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Role of Arginase 2 in Murine Retinopathy Associated with Western Diet-Induced Obesity.

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Western diet-induced obesity is linked to the development of metabolic dysfunctions, including type 2 diabetes and complications that include retinopathy, a leading cause of blindness. Aberrant activation of the inflammasome cascade leads to the progression of obesity-induced pathologies. Our lab

Role of Arginase 2 in Systemic Metabolic Activity and Adipose Tissue Fatty Acid Metabolism in Diet-Induced Obese Mice.

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Visceral adipose tissue (VAT) inflammation and metabolic dysregulation are key components of obesity-induced metabolic disease. Upregulated arginase, a ureahydrolase enzyme with two isoforms (A1-cytosolic and A2-mitochondrial), is implicated in pathologies associated with obesity and diabetes. This

Arginase inhibition ameliorates adipose tissue inflammation in mice with diet-induced obesity.

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This study examined whether oral administration of an arginase inhibitor regulates adipose tissue macrophage infiltration and inflammation in mice with high fat diet (HFD)-induced obesity. Male C57BL/6 mice (n = 30) were randomly assigned to control (CTL, n = 10), HFD only (n = 10), and HFD with

Increased levels of circulating arginase I in overweight compared to normal weight adolescents.

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OBJECTIVE Overweight and the metabolic syndrome have become major problems, especially in children and adolescents. Obesity at a young age increases the risk for cardiovascular diseases and diabetes mellitus later in life. An early event in the development of cardiovascular disease is endothelial

Arginase inhibition ameliorates hepatic metabolic abnormalities in obese mice.

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OBJECTIVE We examined whether arginase inhibition influences hepatic metabolic pathways and whole body adiposity in diet-induced obesity. RESULTS After obesity induction by a high fat diet (HFD), mice were fed either the HFD or the HFD with an arginase inhibitor, Nω-hydroxy-nor-L-arginine

Arginase inhibition prevents the development of hypertension and improves insulin resistance in obese rats.

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This study investigated the temporal activation of arginase in obese Zucker rats (ZR) and determined if arginase inhibition prevents the development of hypertension and improves insulin resistance in these animals. Arginase activity, plasma arginine and nitric oxide (NO) concentration, blood

Arginase promotes endothelial dysfunction and hypertension in obese rats.

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OBJECTIVE This study investigated whether arginase contributes to endothelial dysfunction and hypertension in obese rats. METHODS Endothelial function and arginase expression were examined in skeletal muscle arterioles from lean and obese Zucker rats (ZRs). Arginase activity, arginine

Serum fetuin-A and arginase-1 in human obesity model: Is there any interaction between inflammatory status and arginine metabolism?

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Obesity is a major risk factor for many chronic metabolic diseases such as inflammation, insulin resistance (IR) and fatty liver injury. It was reported that obesity causes some variations on the serum levels of fetuin-A and is associated with arginine metabolism, especially arginase-1 levels. The

p38 mitogen-activated protein kinase is involved in arginase-II-mediated eNOS-uncoupling in obesity.

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BACKGROUND Endothelial nitric oxide synthase (eNOS)-uncoupling links obesity-associated insulin resistance and type-II diabetes to the increased incidence of cardiovascular disease. Studies have indicated that increased arginase is involved in eNOS-uncoupling through competing with the substrate

Arginase I and the very low-density lipoprotein receptor are associated with phenotypic biomarkers for obesity.

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OBJECTIVE Obesity is a serious health problem implicated in many metabolic disorders (i.e., hypertension, dyslipidemia, and cardiovascular disease). We examined whether the mRNA of tested genes were linked to blood lipid concentrations and vascular endothelial function as features of

Genetic Targeting of Arginase-II in Mouse Prevents Renal Oxidative Stress and Inflammation in Diet-Induced Obesity.

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Obesity is associated with development and progression of chronic kidney disease (CKD). Recent evidence demonstrates that enhanced levels of the L-arginine:ureahydrolase, including the two isoenzymes arginase-I (Arg-I) and arginase-II (Arg-II) in vascular endothelial cells promote uncoupling of

Aging Modulates the Influence of Arginase on Endothelial Dysfunction in Obesity.

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Objective- Arginase can reduce NO availability. In this study, we explored arginase as a determinant of endothelial dysfunction in small arteries from obese patients and its relationship with aging and microvascular remodeling. Approach and Results- Small arteries were dissected after subcutaneous

Asymmetric dimethylarginine (ADMA) elevation and arginase up-regulation contribute to endothelial dysfunction related to insulin resistance in rats and morbidly obese humans.

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The presence of insulin resistance (IR) is determinant for endothelial dysfunction associated with obesity. Although recent studies have implicated the involvement of mitochondrial superoxide and inflammation in the defective nitric oxide (NO)-mediated responses and subsequent endothelial

Early obesity leads to increases in hepatic arginase I and related systemic changes in nitric oxide and L-arginine metabolism in mice.

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Obesity is a risk factor for vascular endothelial cell dysfunction characterized by low-grade, chronic inflammation. Increased levels of arginase I and concomitant decreases in L-arginine bioavailability are known to play a role in the pathogenesis of vascular endothelial cell dysfunction. In the

Obesity-induced vascular inflammation involves elevated arginase activity.

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Obesity-induced vascular dysfunction involves pathological remodeling of the visceral adipose tissue (VAT) and increased inflammation. Our previous studies showed that arginase 1 (A1) in endothelial cells (ECs) is critically involved in obesity-induced vascular dysfunction. We tested the hypothesis

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