scholarly journals Clustering of Insulin Resistance With Vascular Dysfunction and Low-Grade Inflammation in Type 2 Diabetes

Diabetes ◽  
2006 ◽  
Vol 55 (4) ◽  
pp. 1133-1140 ◽  
Author(s):  
A. Natali ◽  
E. Toschi ◽  
S. Baldeweg ◽  
D. Ciociaro ◽  
S. Favilla ◽  
...  
2021 ◽  
pp. 1-13

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.


F1000Research ◽  
2018 ◽  
Vol 7 ◽  
pp. 1283 ◽  
Author(s):  
Thomas van Sloten ◽  
Miranda Schram

Depression is twice as common in type 2 diabetes as in the general population and is associated with adverse health outcomes. Growing evidence suggest that type 2 diabetes and depression share biological mechanisms. This brief commentary discusses current understanding of shared biological pathways, focussing on hyperglycaemia, (micro)vascular dysfunction, and low-grade inflammation. Although there is accumulating evidence that these pathways are involved in the link between type 2 diabetes and depression, direct evidence of their temporal associations is lacking because of a paucity of longitudinal studies that focus on the pathobiology of both type 2 diabetes and depression.


Nutrients ◽  
2020 ◽  
Vol 12 (5) ◽  
pp. 1305 ◽  
Author(s):  
Iwona Kojta ◽  
Marta Chacińska ◽  
Agnieszka Błachnio-Zabielska

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.


2018 ◽  
Vol 2018 ◽  
pp. 1-18 ◽  
Author(s):  
Alex S. Yamashita ◽  
Thiago Belchior ◽  
Fábio S. Lira ◽  
Nicolette C. Bishop ◽  
Barbara Wessner ◽  
...  

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.


2016 ◽  
Vol 2016 ◽  
pp. 1-5 ◽  
Author(s):  
Shuang Chen ◽  
Hongmei Jiang ◽  
Xiaosong Wu ◽  
Jun Fang

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.


Author(s):  
L. A. Kharitonova ◽  
O. V. Papisheva ◽  
T. A. Mayatskaya ◽  
G. A. Kotaysh

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.


2016 ◽  
Vol 57 (3) ◽  
pp. 77-90
Author(s):  
V. M. Pushkarev ◽  
L. K. Sokolova ◽  
V. V. Pushkarev ◽  
M. D. Tronko

It was analyzed the cellular and molecular links between chronic low-grade inflammation and caused by inflammation insulin resistance and type 2 diabetes. Particular emphasis is placed on the participation of AMPK and mTORC1 in the development of metabolic diseases caused by obesity. A detailed analysis of the biochemical mechanisms of action of the main drug used in the treatment of insulin resistance and type 2 diabetes — metformin.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1726-P
Author(s):  
MARIE MONLUN ◽  
VINCENT RIGALLEAU ◽  
LAURENCE BLANCO ◽  
KAMEL MOHAMMEDI ◽  
PATRICK BLANCO

Author(s):  
Charmaine S. Tam ◽  
Leanne M. Redman

AbstractObesity is characterized by a state of chronic low-grade inflammation due to increased immune cells, specifically infiltrated macrophages into adipose tissue, which in turn secrete a range of proinflammatory mediators. This nonselective low-grade inflammation of adipose tissue is systemic in nature and can impair insulin signaling pathways, thus, increasing the risk of developing insulin resistance and type 2 diabetes. The aim of this review is to provide an update on clinical studies examining the role of adipose tissue in the development of obesity-associated complications in humans. We will discuss adipose tissue inflammation during different scenarios of energy imbalance and metabolic dysfunction including obesity and overfeeding, weight loss by calorie restriction or bariatric surgery, and conditions of insulin resistance (diabetes, polycystic ovarian syndrome).


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