State of the micro-biota of bowels with dislipidemii in the children

The gut microbiota has attracted increasing attention during the last several years as a key player in the pathophysiology of chronic disease. Microbiome is considered to be the link between metabolic disorders, obesity, insulin resistance, dyslipidemia, diabetes, hypertension and cardiovascular diseases. Recent findings have related the intestinal microbiota to a plethora of pathological conditions, including type 2 diabetes, obesity, cholelithiasis and nonalcoholic steatohepatitis. This review presents potential mechanisms for the development of these diseases in response to changes in the gut microbiota. They involve increased gut permeability, low-grade inflammation and autoantibodies. Many studies contradict each other, which confirms the need for further scientific research in this area.

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Regulation of Metabolic Disease-Associated Inflammation by Nutrient Sensors

Mediators of Inflammation ◽

10.1155/2018/8261432 ◽

2018 ◽

Vol 2018 ◽

pp. 1-18 ◽

Cited By ~ 13

Author(s):

Alex S. Yamashita ◽

Thiago Belchior ◽

Fábio S. Lira ◽

Nicolette C. Bishop ◽

Barbara Wessner ◽

...

Keyword(s):

Metabolic Disease ◽

Insulin Resistance ◽

Type 2 Diabetes ◽

Chronic Disease ◽

Visceral Fat ◽

Visceral Obesity ◽

Low Grade ◽

Cell Dysfunction ◽

Low Grade Inflammation

Visceral obesity is frequently associated with the development of type 2 diabetes (T2D), a highly prevalent chronic disease that features insulin resistance and pancreatic β-cell dysfunction as important hallmarks. Recent evidence indicates that the chronic, low-grade inflammation commonly associated with visceral obesity plays a major role connecting the excessive visceral fat deposition with the development of insulin resistance and pancreatic β-cell dysfunction. Herein, we review the mechanisms by which nutrients modulate obesity-associated inflammation.

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IL-6 as a Surrogate Biomarker: The IL-6 Clinical Value for the Diagnosis of Insulin Resistance and Type 2 Diabetes.

10.46940/semrj.02.1007 ◽

2021 ◽

pp. 1-13

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Molecular Mechanisms ◽

Diagnostic Value ◽

Low Grade ◽

Clinical Value ◽

Insulin Resistant ◽

Tnf Α ◽

Low Grade Inflammation

1. Abstract Insulin Resistance is the leading cause of Type 2 diabetes mellitus (T2D). It occurs as a result of lipid disorders and increased levels of circulating free fatty acids (FFAs). FFAs accumulate within the insulin sensitive tissues such as muscle, liver and adipose tissues exacerbating different molecular mechanisms. Increased levels fatty acid has been documented to be strongly associated with insulin resistant states and obesity causing inflammation that eventually causes type 2-diabetes. Among the biomarkers that are accompanying low grade inflammation include IL-1β, IL-6 and TNF-α. The current review point out the importance of measuring the inflammatory biomarkers especially focusing on the conductance and measurement for IL-6 as a screening laboratory test and its diagnostic value in clinical practice.

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Disrupting phosphatase SHP2 in macrophages protects mice from high-fat diet-induced hepatic steatosis and insulin resistance by elevating IL-18 levels

Journal of Biological Chemistry ◽

10.1074/jbc.ra119.011840 ◽

2020 ◽

Vol 295 (31) ◽

pp. 10842-10856 ◽

Cited By ~ 1

Author(s):

Wen Liu ◽

Ye Yin ◽

Meijing Wang ◽

Ting Fan ◽

Yuyu Zhu ◽

...

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Hepatic Steatosis ◽

High Fat Diet ◽

Metabolic Disorders ◽

Metabolic Diseases ◽

Low Grade ◽

High Fat ◽

Caspase 1

Chronic low-grade inflammation plays an important role in the pathogenesis of type 2 diabetes. Src homology 2 domain-containing tyrosine phosphatase-2 (SHP2) has been reported to play diverse roles in different tissues during the development of metabolic disorders. We previously reported that SHP2 inhibition in macrophages results in increased cytokine production. Here, we investigated the association between SHP2 inhibition in macrophages and the development of metabolic diseases. Unexpectedly, we found that mice with a conditional SHP2 knockout in macrophages (cSHP2-KO) have ameliorated metabolic disorders. cSHP2-KO mice fed a high-fat diet (HFD) gained less body weight and exhibited decreased hepatic steatosis, as well as improved glucose intolerance and insulin sensitivity, compared with HFD-fed WT littermates. Further experiments revealed that SHP2 deficiency leads to hyperactivation of caspase-1 and subsequent elevation of interleukin 18 (IL-18) levels, both in vivo and in vitro. Of note, IL-18 neutralization and caspase-1 knockout reversed the amelioration of hepatic steatosis and insulin resistance observed in the cSHP2-KO mice. Administration of two specific SHP2 inhibitors, SHP099 and Phps1, improved HFD-induced hepatic steatosis and insulin resistance. Our findings provide detailed insights into the role of macrophagic SHP2 in metabolic disorders. We conclude that pharmacological inhibition of SHP2 may represent a therapeutic strategy for the management of type 2 diabetes.

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Involvement of gut microbiota in the development of low-grade inflammation and type 2 diabetes associated with obesity

Gut Microbes ◽

10.4161/gmic.19625 ◽

2012 ◽

Vol 3 (4) ◽

pp. 279-288 ◽

Cited By ~ 381

Author(s):

Patrice D. Cani ◽

Melania Osto ◽

Lucie Geurts ◽

Amandine Everard

Keyword(s):

Type 2 Diabetes ◽

Gut Microbiota ◽

Low Grade ◽

Low Grade Inflammation

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Dietary inulin alleviates diverse stages of type 2 diabetes mellitusviaanti-inflammation and modulating gut microbiota in db/db mice

Food & Function ◽

10.1039/c8fo02265h ◽

2019 ◽

Vol 10 (4) ◽

pp. 1915-1927 ◽

Cited By ~ 35

Author(s):

Ke Li ◽

Li Zhang ◽

Jing Xue ◽

Xiaoli Yang ◽

Xiaoying Dong ◽

...

Keyword(s):

Diabetes Mellitus ◽

Type 2 Diabetes ◽

Type 2 Diabetes Mellitus ◽

Gut Microbiota ◽

Low Grade ◽

Gut Dysbiosis ◽

P Type ◽

Low Grade Inflammation

Type 2 diabetes mellitus (T2DM) is closely correlated with chronic low-grade inflammation and gut dysbiosis.

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Obesity, Bioactive Lipids, and Adipose Tissue Inflammation in Insulin Resistance

Nutrients ◽

10.3390/nu12051305 ◽

2020 ◽

Vol 12 (5) ◽

pp. 1305 ◽

Cited By ~ 8

Author(s):

Iwona Kojta ◽

Marta Chacińska ◽

Agnieszka Błachnio-Zabielska

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Adipose Tissue ◽

Biologically Active ◽

Bioactive Molecules ◽

Low Grade ◽

Bioactive Lipids ◽

Chain Acyl ◽

Low Grade Inflammation

Obesity is a major risk factor for the development of insulin resistance and type 2 diabetes. The exact mechanism by which adipose tissue induces insulin resistance is still unclear. It has been demonstrated that obesity is associated with the adipocyte dysfunction, macrophage infiltration, and low-grade inflammation, which probably contributes to the induction of insulin resistance. Adipose tissue synthesizes and secretes numerous bioactive molecules, namely adipokines and cytokines, which affect the metabolism of both lipids and glucose. Disorders in the synthesis of adipokines and cytokines that occur in obesity lead to changes in lipid and carbohydrates metabolism and, as a consequence, may lead to insulin resistance and type 2 diabetes. Obesity is also associated with the accumulation of lipids. A special group of lipids that are able to regulate the activity of intracellular enzymes are biologically active lipids: long-chain acyl-CoAs, ceramides, and diacylglycerols. According to the latest data, the accumulation of these lipids in adipocytes is probably related to the development of insulin resistance. Recent studies indicate that the accumulation of biologically active lipids in adipose tissue may regulate the synthesis/secretion of adipokines and proinflammatory cytokines. Although studies have revealed that inflammation caused by excessive fat accumulation and abnormalities in lipid metabolism can contribute to the development of obesity-related insulin resistance, further research is needed to determine the exact mechanism by which obesity-related insulin resistance is induced.

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Therapeutic Effects of Quercetin on Inflammation, Obesity, and Type 2 Diabetes

Mediators of Inflammation ◽

10.1155/2016/9340637 ◽

2016 ◽

Vol 2016 ◽

pp. 1-5 ◽

Cited By ~ 58

Author(s):

Shuang Chen ◽

Hongmei Jiang ◽

Xiaosong Wu ◽

Jun Fang

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Capillary Permeability ◽

Therapeutic Effects ◽

Low Grade ◽

Beneficial Effects ◽

Anti Inflammatory ◽

Low Grade Inflammation

In previous studies, abdominal obesity has been related to total low-grade inflammation and in some cases has resulted in insulin resistance and other metabolism related disorders such as diabetes. Quercetin is a polyphenol, which is a derivative of plants, and has been shownin vitroas well as in a few animal models to have several potential anti-inflammatory as well as anticarcinogenic applications. The substance has also been shown to aid in the attenuation of lipid peroxidation, platelet aggregation, and capillary permeability. However, further research is called for to gain a better understanding of how quercetin is able to provide these beneficial effects. This manuscript reviewed quercetin’s anti-inflammatory properties in relation to obesity and type 2 diabetes.

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Gut microbiota controls adipose tissue expansion, gut barrier and glucose metabolism: novel insights into molecular targets and interventions using prebiotics

Beneficial Microbes ◽

10.3920/bm2012.0065 ◽

2014 ◽

Vol 5 (1) ◽

pp. 3-17 ◽

Cited By ~ 149

Author(s):

L. Geurts ◽

A.M. Neyrinck ◽

N.M. Delzenne ◽

C. Knauf ◽

P.D. Cani

Keyword(s):

Insulin Resistance ◽

Type 2 Diabetes ◽

Adipose Tissue ◽

Glucose Metabolism ◽

Gut Microbiota ◽

Endocannabinoid System ◽

Gut Permeability ◽

Gut Barrier ◽

Glucagon Like Peptide

Crosstalk between organs is crucial for controlling numerous homeostatic systems (e.g. energy balance, glucose metabolism and immunity). Several pathological conditions, such as obesity and type 2 diabetes, are characterised by a loss of or excessive inter-organ communication that contributes to the development of disease. Recently, we and others have identified several mechanisms linking the gut microbiota with the development of obesity and associated disorders (e.g. insulin resistance, type 2 diabetes, hepatic steatosis). Among these, we described the concept of metabolic endotoxaemia (increase in plasma lipopolysaccharide levels) as one of the triggering factors leading to the development of metabolic inflammation and insulin resistance. Growing evidence suggests that gut microbes contribute to the onset of low-grade inflammation characterising these metabolic disorders via mechanisms associated with gut barrier dysfunctions. We have demonstrated that enteroendocrine cells (producing glucagon-like peptide-1, peptide YY and glucagon-like peptide-2) and the endocannabinoid system control gut permeability and metabolic endotoxaemia. Recently, we hypothesised that specific metabolic dysregulations occurring at the level of numerous organs (e.g. gut, adipose tissue, muscles, liver and brain) rely from gut microbiota modifications. In this review, we discuss the mechanisms linking gut permeability, adipose tissue metabolism, and glucose homeostasis, and recent findings that show interactions between the gut microbiota, the endocannabinoid system and the apelinergic system. These specific systems are discussed in the context of the gut-to-peripheral organ axis (intestine, adipose tissue and brain) and impacts on metabolic regulation. In the present review, we also briefly describe the impact of a variety of non-digestible nutrients (i.e. inulin-type fructans, arabinoxylans, chitin glucans and polyphenols). Their effects on the composition of the gut microbiota and activity are discussed in the context of obesity and type 2 diabetes.

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