In: American Journal of Physiology - Endocrinology and Metabolism, 2007, vol. 293, p. E91-E95
Glitazones are peroxisome proliferator-activated receptor (PPAR)-Γ agonists with powerful insulin-sensitizing properties. They promote the development of metabolically active adipocytes that can lead to a substantial gain in fat mass. Telmisartan is an ANG II type 1 receptor antagonist with partial PPAR-Γ agonistic properties. Recently, telmisartan has been reported to prevent weight gain and...
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In: Cardiovascular Diabetology, 2014, vol. 13, no. 1, p. 113
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 L-arginine. Given that arginase-II (Arg-II) exerts some of its biological functions through crosstalk...
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In: Cell Death & Disease, 2018, vol. 9, no. 3, p. 313
Type-II L-arginine:ureahydrolase, arginase-II (Arg-II), is shown to activate mechanistic target of rapamycin complex 1 (mTORC1) pathway and contributes to cell senescence and apoptosis. In an attempt to elucidate the underlying mechanism, we identified myosin-1b (Myo1b) as a mediator. Overexpression of Arg-II induces re-distribution of lysosome and mTOR but not of tuberous sclerosis complex...
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In: Journal of Visualized Experiments, 2016, no. 108, p. -
Endothelium-derived nitric oxide (NO) produced from endothelial NO-synthase (eNOS) is one of the most important vasoprotective molecules in cardiovascular physiology. Dysfunctional eNOS such as uncoupling of eNOS leads to decrease in NO bioavailability and increase in superoxide anion (O₂.−) production, and in turn promotes cardiovascular diseases. Therefore, appropriate...
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In: British Journal of Nutrition, 2011, vol. 105, no. 12, p. 1750-1763
The present study investigates whether excessive fat accumulation and hyperinsulinaemia during catch-up growth on high-fat diets are altered by n-6 and n-3 PUFA derived from oils rich in either linoleic acid (LA), α-linolenic acid (ALA), arachidonic acid (AA) or DHA. It has been shown that, compared with food-restricted rats refed a high-fat (lard) diet low in PUFA, those...
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In: British Journal of Nutrition, 2011, vol. 105, no. 12, p. 1750-1763
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In: Aging Cell, 2012, p. -
Augmented activities of both arginase and S6K1 are involved in endothelial dysfunction in aging. This study was to investigate whether or not there is a crosstalk between arginase and S6K1 in endothelial inflammation and aging in senescent human umbilical vein endothelial cells and in aging mouse models. We show increased arginase-II (Arg-II) expression/activity in senescent endothelial cells....
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In: Immunology, Endocrine & Metabolic Agents - Medicinal Chemistry, 2007, vol. 7, no. 2, p. 137-141
Clinical and experimental studies provide increasing evidence that obesity is a major cardiovascular risk factor and that the adipose tissue is not just for regulation of lipid and energy homeostasis. Accordingly, the endocrine secretion of adipose tissue is implicated in the pathogenesis of vascular diseases. Whilst the functions of visceral and subcutaneous adipose tissue are relatively...
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In: Diabetes, 2017, vol. 66, no. 6, p. 1636–1649
Aging is associated with glucose intolerance. Arginase-II (Arg-II), the type-II L-arginine- ureahydrolase, is highly expressed in pancreas. However, its role in regulation of pancreatic β-cell function is not known. Here we show that female (not male) mice deficient in Arg-II (Arg-II−/−) are protected from age-associated glucose intolerance and reveal greater glucose induced-insulin...
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In: Frontiers in Physiology, 2017, vol. 8, p. -
The mitochondrial arginase type II (Arg-II) has been shown to interact with ribosomal protein S6 kinase 1 (S6K1) and mitochondrial p66Shc and to promote cell senescence, apoptosis and inflammation under pathological conditions. However, the impact of Arg-II on organismal lifespan is not known. In this study, we demonstrate a significant lifespan extension in mice with Arg-II gene deficiency...
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