Inflammation and Metabolic Syndrome: An Overview

Hinal Patel,V H Patel

doi:10.12944/crnfsj.3.3.10

Abstract

Inflammation is a reaction to a disrupted tissue homeostasis. Basically it is a tissue-destroying process that involves the recruitment of blood-derived products. Rapidly destroy or isolate the underlying source of the disturbance, removes damaged tissue and restore tissue homeostasis is the primary function of inflammation. Inflammatory and chronic metabolic alterations that together are termed metabolic syndrome. The risk of developing serious pathological conditions such as cardiovascular disease (CVD), type 2 diabetes mellitus (T2DM) and non-alcoholic fatty liver disease (NAFLD) is significantly associated with inflammation and its concurrent multi-organ abnormalities which represent a great burden upon societies, as they require significant resources from health care systems. Thus, understanding the tissue-specific pathogenic processes that lead to disease progression is required for the development of more effective therapeutic approaches.

Highlights

Inflammation Infection by microbial invaders is often implicated as the major convict that promotes inflammatory responses (Figure 1a)
Isolation or rapidly destroy the underlying source of the disturbance, remove damaged tissue and restore tissue homeostasis is the primary functions of inflammation[1]
The first link between inflammation and insulin sensitivity came from early studies that demonstrated that the levels of pro-inflammatory cytokines were increased in the circulation and adipose tissue of obese and diabetic subjects . 21-23 Studies using mouse models demonstrated that pro-inflammatory cytokines inhibit insulin signalling by direct serine phosphorylation of insulin receptor substrate-1 (IRS-1)[24]

Summary

Introduction

Inflammation Infection by microbial invaders is often implicated as the major convict that promotes inflammatory responses (Figure 1a). Regulation of immune cells is the primary role of this cytokine but studies showed that in obese subjects its level increases in adipose tissue (visceral than subcutaneous) and reduces as weight decreases[11]. IL-11 It is found mainly in stromal cells and fibroblasts which inhibits pro-inflummatory cytokine response This marker can be used to see inflammatory bowel disease, thrombocytopenia, chemotherapy-induced mucositis and psoriasis[17]. The first link between inflammation and insulin sensitivity came from early studies that demonstrated that the levels of pro-inflammatory cytokines were increased in the circulation and adipose tissue of obese and diabetic subjects . Chronic levels of free fatty acids and glucose induces inflammation, results in increased apoptosis and impaired insulin secretion of â cells, which prompts the progression from obesity and insulin resistance to overt T2DM26. Clinical studies on gout shows that blockade of IL-1a significantly reduce severity of disease[32]

Conclusion

Kinase Promotes Insulin Resistance During

Abrogation Of Adiponectin Binding And

Findings

Of Surrogate Markers Of Atherosclerosis In