Endothelial dysfunction in pre-diabetes
Endothelial dysfunction in pre-diabetes
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array:17 [ "pii" => "8633" "issn" => "15750922" "estado" => "S300" "fechaPublicacion" => "1999-11-01" "documento" => "article" "crossmark" => 0 "subdocumento" => "fla" "cita" => "Endocrinol Nutr. 1999;46:279" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 1634 "formatos" => array:3 [ "EPUB" => 13 "HTML" => 1526 "PDF" => 95 ] ] "itemSiguiente" => array:15 [ "pii" => "8634" "issn" => "15750922" "estado" => "S300" "fechaPublicacion" => "1999-11-01" "documento" => "article" "crossmark" => 0 "subdocumento" => "fla" "cita" => "Endocrinol Nutr. 1999;46:282" "abierto" => array:3 [ "ES" => false "ES2" => false "LATM" => false ] "gratuito" => false "lecturas" => array:2 [ "total" => 2581 "formatos" => array:3 [ "EPUB" => 10 "HTML" => 2532 "PDF" => 39 ] ] "es" => array:7 [ "idiomaDefecto" => true "titulo" => "Propiedades de medición y utilidad clínica de la versión española del QoL-AGHDA: un instrumento de medida de la calidad de vida relacionada con la salud específico para pacientes adultos con déficit de hormona del crecimiento" "tieneTextoCompleto" => "es" "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "282" ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Measurement properties and clinical usefulness of QoL-AGHDA version: an instrument for quality of life measurement specific for adult patients with growth hormone deficiency" ] ] "contieneTextoCompleto" => array:1 [ "es" => true ] "autores" => array:1 [ 0 => array:2 [ "autoresLista" => "A Lucas, A Gilsanz, A Leal, X Badia, M Herdman, MA Ulie" "autores" => array:6 [ 0 => array:2 [ "Iniciales" => "A" "apellidos" => "Lucas" ] 1 => array:2 [ "Iniciales" => "A" "apellidos" => "Gilsanz" ] 2 => array:2 [ "Iniciales" => "A" "apellidos" => "Leal" ] 3 => array:2 [ "Iniciales" => "X" "apellidos" => "Badia" ] 4 => array:2 [ "Iniciales" => "M" "apellidos" => "Herdman" ] 5 => array:2 [ "Iniciales" => "MA" "apellidos" => "Ulie" ] ] ] ] ] "idiomaDefecto" => "es" "EPUB" => "https://multimedia.elsevier.es/PublicationsMultimediaV1/item/epub/8634?idApp=UINPBA00004N" "url" => "/15750922/0000004600000009/v0_201307121156/8634/v0_201307121156/es/main.assets" ] "en" => array:9 [ "idiomaDefecto" => true "titulo" => "Endothelial dysfunction in pre-diabetes" "tieneTextoCompleto" => true "paginas" => array:1 [ 0 => array:1 [ "paginaInicial" => "279" ] ] "autores" => array:1 [ 0 => array:3 [ "autoresLista" => "E ANASTASIOU" "autores" => array:1 [ 0 => array:3 [ "Iniciales" => "E" "apellidos" => "ANASTASIOU" "referencia" => array:1 [ 0 => array:2 [ "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "afiliaciones" => array:1 [ 0 => array:3 [ "entidad" => "MD. 1st Endocrine Section-Diabetes Center.Alexandra General Hospital. Athens. Greece" "etiqueta" => "<span class="elsevierStyleSup">a</span>" "identificador" => "affa" ] ] ] ] "titulosAlternativos" => array:1 [ "en" => array:1 [ "titulo" => "Endothelial dysfunction in pre-diabetes" ] ] "textoCompleto" => "<p class="elsevierStylePara">Cardiovascular complications are the principal cause of morbidity and mortality among patients with NIDDM, mainly as a result of an acceleration of atherosclerosis and increased thrombosis<span class="elsevierStyleSup">1</span>. One of the early signs in the development of atherosclerosis is endothelial dysfunction. Vascular endothelium is considered as the organ of first-line defense against atherosclerosis: by secreting a variety of dilating and constricting substances it modulates vascular tone. Furthermore it can affect platelet adhesion and aggregation influencing thrombogenicity of the blood, and over the long term participate in cell proliferation and, consequently, in the development and progression of atherosclerosis<span class="elsevierStyleSup">2,3</span>.</p><p class="elsevierStylePara">The predominant relaxing factor secreted by the endothelium is nitric oxide (NO), which is synthesized from the amino acid L-arginine by constitutive activity of nitic oxide synthase, an enzyme present in endothelial cells. Nitric oxide release activates the smooth muscle cell guanylyl cyclase, leading to increased cGMP production and subsequent relaxation<span class="elsevierStyleSup">4</span>.</p><p class="elsevierStylePara">Endothelial function may be clinically assessed through measurements of endothelium dependent vasodilation. Several tests have been developed using either pharmacological or mechanical stimuli; a preserved vasodilatory response is an indication of endothelial integrity. Numerous endothelium dependent agonists have been identified, including acetylcholine, serotonin, bradykinin, thrombin and substance P<span class="elsevierStyleSup">5</span>. In addition, mechanical stimuli, such as an increase in blood flow, result in increased shear stress at the endothelial cell surface leading to enhanced synthesis and release of endothelium-derived NO<span class="elsevierStyleSup">6</span>. The above mentioned pharmacological and mechanical stimuly activate receptors that mediate calcium influx into the endothelial cells. The increased intracelular free calcium levels activate the nitric oxide synthase resulting in NO production<span class="elsevierStyleSup">7</span>. Endothelium dependent vasodilation has been studied in both the coronary and peripheral vessels.</p><p class="elsevierStylePara">Three clinical measures are usually employed in order to assess endogenous NO activity, namely quantitative coronary arteriographic diameter changes in response to varying concentrations of acetylcholine, venous plethysmographic changes in forearm blood flow after acetylcholine infusion and high-resolution ultrasonography. The latter technique is a non-invasive approach suitable for young symptom-free subjects. It assesses changes in the diameter of a conduit artery (such as the brachial artery) caused by a reactive hyperemia induced by a shear stress after vessel occlusion and release<span class="elsevierStyleSup">8</span>. Moreover, it has been shown that abnormalities of flow-mediated dilation (FMD) of the brachial artery correlate significantly with acetylcholine-induced coronary artery vasodilation<span class="elsevierStyleSup">9,10</span>. The three above-mentioned techniques include the concomitant measurement of endothelium independent vasodilation induced through the administration of an exogenous NO donor, such as sodium nitroprusside or nitroglycerine to assess the integrity of smooth muscle cell response.</p><p class="elsevierStylePara">Recently, endothelial dysfunction in both the coronary and brachial arteries has been found to be associated with the presence of the traditional coronary risk factors, before any evidence of atherosclerosis is detected even by intravascular ultrasound. Specifically, it has been associated with hypertension<span class="elsevierStyleSup">11</span>, hypercholesterolemia<span class="elsevierStyleSup">12</span>, smoking<span class="elsevierStyleSup">13</span>, obesi ty<span class="elsevierStyleSup">14</span>. Futhermore, improvement in indothelial function has been demonstrated after interventions that are know to reduce cardiovascular risk factors (e.g. exercise<span class="elsevierStyleSup">15</span> reduction of cholesterol in cholesterol lowering trials<span class="elsevierStyleSup">16</span>).</p><p class="elsevierStylePara">Based on the above, an attractive current hypothesis is that the assessment of endothelial function may serve as an integrating index of overall coronary risk factors.</p><p class="elsevierStylePara">Diabetes mellitus, both type 1<span class="elsevierStyleSup">17,18</span> and type 2<span class="elsevierStyleSup">19,20</span>, has been associated with endothelial dysfunction in several studies. The mechanisms responsible for the impaired vasodilation are incompletely understood, as impaired NO activity by either impaired synthesis or increased breakdown or both may be involved<span class="elsevierStyleSup">21</span>. A factor which plays an important role in endothelial dysfunction is hyperglycemia: acute hyperglycemia impairs endothelium-dependent vasodilation in healthy humans <span class="elsevierStyleItalic">in vivo</span><span class="elsevierStyleSup">22</span>, while chronic hyperglycemia may lead to formation of free radicals directly by glucose auto-oxidation<span class="elsevierStyleSup">23</span> or as a byproduct of increased prostaglandin synthesis<span class="elsevierStyleSup">24</span>. Endothelium-derived NO is thus inactivated. Another proposed mechanisms is hyperglycemia-mediated activation of protein kinase C thorugh increases synthesis of diacylglycerol. Activated protein kinase C results in increased generation of vasoconstrictor prostanoids, which contribute to the formation of reactive oxygen species and perhaps decreased NO synthesis and activity<span class="elsevierStyleSup">25,26</span>. A third possible mechanisms is through formation of advanced glycosilation end-products which form during hyperglycemia via non enzymatic protein glycosilation, and result in NO inactivation and endothelium dysfunction<span class="elsevierStyleSup">27</span>. Moreover, patients with type 2 diabetes mellitus usually also have additional cardiovascular risk factors, such as dyslipemia, which in themselves contribute to varying degress of endothelial dysfunction.</p><p class="elsevierStylePara">Gestational diabetes mellitus (GDM) refers to glucose intolerance that has its onset or first recognition during pregnancy. Pregnancy itself is characterized by the development of significant insulin resistance which, when superimposed on pre-existing defects in insulin action, unmasks even the slightest defects in insulin secretion, resulting in GDM. The vast majority of GDM women will return to normal glucose tolerance after delivery, but are at markedly increased risk to develop type 2 DM in later life. In this way GDM is considered a pre-diabetic state and offers an opportunity to study abnormalities that may appear very early in the natural history of DM type 2<span class="elsevierStyleSup">28,29</span>.</p><p class="elsevierStylePara">In view of the above, we recently assessed endothelial function using FMD of the brachial artery as an index in both non-obese normotensive, normoglycemic women with a history of GDM, and in non obese controls who had normal glucose tolerance during pregnancy<span class="elsevierStyleSup">30</span>. Both groups of women with previous GDM had markedly decreased FMD in the brachial artery compared with control subjects. Furthermore, repeated studies performed after a one-year period in a subgroup of these previous GDM women showed similar results suggesting that endothelial dysfunction is a consistent findings in women with a history of GDM. Flow-mediated dilation was significantly inversely correlated with serum uric acid levels, basal insulin resistance as calculated by homeostasis model assessment, BMI, and serum total cholesterol levels.</p><p class="elsevierStylePara">This effect could either be secondary to the known risk factors related to the insulin resistance syndrome or alternatively it could be due to a more basic pre-existing abnormality. An interesting possibility is that early endothelial dysfunction could be related to the chronic insulin resistance that is known to characterize this group<span class="elsevierStyleSup">31</span>. It has been shown that there is a positive correlation between basal vascular endothelial nitric oxide production and insulin sensitivity in healthy individuals<span class="elsevierStyleSup">32</span>. Furthermore it has been postulated that a defect in the phosphatidylinositol 3-kinase (PI3-K), a signaling pathway of insulin action, may be common in both insulin mediated glucose uptake in muscle cells as well as in insulin stimulated NO production in endothelial cells<span class="elsevierStyleSup">33</span>. The highly significant inverse correlation of FMD with uric levels is in agreement with this explanation, as the latter have been associated with insulin resistance<span class="elsevierStyleSup">34,35</span>. Similar evidence that endothelial dysfunction is present very early and is associated with insulin resistance is provided by a study of normal glucose tolerant first-degree relatives of patients with DM type 2<span class="elsevierStyleSup">36</span>.</p><p class="elsevierStylePara">Apart from the above mentioned hypothesis that this dysfunction may be intrinsic to the insulin resistance state, Took and Goh<span class="elsevierStyleSup">37</span> suggest other interesting mechanisms such as a generalized change in cell membrane biophysical propertial that might alter the presentation of insulin and shear receptors<span class="elsevierStyleSup">38</span>. Another attractive hypothesis, widely discussed currently, is the association of reduced fetal growth with insulin resistance and the future development of type 2 diabetes<span class="elsevierStyleSup">39,40</span>. Interestingly Leeson et al<span class="elsevierStyleSup">41</span> showed that low birth weight was associated with impaired endothelial function in 9 to 11 year old children independently of conventional cardiovascular risk factors.</p><p class="elsevierStylePara">Nevertheless, we cannot exclude the possibility that other abnormalities which accompany the insulin resistance syndrome such as disturbances in lipid metabolism or oxidative stress have a synergistic detrimental effect of endothelial impairment. Dyslipidemia, a feature of the insulin resistance syndrome, is a well-known factor causing endothelial dysfunction<span class="elsevierStyleSup">12,42</span> although according to our findings, non-obese previous GDM women have no significant differences in lipid levels compared to controls. Another possible mechanism that may link the insulin resistance syndrome and endothelial dysfunction is oxidative stress<span class="elsevierStyleSup">43</span>. We recently showed that oral administration of ascorbic acid, a know anti-oxidant, acutely improves endothelium dependent vasodilation of brachial artery<span class="elsevierStyleSup">44</span>.</p><p class="elsevierStylePara">In conclusion, it seems that endothelial dysfunction and possible increased risk of atherogenesis is already present in the prediabetic state. Further investigation is needed to explore the full mechanism that links endothelial dysfunction with the insulin resistance state.</p>" "tienePdf" => false "bibliografia" => array:2 [ "titulo" => "Bibliography" "seccion" => array:1 [ 0 => array:1 [ "bibliografiaReferencia" => array:44 [ 0 => array:3 [ "identificador" => "bib1" "etiqueta" => "1" "referencia" => array:1 [ 0 => array:2 [ "contribucion" => array:1 [ 0 => array:3 [ "titulo" => "The changing faces of macrovascular disease in non-insulin-dependent diabetes mellitus: an epidemic in progress." 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| 2021 December | 16 | 0 | 16 |
| 2021 November | 18 | 1 | 19 |
| 2021 October | 11 | 0 | 11 |
| 2021 September | 23 | 2 | 25 |
| 2021 August | 17 | 1 | 18 |
| 2021 July | 6 | 1 | 7 |
| 2021 June | 14 | 2 | 16 |
| 2021 May | 16 | 3 | 19 |
| 2021 April | 61 | 6 | 67 |
| 2021 March | 39 | 1 | 40 |
| 2021 February | 12 | 1 | 13 |
| 2021 January | 22 | 1 | 23 |
| 2020 December | 19 | 1 | 20 |
| 2020 November | 16 | 0 | 16 |
| 2020 October | 7 | 1 | 8 |
| 2020 September | 12 | 0 | 12 |
| 2020 August | 12 | 1 | 13 |
| 2020 July | 12 | 1 | 13 |
| 2020 June | 21 | 0 | 21 |
| 2020 May | 22 | 0 | 22 |
| 2020 April | 19 | 0 | 19 |
| 2020 March | 13 | 0 | 13 |
| 2020 February | 20 | 0 | 20 |
| 2020 January | 24 | 2 | 26 |
| 2019 December | 18 | 4 | 22 |
| 2019 November | 16 | 0 | 16 |
| 2019 October | 17 | 0 | 17 |
| 2019 September | 15 | 0 | 15 |
| 2019 August | 7 | 2 | 9 |
| 2019 July | 14 | 0 | 14 |
| 2019 June | 26 | 2 | 28 |
| 2019 May | 60 | 0 | 60 |
| 2019 April | 27 | 1 | 28 |
| 2019 March | 9 | 0 | 9 |
| 2019 February | 8 | 0 | 8 |
| 2019 January | 16 | 5 | 21 |
| 2018 December | 9 | 2 | 11 |
| 2018 November | 12 | 5 | 17 |
| 2018 October | 10 | 1 | 11 |
| 2018 September | 7 | 0 | 7 |
| 2018 August | 5 | 0 | 5 |
| 2018 July | 6 | 0 | 6 |
| 2018 June | 5 | 0 | 5 |
| 2018 May | 6 | 0 | 6 |
| 2018 April | 4 | 0 | 4 |
| 2018 March | 4 | 0 | 4 |
| 2018 February | 2 | 0 | 2 |
| 2018 January | 8 | 0 | 8 |
| 2017 December | 6 | 0 | 6 |
| 2017 November | 5 | 0 | 5 |
| 2017 October | 4 | 0 | 4 |
| 2017 September | 9 | 0 | 9 |
| 2017 August | 10 | 0 | 10 |
| 2017 July | 9 | 15 | 24 |
| 2017 June | 9 | 16 | 25 |
| 2017 May | 13 | 7 | 20 |
| 2017 April | 16 | 12 | 28 |
| 2017 March | 8 | 0 | 8 |
| 2017 February | 9 | 0 | 9 |
| 2017 January | 9 | 0 | 9 |
| 2016 December | 15 | 3 | 18 |
| 2016 November | 12 | 0 | 12 |
| 2016 October | 27 | 1 | 28 |
| 2016 September | 19 | 1 | 20 |
| 2016 August | 16 | 4 | 20 |
| 2016 July | 21 | 3 | 24 |
| 2016 June | 34 | 1 | 35 |
| 2016 May | 17 | 3 | 20 |
| 2016 April | 18 | 0 | 18 |
| 2016 March | 15 | 4 | 19 |
| 2016 February | 12 | 1 | 13 |
| 2016 January | 15 | 0 | 15 |
| 2015 December | 18 | 0 | 18 |
| 2015 November | 18 | 0 | 18 |
| 2015 October | 30 | 0 | 30 |
| 2015 September | 17 | 0 | 17 |
| 2015 August | 9 | 0 | 9 |
| 2015 July | 18 | 0 | 18 |
| 2015 June | 7 | 0 | 7 |
| 2015 May | 8 | 0 | 8 |
| 2015 April | 11 | 0 | 11 |
| 2015 March | 10 | 0 | 10 |
| 2015 February | 21 | 0 | 21 |
| 2015 January | 13 | 0 | 13 |
| 2014 December | 15 | 0 | 15 |
| 2014 November | 6 | 0 | 6 |
| 2014 October | 8 | 0 | 8 |
| 2014 September | 2 | 0 | 2 |
| 2014 August | 3 | 0 | 3 |
| 2014 July | 5 | 0 | 5 |
| 2014 June | 4 | 0 | 4 |
| 2014 May | 1 | 0 | 1 |
| 2014 April | 23 | 0 | 23 |
| 2014 March | 4 | 0 | 4 |
| 2014 February | 2 | 0 | 2 |
| 2014 January | 6 | 0 | 6 |
| 2013 December | 3 | 0 | 3 |
| 2013 November | 7 | 0 | 7 |
| 2013 October | 5 | 0 | 5 |
| 2013 September | 11 | 0 | 11 |
| 2013 August | 6 | 0 | 6 |
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