Advanced glycation end-products regulate extracellular matrix-adipocyte metabolic crosstalk in diabetes

Strieder‐Barboza, Clarissa; Baker, Nicki A.; Flesher, Carmen G.; Karmakar, Monita; Neeley, Christopher K.; Polsinelli, Dominic; Dimick, Justin B.; Finks, Jonathan F.; Ghaferi, Amir A.; Varban, Oliver A.; Lumeng, Carey N.; O’Rourke, Robert W.

doi:10.1038/s41598-019-56242-z

Cited by 34 publications

(33 citation statements)

References 69 publications

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“…As β-cell function declines and diabetes progresses, poorly controlled blood glucose levels in the form of chronic hyperglycaemia contributes significantly to abnormal protein glycation throughout the islets and other non-pancreatic tissues ( 97 , 98 ). The advanced glycation end-products (AGEs) formed by this process are implicated in both worsening β-cell function as well as in development of long-term diabetic complications including diabetic retinopathy ( 99 , 100 ), nephropathy ( 100 , 101 ), and decreased insulin sensitivity in adipose tissues ( 102 ).…”

Section: Involvement Of Islet Vascular Cells In Diabetesmentioning

confidence: 99%

The Role of Vascular Cells in Pancreatic Beta-Cell Function

et al. 2021

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Insulin-producing β-cells constitute the majority of the cells in the pancreatic islets. Dysfunction of these cells is a key factor in the loss of glucose regulation that characterizes type 2 diabetes. The regulation of many of the functions of β-cells relies on their close interaction with the intra-islet microvasculature, comprised of endothelial cells and pericytes. In addition to providing islet blood supply, cells of the islet vasculature directly regulate β-cell activity through the secretion of growth factors and other molecules. These factors come from capillary mural pericytes and endothelial cells, and have been shown to promote insulin gene expression, insulin secretion, and β-cell proliferation. This review focuses on the intimate crosstalk of the vascular cells and β-cells and its role in glucose homeostasis and diabetes.

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Section: Involvement Of Islet Vascular Cells In Diabetesmentioning

confidence: 99%

The Role of Vascular Cells in Pancreatic Beta-Cell Function

et al. 2021

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“…AGEs’ interaction with the ECM reduces glucose uptake and favors the development of insulin resistance. CD36 is a receptor for AGEs, but it is not involved in this pathomechanism [ 104 ]. However, the interaction of AGE, glycolaldehyde-modified BSA (GA-BSA) or oxLDL with CD36 downregulates leptin expression in adipocytes [ 105 , 106 ] which is associated with ectopic fat deposition and lipotoxicity [ 107 ].…”

Section: The Role Of Cd36 In the Pathogenesis Of Dmmentioning

confidence: 99%

The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications—Update in Pathogenesis, Treatment and Monitoring

Puchałowicz

Rać

2020

Cells

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CD36 is a multiligand receptor contributing to glucose and lipid metabolism, immune response, inflammation, thrombosis, and fibrosis. A wide range of tissue expression includes cells sensitive to metabolic abnormalities associated with metabolic syndrome and diabetes mellitus (DM), such as monocytes and macrophages, epithelial cells, adipocytes, hepatocytes, skeletal and cardiac myocytes, pancreatic β-cells, kidney glomeruli and tubules cells, pericytes and pigment epithelium cells of the retina, and Schwann cells. These features make CD36 an important component of the pathogenesis of DM and its complications, but also a promising target in the treatment of these disorders. The detrimental effects of CD36 signaling are mediated by the uptake of fatty acids and modified lipoproteins, deposition of lipids and their lipotoxicity, alterations in insulin response and the utilization of energy substrates, oxidative stress, inflammation, apoptosis, and fibrosis leading to the progressive, often irreversible organ dysfunction. This review summarizes the extensive knowledge of the contribution of CD36 to DM and its complications, including nephropathy, retinopathy, peripheral neuropathy, and cardiomyopathy.

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“…Diaphanous1 (DIAPH1) is a type of formin which is intracellular bind domain of RAGE. The interaction between DIAPH1 with RAGE is essential for RAGE ligand-mediated signalling in multiple cell types [7][8][9].…”

Section: The Biology Of Ragementioning

confidence: 99%

RAGE signalling in obesity and diabetes: focus on the adipose tissue macrophage

Feng

Zhu

2020

Adipocyte

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The advanced glycosylation end product receptor (RAGE) acts as a recognition receptor and interacts with different types of ligands that form and accumulate in the tissues and circulation, such as diabetes, inflammation, insulin resistance, and obesity. In these environments, RAGE is expressed on the surface of various cells associated with tissue disturbance. This review mainly summarizes the characteristics of RAGE-related signalling, with a particular emphasis on the role of RAGE in the development of obesity. We also briefly describe the phenotypes and characteristics of macrophages and focus on the role of adipose tissue macrophages (ATMs) and the regulatory mechanisms in obesity, diabetes, and other related metabolic diseases. Besides, we will also elaborate on the prospect of new strategies for treating diabetes and obesity-related metabolic diseases by inhibiting RAGE signalling and regulating ATMs recruitment and polarization.

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Advanced glycation end-products regulate extracellular matrix-adipocyte metabolic crosstalk in diabetes

Cited by 34 publications

References 69 publications

The Role of Vascular Cells in Pancreatic Beta-Cell Function

The Role of Vascular Cells in Pancreatic Beta-Cell Function

The Multifunctionality of CD36 in Diabetes Mellitus and Its Complications—Update in Pathogenesis, Treatment and Monitoring

RAGE signalling in obesity and diabetes: focus on the adipose tissue macrophage

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