“Adipokines and Obesity: Bridging the Knowledge Gap”

Leptin

Adiponectin

Apelin

chemerin

interleukin-6 (IL-6)

monocyte chemotactic

protein-1 (MCP-1)

plasminogen activator inhibitor-1 (PAI-1)

Retinol-binding protein 4 (RBP4)

tumour necrosis factor-alpha (TNFα)

visfatin

omentin

vaspin (SERPINA12)

progranulin

CTRP-4

Adipokines are responsible for various processes, including inflammation; energy and appetite modulation; lipid and glucose metabolism; insulin sensitivity; endothelial cell functioning; angiogenesis; the regulation of blood pressure; and hemostasis.

Abnormal or excessive fat accumulation will lead to obesity. Obesity is the primary cause of the development of non-infectious diseases such as type 2 diabetes, cardiovascular disease (CVD), non-alcoholic fatty liver disease (NAFLD), hypertension, stroke, various forms of cancer, and mental health problems. According to The World Obesity Federation, one million people across the globe will be living with obesity as we enter 2030. hyperinsulinemia, insulin resistance, hormonal regulation, and chronic systemic inflammation are major pathogenetic factors in obesity-related complications and their chronicity.

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In obesity, there is an increased accumulation of white adipose tissue (WAT), especially in the visceral region (vwat) influences the adipokines synthesis and secretion, and it is associated with metabolic and cardiovascular disorders due to reduced sensitivity to insulin, low angiogenic potential, and
increased lipolytic activity of (vWAT) adipocytes.

Visceral Adipose tissues are associated with the accumulation of increased visceral fat deposits which enhances the transport of free fatty acid (FFA) to the liver through portal circulation and
disrupts insulin signalling.

A dormant lifestyle and obesity accompany morbid changes in white adipose tissue (WAT) and brown adipose tissue (BAT) morphology and physiology. Major changes are

1.    Adipocyte hypertrophy or hyperplasia.

2.    Inflammation and fibrosis in Adipose tissues.

3.    Adipose-derived signal secretion deregulation.

4.    Reduce BAT mass or activity.

Obesity will cause abnormally increased adipose tissues and increased levels of biologically active adipokines. The size of the Adipocyte rather than its number correlates with the risk of
nutritional-related disorders.

The disproportion between food intake and energy consumption in the body’s metabolic processes causes high levels of adipose tissues. As a result, adipose tissues secrete immoderate levels of adipokines that influence the body’s metabolism. Adipose tissue and the Hypothalamus association authorize practical elucidation of hunger and satiety signals.

It has been proven that in obesity potential of adipose tissue expansion to store extra fat reservoirs causes
metabolic disorders.

Hypertrophic adipocytes show proinflammatory potential and stimulate insulin resistance. These cells synthesize high levels of proinflammatory cytokines, including interleukin 1 beta (IL1β), interleukin 6 (IL6), and tumour necrosis factor-alpha (TNFα), favor the development of civilization-related diseases, including obesity-induced insulin resistance.

Adipose tissues and their Adipokines in the typical optimum environment. Adipokines in the specific optimum environment maintain body homeostasis, including energy, lipid and carbohydrate metabolism, and immune system activity.

In obesity, Adipokines are unable to perform their homeostatic functions in the body anymore, which leads to cause the development of various metabolic disorders.

 

The changes that occur as a result of obesity are unique. Increased lipid storage will cause adipocyte hypertrophy, hypoxia, and cell death. This adipose tissue dysfunction promotes a microenvironment in which the adipocytes begin to secrete proinflammatory cytokines, including TNF-α, IL-6, IL-8, and MCP-1. MCP-1 and other chemokines produced by adipocytes and immune cells promote increased infiltration of
circulating monocytes and other innate and adaptive immune cells into the adipose tissue. Increased monocyte infiltration, self-renewal of tissue-resident adipose tissue macrophages (ATMs), and tissue retention of macrophages all contribute to profound increases in the number of macrophages
within obese adipose.

Obesity is directly associated with an elevated risk of Chronic Kidney disease (CKD). The molecular mechanism which interlinked the two conditions is still debatable. The role of Adipokine is important in obesity-related kidney damage.
In obesity, lipotoxicity and the alteration of the Adipose Tissue secretion profile (Adipokine) promote inflammation, oxidative stress, and fibrosis in the kidney, which ultimately leads to impaired renal function. Adaptation in secretion and signaling mechanism of Adipose Tissues during obesity leads to hypersecretion of proinflammatory cytokines, which stimulate endothelial cells and leucocytes inside the intrarenal blood vessels affecting endothelial barrier function and leading to irreversible tubular injury and nephron failure. Circulating levels of TNFα and IL-6 are correlated with the incidence of CKD.

Impaired Adipose Tissue function during obesity will disrupt normal renal function. Abnormal hypertrophy in the obese Adipose Tissue causes lipotoxicity and altered adipocytokine secretion. Changes in the secretion of adipokines and inflammatory and fibrotic parameters may induce glomerulosclerosis, glomerular and podocyte hypertrophy, albuminuria, and, therefore, chronic renal dysfunction.