Abstract
Proteoglycans are a specific subset of glycoproteins found at the cell surface and in the extracellular matrix, where they interact with a plethora of proteins involved in metabolic homeostasis and meta-inflammation. Over the last decade, new insights have emerged on the mechanism and biological significance of these interactions in the context of diet-induced disorders such as obesity and type-2 diabetes. Complications of energy metabolism drive most diet-induced metabolic disorders, which results in low-grade chronic inflammation, thereby affecting proper function of many vital organs involved in energy homeostasis, such as the brain, liver, kidney, heart and adipose tissue. Here, we discuss how heparan, chondroitin and keratan sulfate proteoglycans modulate obesity-induced metabolic dysfunction and low-grade inflammation that impact the initiation and progression of obesity-associated morbidities.
Highlights
Obesity and its co-morbidities are responsible for a global health problem carrying a significant economic burden
In this review we will describe the central role of heparan, chondroitin and keratan sulfate proteoglycans found in the extracellular matrix (ECM) in processes critical for initiation, progression and the chronic nature of meta-inflammation in the context of obesity and type-2 diabetes (T2D)
Plasma SDC1 correlates with T1D and diabetic kidney disease (DKD) [77] and hypertriglyceridemia in T2D patients [84]; Single nucleotide polymorphisms (SNPs) in SDC4 linked with predisposition to T2D and obesity [78, 79, 80]
Summary
Obesity and its co-morbidities are responsible for a global health problem carrying a significant economic burden. The most common obesity-mediated complications include type-2 diabetes (T2D), cardiovascular disease and chronic kidney disease, yet the contributing mechanisms to these diseases remain to be fully established [1, 2]. Obesity and in particular central adiposity – the excess deposition of visceral fat – is associated with increased serum levels of pro-inflammatory cytokines such as interleukin 6 (IL-6), C-reactive protein (CRP), and tumor necrosis factor (TNF) [3,4,5] This type of low-grade tissue inflammation, called meta-inflammation, of multiple organs such as liver, adipose tissue, pancreas, kidney, heart, and brain is an important contributing risk factor for the development of insulin resistance
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