1,721,084 research outputs found
Recent acquisitions on the pathophysiology of metabolic syndrome [Recenti progressi nelle conoscenze della patogenesi della sindrome metabolica]
No full textThe metabolic syndrome is characterized by metabolic and cardiovascular disorders, including obesity, hypertension, impaired glucose tolerance and dyslipidemia. Recently, metabolic syndrome has been associated with a greater risk of atherosclerotic cardiovascular disease than any of its individual components. Its pathophysiology seems to be largely due to insulin resistance and visceral adiposity, leading to a proinflammatory and prothrombotic milieu that potentiates atherosclerosis. Recent knowledge implies a role for fat-derived "adipokines," as pathogenic contributors or protective factors. Furthermore, low plasma levels of ghrelin, an orexigenic peptide that promotes a positive energy balance, have been associated with the presence of vascular damage in patients with metabolic syndrome
Increased endothelin-1-mediated vasoconstrictor tone in human obesity: effects of gut hormones
No full textThe heavy impact of obesity on the development and progression of cardiovascular disease has sparked sustained efforts to uncover the mechanisms linking excess adiposity to vascular dysfunction. Impaired vasodilator reactivity has been recognized as an early hemodynamic abnormality in obese patients, but also increased vasoconstrictor tone importantly contributes to their vascular damage. In particular, upregulation of the endothelin (ET)-1 system, consistently reported in these patients, might accelerate atherosclerosis and its complication, given the pro-inflammatory and mitogenic properties of ET-1. In recent years, a number of gut hormones, in addition to their role as modulators of food intake, energy balance, glucose and lipid metabolism, and insulin secretion and action, have demonstrated favorable vascular actions. They increase the bioavailability of vasodilator mediators like nitric oxide, but they have also been shown to inhibit the ET-1 system. These features make gut hormones promising tools for targeting both the metabolic and cardiovascular complications of obesity, a view supported by recent large-scale clinical trials indicating that novel drugs for type 2 diabetes with cardiovascular potential may translate into clinically significant advantages. Therefore, there is real hope that better understanding of the properties of gut-derived substances might provide more effective therapies for the obesity-related cardiometabolic syndrome
Obesity, blood vessels and metabolic syndrome
No full textObesity is rising worldwide at an alarming rate and so is the incidence of obesity-related disorders, such as the metabolic syndrome, type 2 diabetes and cardiovascular diseases. The obesity-dependent vascular damage appears to be derived from a variety of changes in the adipose tissue, leading to a chronic inflammatory state and dysregulation of adipocyte-derived factors. This, in turn, impairs vascular homeostasis by determining an unbalance between the protective effect of the nitric oxide pathway and the unfavourable action of the endothelin-1 system. In addition, hyperinsulinemia and insulin resistance contribute to vascular dysfunction because the opposing endothelium-dependent vasodilating and vasoconstrictor effects of insulin are shifted towards a predominant vasoconstriction in patients with obesity. Importantly, emerging evidence suggests that the vascular dysfunction of obesity is not only limited to the endothelium but also involves the other layers of the vessel wall. In particular, obesity-related changes in vascular smooth muscle seem to disrupt the physiological facilitatory action of insulin on the responsiveness to vasodilator stimuli, whereas the adventitia and the perivascular fat appear to be a source of proinflammatory and vasoactive factors that may contribute to endothelial and smooth muscle cell dysfunction and to the pathogenesis of vascular disease
Product Innovation and Imperfect Competition in the Italian fruit-Drink Industry
No full textIn this paper, the case of the Italian fruit-drink industry is presented to discuss the strategic issues of product-innovation in imperfectly competitive markets. In particular, three main topics are addressed: the incentives to the adoption of innovation-based strategies, R&D investments in imperfectly competitive markets and the role of vertical coordination. To address the topics, a brief description of the industry, a game-theory conceptual framework and a strategic analysis of the marketing channels are proposed. The major conclusions can be summarized as follows: (i) product-innovation strategies are the result of an evaluation of the option value of the R&D investments, the risk of failure and competitors' strategies (ii) demand pull only may be insufficient to trigger innovation: an efficient retailing system, costs of failure and production efficiency may influence the firm's strategic approach to innovation
The efficiency of a threshold approach based on farm size to exclude farmers from the benefit of direct payments
No full textThe paper discusses the efficiency of a threshold approach based on farm size to exclude farmers from the benefit of direct payments, as per the Reg. (EU) 1307/13. We use farm-level census data to compare the outcome of the threshold approach with a classification of strategic profiles that identifies agricultural firms with a “non-negligible” farming activities. The empirical analysis concludes that the choice of the efficient threshold depends on the relative weights that are given to two conflicting objectives: the concentration of financial resources on one hand and the support to productive small farmers. In particular the 1-hectare threshold (art. 10 of the abovementioned regulation) is efficient only if the two weights are approximately equal. A spatial analysis suggested that lower threshold should applied in mountain areas or compensation should considered for small farmers using associations or local markets to market their productions
Vascular hyperpolarization in human physiology and cardiovascular risk conditions and disease
No full textHyperpolarization causing smooth muscle relaxation contributes to the maintenance of vascular homeostasis, particularly in small-calibre arteries and arterioles. It may also become a compensatory vasodilator mechanism upregulated in states with impaired nitric oxide (NO) availability. Bioassay of vascular hyperpolarization in the human circulation has been hampered by the complexity of mechanisms involved and the limited availability of investigational tools. Firm evidence, however, supports the notion that hyperpolarization participates in the regulation of resting vasodilator tone and vascular reactivity in healthy subjects. In addition, an enhanced endothelium-derived hyperpolarization contributes to both resting and agonist-stimulated vasodilation in a variety of cardiovascular risk conditions and disease. Thus, hyperpolarization mediated by epoxyeicosatrienoic acids (EETs) and H2 O2 has been observed in coronary arterioles of patients with coronary artery disease. Similarly, ouabain-sensitive and EETs-mediated hyperpolarization has been observed to compensate for NO deficiency in patients with essential hypertension. Moreover, in non-hypertensive patients with multiple cardiovascular risk factors and in hypercholesterolaemia, KCa channel-mediated vasodilation appears to be activated. A novel paradigm establishes that perivascular adipose tissue (PVAT) is an additional regulator of vascular tone/function and endothelium is not the only agent in vascular hyperpolarization. Indeed, some PVAT-derived relaxing substances, such as adiponectin and angiotensin 1-7, may exert anticontractile and vasodilator actions by the opening of KCa channels in smooth muscle cells. Conversely, PVAT-derived factors impair coronary vasodilation via differential inhibition of some K(+) channels. In view of adipose tissue abnormalities occurring in human obesity, changes in PVAT-dependent hyperpolarization may be relevant for vascular dysfunction also in this condition
Osteoprotegerin and outcomes in acute coronary syndromes--when the culprit is not the plaque
No full textNot available
Cardiovascular and metabolic effects of ghrelin
No full textGhrelin is an orexigenic peptide hormone secreted into the systemic circulation predominantly by the X/A-like cells in the mucosa of the stomach. In addiction to central effects on food intake and growth hormone release, ghrelin has also important vascular and metabolic actions. Our laboratory has shown that administration of exogenous ghrelin acutely improves endothelial function by increasing nitric oxide bioavailability and normalizing the alterate balance between endothelin 1/nitric oxide (ET-1/NO) within the vasculature of individuals with metabolic syndrome. Additionally, in endothelial cell cultures, it has been shown that ghrelin directly stimulates NO production using a signaling pathway that involves GHSR-1a, PI 3-kinase, Akt, and eNOS. Other cardiovascular effects of ghrelin include lowering of peripheral resistance, improvement of contractility and cardiac output. In addition ghrelin plays a significant role in the regulation of glucose homeostasis, lipid profiles and body composition. Importantly, ghrelin has antinflammatory and antiapoptotic effects both in vivo and in vitro. This review focuses on the physiological roles of ghrelin in regulating metabolic and endothelial function and on the potential of ghrelin as the therapeutic target to treat metabolic and cardiovascular disorders
Vascular effects of insulin and their relation to endothelial dysfunction, insulin resistance and hypertension
No full text[Endothelial dysfunction and diabetes: possible role in kidney damage]
No full textEndothelial damage, with loss of the vascular protective effects of nitric oxide (NO), is an important early step in the development of microvascular and macrovascular complications of diabetes. Endothelial dysfunction is closely associated with diabetic nephropathy in type 1 and 2 diabetes. In this review we will discuss the mechanisms by which hyperglycemia may cause kidney damage and endothelial dysfunction. Hyperglycemia causes microvascular dysfunction, which contributes to the development of end stage renal disease. Determining the role of endothelial abnormalities in the development of diabetic nephropathy is critical to understanding the etiology and pathogenesis of the microvascular complications of diabetes. Endothelial function can be assessed by invasive and noninvasive techniques both in the coronary and peripheral circulation. Endothelial dysfunction is considered a reversible phenomenon; pharmacological intervention with hypolipidemic agents, insulin sensitizers, ACE inhibitors and angiotensin II receptor blockers (ARB) as well as dietary and lifestyle modifications have been shown to reverse it
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