable of interacting with gut microbiota and have a non-beneficial health effect. Based on the current study, we propose the hypothesis of “gut microenvironment baseline drift”. According to this “baseline drift” theory, gut microbiota is a temporarily combined cluster of species sharing the same environmental stresses for a short period, which would change quickly under the influence of different environmental factors. This indicates that the microbial species in the gut do not have a long-term relationship; any split, division, or recombination may occur in different environments. Nonetheless, the “baseline drift” theory considers the critical role of the response of the whole gut microbiome. Undoubtedly, this hypothesis implies that the gut microbiota response is not merely a “cross junction” switch; in contrast, the human health or disease is a result of a rich palette of gut-microbiota-driven multiple-pathway responses. In summary, environmental factors, including hazardous and normal factors, are critical to the biological impact of the gut microbiota responses and the dual effect of the gut microbiota on the regulation of biological functions. Novel appreciation of the role of gut microbiota and environmental hazards in the insulin resistance would shed new light on insulin resistance and also promote the development of new research direction and new overcoming strategies for patients.

scholarly journals CD44 contributes to hyaluronan-mediated insulin resistance in skeletal muscle of high-fat-fed C57BL/6 mice

2019 ◽  
Vol 317 (6) ◽  
pp. E973-E983 ◽  
Author(s):  
Annie Hasib ◽  
Chandani K. Hennayake ◽  
Deanna P. Bracy ◽  
Aimée R. Bugler-Lamb ◽  
Louise Lantier ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
High Fat Diet ◽  
Critical Role ◽  
Chow Diet ◽  
Wild Type ◽  
High Fat ◽  
Insulin Resistant ◽  
Beneficial Effects

Extracellular matrix hyaluronan is increased in skeletal muscle of high-fat-fed insulin-resistant mice, and reduction of hyaluronan by PEGPH20 hyaluronidase ameliorates diet-induced insulin resistance (IR). CD44, the main hyaluronan receptor, is positively correlated with type 2 diabetes. This study determines the role of CD44 in skeletal muscle IR. Global CD44-deficient ( cd44−/−) mice and wild-type littermates ( cd44+/+) were fed a chow diet or 60% high-fat diet for 16 wk. High-fat-fed cd44−/− mice were also treated with PEGPH20 to evaluate its CD44-dependent action. Insulin sensitivity was measured by hyperinsulinemic-euglycemic clamp (ICv). High-fat feeding increased muscle CD44 protein expression. In the absence of differences in body weight and composition, despite lower clamp insulin during ICv, the cd44−/− mice had sustained glucose infusion rate (GIR) regardless of diet. High-fat diet-induced muscle IR as evidenced by decreased muscle glucose uptake (Rg) was exhibited in cd44+/+ mice but absent in cd44−/− mice. Moreover, gastrocnemius Rg remained unchanged between genotypes on chow diet but was increased in high-fat-fed cd44−/− compared with cd44+/+ when normalized to clamp insulin concentrations. Ameliorated muscle IR in high-fat-fed cd44−/− mice was associated with increased vascularization. In contrast to previously observed increases in wild-type mice, PEGPH20 treatment in high-fat-fed cd44−/− mice did not change GIR or muscle Rg during ICv, suggesting a CD44-dependent action. In conclusion, genetic CD44 deletion improves muscle IR, and the beneficial effects of PEGPH20 are CD44-dependent. These results suggest a critical role of CD44 in promoting hyaluronan-mediated muscle IR, therefore representing a potential therapeutic target for diabetes.

scholarly journals Role of T Lymphocytes in Type 2 Diabetes and Diabetes-Associated Inflammation

2017 ◽  
Vol 2017 ◽  
pp. 1-6 ◽  
Author(s):  
Chang Xia ◽  
Xiaoquan Rao ◽  
Jixin Zhong
Keyword(s):  
Insulin Resistance ◽  
Type 2 Diabetes ◽  
T Cells ◽  
Immune System ◽  
Critical Role ◽  
Adaptive Immune System ◽  
Metabolic Inflammation ◽  
Adaptive Immune

Although a critical role of adaptive immune system has been confirmed in driving local and systemic inflammation in type 2 diabetes and promoting insulin resistance, the underlying mechanism is not completely understood. Inflammatory regulation has been focused on innate immunity especially macrophage for a long time, while increasing evidence suggests T cells are crucial for the development of metabolic inflammation and insulin resistance since 2009. There was growing evidence supporting the critical implication of T cells in the pathogenesis of type 2 diabetes. We will discuss the available effect of T cells subsets in adaptive immune system associated with the procession of T2DM, which may unveil several potential strategies that could provide successful therapies in the future.

scholarly journals The role of added feed enzymes in promoting gut health in swine and poultry

2013 ◽  
Vol 26 (1) ◽  
pp. 71-88 ◽  
Author(s):  
Elijah Kiarie ◽  
Luis F. Romero ◽  
Charles M. Nyachoti
Keyword(s):  
Gut Microbiota ◽  
Broiler Chickens ◽  
Critical Role ◽  
Gut Health ◽  
Pathogen Challenge ◽  
Nutrient Utilisation ◽  
Host Nutrition ◽  
Feed Enzymes ◽  
The Impact

The value of added feed enzymes (FE) in promoting growth and efficiency of nutrient utilisation is well recognised in single-stomached animal production. However, the effects of FE on the microbiome of the gastrointestinal tract (GIT) are largely unrecognised. A critical role in host nutrition, health, performance and quality of the products produced is played by the intestinal microbiota. FE can make an impact on GIT microbial ecology by reducing undigested substrates and anti-nutritive factors and producing oligosaccharidesin situfrom dietary NSP with potential prebiotic effects. Investigations with molecular microbiology techniques have demonstrated FE-mediated responses on energy utilisation in broiler chickens that were associated with certain clusters of GIT bacteria. Furthermore, investigations using specific enteric pathogen challenge models have demonstrated the efficacy of FE in modulating gut health. Because FE probably change the substrate characteristics along the GIT, subsequent microbiota responses will vary according to the populations present at the time of administration and their reaction to such changes. Therefore, the microbiota responses to FE administration, rather than being absolute, are a continuum or a population of responses. However, recognition that FE can make an impact on the gut microbiota and thus gut health will probably stimulate development of FE capable of modulating gut microbiota to the benefit of host health under specific production conditions. The present review brings to light opportunities and challenges for the role of major FE (carbohydrases and phytase) on the gut health of poultry and swine species with a specific focus on the impact on GIT microbiota.

scholarly journals Genetic and epigenetic factors of caries

2021 ◽  
Vol 105 (1) ◽  
pp. 18-22
Author(s):  
O. Bilynskyi ◽  
◽  
Ye. Kostenko ◽  
Keyword(s):  
Environmental Factors ◽  
Critical Role ◽  
Genetic Component ◽  
Caries Prevalence ◽  
Epigenetic Factors ◽  
Poor Oral Hygiene ◽  
Population Characteristic ◽  
Component Type ◽  
Analytical Approaches

Summary. The paper analyzes the literature on the causes of caries, including the most common epigenetic factors, such as poor oral hygiene, adequate or deficient nutrition, the nature of food, biogeochemical and territorial factors, the content of microelements of water and soil, the level of environmental pollution, etc., as well as considering the genetic component, type of blood group, the structure of the hard tissues of the tooth, including a set of genes responsible for the occurrence and development of carious pathology. It was found that in conditions of fluoride and iodine deficiency, environmental factors have a critical role in the formation of the population-characteristic pattern of changes in dental status associated with the prevalence and intensity of caries. However, variations in these indicators may be partly mediated by the influence of genetically associated factors. The results of the analysis allowed to identify opportunities for the formulation of several independent analytical approaches that would help establish the significance of the genetic component in the structure of caries prognosis in terms of interaction with environmental conditions, actually determining how certain environmental factors can influence changes in genetic predisposition to caries. It can be summarized, that all currently available studies of the role of heredity in the risk structure of caries pathology is divided into two broad categories: identification of specific localized changes in genotype and verification of combinations or sets of such changes that can determine caries risk. Key words: caries, caries intensity, caries prevalence, genetics, twins, epigenetics, environment, saliva pH.

scholarly journals Liver Steatosis, Gut-Liver Axis, Microbiome and Environmental Factors. A Never-Ending Bidirectional Cross-Talk

2020 ◽  
Vol 9 (8) ◽  
pp. 2648 ◽  
Author(s):  
Agostino Di Ciaula ◽  
Jacek Baj ◽  
Gabriella Garruti ◽  
Giuseppe Celano ◽  
Maria De Angelis ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Gut Microbiota ◽  
Intestinal Permeability ◽  
Immune Cells ◽  
Critical Role ◽  
Liver Steatosis ◽  
Food Contaminants ◽  
Microbial Composition ◽  
Alcoholic Fatty Liver ◽  
Molecular Patterns

The prevalence of non-alcoholic fatty liver disease (NAFLD) is increasing worldwide and parallels comorbidities such as obesity, metabolic syndrome, dyslipidemia, and diabetes. Recent studies describe the presence of NAFLD in non-obese individuals, with mechanisms partially independent from excessive caloric intake. Increasing evidences, in particular, point towards a close interaction between dietary and environmental factors (including food contaminants), gut, blood flow, and liver metabolism, with pathways involving intestinal permeability, the composition of gut microbiota, bacterial products, immunity, local, and systemic inflammation. These factors play a critical role in the maintenance of intestinal, liver, and metabolic homeostasis. An anomalous or imbalanced gut microbial composition may favor an increased intestinal permeability, predisposing to portal translocation of microorganisms, microbial products, and cell wall components. These components form microbial-associated molecular patterns (MAMPs) or pathogen-associated molecular patterns (PAMPs), with potentials to interact in the intestine lamina propria enriched in immune cells, and in the liver at the level of the immune cells, i.e., Kupffer cells and stellate cells. The resulting inflammatory environment ultimately leads to liver fibrosis with potentials to progression towards necrotic and fibrotic changes, cirrhosis. and hepatocellular carcinoma. By contrast, measures able to modulate the composition of gut microbiota and to preserve gut vascular barrier might prevent or reverse NAFLD.

scholarly journals Emerging Role of microRNAs and Long Non-Coding RNAs in Sjögren’s Syndrome

Genes ◽  
2021 ◽  
Vol 12 (6) ◽  
pp. 903
Author(s):  
Giada De Benedittis ◽  
Cinzia Ciccacci ◽  
Andrea Latini ◽  
Lucia Novelli ◽  
Giuseppe Novelli ◽  
...  
Keyword(s):  
Environmental Factors ◽  
Sjögren’S Syndrome ◽  
Genetic Predisposition ◽  
Sjögren's Syndrome ◽  
Critical Role ◽  
Sjogren’S Syndrome ◽  
Sjogren's Syndrome ◽  
Non Coding Rnas ◽  
Sjögren‘S Syndrome

Sjögren’s Syndrome (SS) is a chronic autoimmune inflammatory disease. It is considered a multifactorial pathology, in which underlying genetic predisposition, epigenetic mechanisms and environmental factors contribute to development. The epigenetic regulations represent a link between genetic predisposition and environmental factors. Recent studies suggested a regulatory role for non-coding RNAs in critical biological and disease processes. Among non-coding RNAs, microRNAs (miRNAs) and long non-coding RNAs (lncRNAs) play a critical role in the post-transcriptional mRNA expression, forming a complex network of gene expression regulation. This review aims to give an overview of the latest studies that have investigated the role of miRNAs and lncRNAs in the SS. We included papers that investigated the expression of non-coding RNAs on different tissues, in particular on peripheral blood mononuclear cells and salivary glands. However, regarding the involvement of non-coding RNAs genetic variability in SS susceptibility very few data are available. Further research could help to elucidate underlying pathogenic processes of SS and provide new opportunities for the development of targeted therapies.

scholarly journals Hepatocellular Carcinoma Immunotherapy and the Potential Influence of Gut Microbiome

2021 ◽  
Vol 22 (15) ◽  
pp. 7800
Author(s):  
Sally Temraz ◽  
Farah Nassar ◽  
Firas Kreidieh ◽  
Deborah Mukherji ◽  
Ali Shamseddine ◽  
...  
Keyword(s):  
Hepatocellular Carcinoma ◽  
Gut Microbiota ◽  
Gut Microbiome ◽  
Immune Checkpoint ◽  
Immune Checkpoint Inhibitors ◽  
Checkpoint Inhibitors ◽  
Critical Role ◽  
Hepatic Carcinogenesis ◽  
Host Metabolism

Disruptions in the human gut microbiome have been associated with a cycle of hepatocyte injury and regeneration characteristic of chronic liver disease. Evidence suggests that the gut microbiota can promote the development of hepatocellular carcinoma through the persistence of this inflammation by inducing genetic and epigenetic changes leading to cancer. As the gut microbiome is known for its effect on host metabolism and immune response, it comes as no surprise that the gut microbiome may have a role in the response to therapeutic strategies such as immunotherapy and chemotherapy for liver cancer. Gut microbiota may influence the efficacy of immunotherapy by regulating the responses to immune checkpoint inhibitors in patients with hepatocellular carcinoma. Here, we review the mechanisms by which gut microbiota influences hepatic carcinogenesis, the immune checkpoint inhibitors currently being used to treat hepatocellular carcinoma, as well as summarize the current findings to support the potential critical role of gut microbiome in hepatocellular carcinoma (HCC) immunotherapy.

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