scholarly journals Metabolic disturbances linked to obesity: the role of impaired tissue perfusion

2009 ◽  
Vol 53 (2) ◽  
pp. 238-245 ◽  
Author(s):  
Nivaldo Ribeiro Villela ◽  
Luiz Guilherme Kramer-Aguiar ◽  
Daniel Alexandre Bottino ◽  
Nicolas Wiernsperger ◽  
Eliete Bouskela

Associated with elevated risk of cardiovascular events and cancer, obesity is a worldwide problem affecting developed and developing countries. Microcirculatory vessels, represented by arterioles, capillaries and venules (mean internal diameter < 100 µm), are the place where blood/tissue nutrition and exchange effectively take place. Microvascular dysfunction is an early event in obesity probably secondary to endothelial dysfunction and capillaries rarefaction. New research techniques allow the investigation of the microcirculation in different vascular beds in humans. Studies suggest a link between endothelial dysfunction and visceral obesity. Oxidative stress, inflammation and rennin-angiotensin system are among factors considered to be involved on microvascular dysfunction in obesity. Microcirculatory impairment present in obesity suggests that it could be an important causal factor in obesity-related disorders such as insulin resistance and hypertension.

2013 ◽  
Vol 59 (8) ◽  
pp. 1166-1174 ◽  
Author(s):  
Fina Lovren ◽  
Subodh Verma

BACKGROUND Endothelial dysfunction is an early event in the development and progression of a wide range of cardiovascular diseases. Various human studies have identified that measures of endothelial dysfunction may offer prognostic information with respect to vascular events. Microparticles (MPs) are a heterogeneous population of small membrane fragments shed from various cell types. The endothelium is one of the primary targets of circulating MPs, and MPs isolated from blood have been considered biomarkers of vascular injury and inflammation. CONTENT This review summarizes current knowledge of the potential functional role of circulating MPs in promoting endothelial dysfunction. Cells exposed to different stimuli such as shear stress, physiological agonists, proapoptotic stimulation, or damage release MPs, which contribute to endothelial dysfunction and the development of cardiovascular diseases. Numerous studies indicate that MPs may trigger endothelial dysfunction by disrupting production of nitric oxide release from vascular endothelial cells and subsequently modifying vascular tone. Circulating MPs affect both proinflammatory and proatherosclerotic processes in endothelial cells. In addition, MPs can promote coagulation and inflammation or alter angiogenesis and apoptosis in endothelial cells. SUMMARY MPs play an important role in promoting endothelial dysfunction and may prove to be true biomarkers of disease state and progression.


2010 ◽  
Vol 7 (2) ◽  
pp. 115
Author(s):  
Antonio Aversa ◽  
Roberto Bruzziches ◽  
Davide Francomano ◽  
Emanuela A Greco ◽  
Silvia Migliaccio ◽  
...  

Normal vascular endothelium is essential for the synthesis and release of substances affecting vascular tone, cell adhesion and the homoeostasis of clotting and fibrinolysis. The degeneration of endothelial integrity promotes adverse events leading to atherogenesis. Circulating levels of endogenous hormones decline during ageing and this may contribute to the occurrence of major adverse cardiovascular events, independently of gender differences. During the last decade more attention has been drawn to the importance of testosterone, oestradiol and adrenal androgens in the pathophysiology, prevention and treatment of male ageing-associated diseases. A considerable body of literature is available indicating that steroid hormones, particularly the sex steroids, are known to modulate endothelial function in all vascular beds and their deficiency may promote endothelial dysfunction. Testosterone decrease and increased mineralocorticoid activity in the ageing male are frequent and may yield endothelial dysfunction and increased cardiovascular burden; we recommend careful hormonal investigations in men who present comorbidities such as diabetes, hypertension and dyslipidaemia.


2017 ◽  
Vol 45 (6) ◽  
pp. 1901-1929 ◽  
Author(s):  
Aleksandar Kibel ◽  
Kristina Selthofer-Relatic ◽  
Ines Drenjancevic ◽  
Tatjana Bacun ◽  
Ivica Bosnjak ◽  
...  

The significance, mechanisms and consequences of coronary microvascular dysfunction associated with diabetes mellitus are topics into which we have insufficient insight at this time. It is widely recognized that endothelial dysfunction that is caused by diabetes in various vascular beds contributes to a wide range of complications and exerts unfavorable effects on microcirculatory regulation. The coronary microcirculation is precisely regulated through a number of interconnected physiological processes with the purpose of matching local blood flow to myocardial metabolic demands. Dysregulation of this network might contribute to varying degrees of pathological consequences. This review discusses the most important findings regarding coronary microvascular dysfunction in diabetes from pre-clinical and clinical perspectives.


2012 ◽  
Vol 113 (2) ◽  
pp. 184-191 ◽  
Author(s):  
Sophocles Chrissobolis ◽  
Botond Banfi ◽  
Christopher G. Sobey ◽  
Frank M. Faraci

Angiotensin II (Ang II) promotes vascular disease through several mechanisms including by producing oxidative stress and endothelial dysfunction. Although multiple potential sources of reactive oxygen species exist, the relative importance of each is unclear, particularly in individual vascular beds. In these experiments, we examined the role of NADPH oxidase (Nox1 and Nox2) in Ang II-induced endothelial dysfunction in the cerebral circulation. Treatment with Ang II (1.4 mg·kg−1·day−1 for 7 days), but not vehicle, increased blood pressure in all groups. In wild-type (WT; C57Bl/6) mice, Ang II reduced dilation of the basilar artery to the endothelium-dependent agonist acetylcholine compared with vehicle but had no effect on responses in Nox2-deficient (Nox2−/y) mice. Ang II impaired responses to acetylcholine in Nox1 WT (Nox1+/y) and caused a small reduction in responses to acetylcholine in Nox1-deficient (Nox1−/y) mice. Ang II did not impair responses to the endothelium-independent agonists nitroprusside or papaverine in either group. In WT mice, Ang II increased basal and phorbol-dibutyrate-stimulated superoxide production in the cerebrovasculature, and these increases were abolished in Nox2−/y mice. Overall, these data suggest that Nox2 plays a relatively prominent role in mediating Ang II-induced oxidative stress and cerebral endothelial dysfunction, with a minor role for Nox1.


2011 ◽  
Vol 07 (02) ◽  
pp. 145
Author(s):  
Antonio Aversa ◽  
Roberto Bruzziches ◽  
Davide Francomano ◽  
Emanuela A Greco ◽  
Silvia Migliaccio ◽  
...  

Normal vascular endothelium is essential for the synthesis and release of substances affecting vascular tone, cell adhesion, and the homoeostasis of clotting and fibrinolysis. The degeneration of endothelial integrity promotes adverse events leading to atherogenesis. Circulating levels of endogenous hormones decline during aging and this may contribute to the occurrence of major adverse cardiovascular events, independently of gender differences. During the last decade, more attention has been drawn to the importance of testosterone, estradiol and adrenal androgens in the pathophysiology, prevention, and treatment of male aging-associated diseases. A considerable body of literature is available indicating that steroid hormones, particularly the sex steroids, are known to modulate endothelial function in all vascular beds and that their deficiency may promote endothelial dysfunction. Testosterone decrease and increased mineralocorticoid activity in the aging male are frequent and may yield endothelial dysfunction and increased cardiovascular burden. We recommend careful hormonal investigations in men who present comorbidities such as diabetes, hypertension and dyslipidemia.


2011 ◽  
Vol 10 (3) ◽  
pp. 72-75 ◽  
Author(s):  
S. N. Tolstov ◽  
V. B. Mychka

The paper presents modern views on cardiovascular aspects of menopause and metabolic therapy of menopausal disturbances with meldonium (Mildronate®). The role of estrogen deficiency in climacteric disturbance development, key pathogenetic mechanisms of menopausal metabolic syndrome (MS), and relevant features of arterial hypertension and endothelial dysfunction development are discussed. The data on Mildronate® clinical use for cardiovascular prevention are summarized. The wide prevalence and multiple clinical manifestations of menopausal disturbances point to the need for their complex therapy. Mildronate® therapy is a new approach for systemic correction of metabolic disturbances in women with climacteric symptoms and menopausal MS.


Author(s):  
Daniela Menichini ◽  
Gianpiero Forte ◽  
Beatrice Orrù ◽  
Giuseppe Gullo ◽  
Vittorio Unfer ◽  
...  

Abstract. Vitamin D is a secosteroid hormone that plays a pivotal role in several metabolic and reproductive pathways in humans. Increasing evidence supports the role of vitamin D deficiency in metabolic disturbances and infertility in women with polycystic ovary syndrome (PCOS). Indeed, supplementation with vitamin D seems to have a beneficial role on insulin resistance and endometrial receptivity. On the other hand, exceedingly high levels of vitamin D appear to play a detrimental role on oocytes development and embryo quality. In the current review, we summarize the available evidence about the topic, aiming to suggest the best supplementation strategy in women with PCOS or, more generally, in those with metabolic disturbances and infertility. Based on the retrieved data, vitamin D seems to have a beneficial role on IR, insulin sensitivity and endometrial receptivity, but high levels and incorrect timing of administration seem to have a detrimental role on oocytes development and embryo quality. Therefore, we encourage a low dose supplementation (400–800 IU/day) particularly in vitamin D deficient women that present metabolic disturbances like PCOS. As far as the reproductive health, we advise vitamin D supplementation in selected populations, only during specific moments of the ovarian cycle, to support the luteal phase. However, ambiguities about dosage and timing of the supplementation still emerge from the clinical studies published to date and further studies are required.


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