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      TheACE2G8790A Polymorphism: Involvement in Type 2 Diabetes Mellitus Combined with Cerebral Stroke

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          Abstract

          <div class="section"> <a class="named-anchor" id="jcla22033-sec-0001"> <!-- named anchor --> </a> <h5 class="section-title" id="d1200685e184">Background</h5> <p id="d1200685e186">We aimed to investigate the correlations between <i> <span style="fixed-case">ACE</span>2 </i> polymorphisms and type 2 diabetes mellitus ( <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span>) combined with cerebral stroke ( <span style="fixed-case">CS</span>). </p> </div><div class="section"> <a class="named-anchor" id="jcla22033-sec-0002"> <!-- named anchor --> </a> <h5 class="section-title" id="d1200685e204">Methods</h5> <p id="d1200685e206">A total of 346 patients treated or hospitalized in our hospital were enrolled, including 181 cases without cerebrovascular complications ( <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span> group) and 165 cases combined with <span style="fixed-case">CS</span> (T2 <span style="fixed-case">DM</span> + <span style="fixed-case">CS</span> group); 284 healthy individuals were selected as the control group. <span style="fixed-case">PCR</span>‐ <span style="fixed-case">RFLP</span> and <span style="fixed-case">ELISA</span> were used to analyze <i> <span style="fixed-case">ACE</span>2 </i> G8790A polymorphisms and serum <span style="fixed-case">ACE</span>2 levels, respectively. </p> </div><div class="section"> <a class="named-anchor" id="jcla22033-sec-0003"> <!-- named anchor --> </a> <h5 class="section-title" id="d1200685e243">Results</h5> <p id="d1200685e245">Significant differences were observed in the genotype/allele frequency of <i> <span style="fixed-case">ACE</span>2 </i> G8790A between the T2 <span style="fixed-case">DM</span> + <span style="fixed-case">CS</span> and control groups, and the T2 <span style="fixed-case">DM</span> and T2 <span style="fixed-case">DM</span> + <span style="fixed-case">CS</span> groups, and in the genotype frequency of <i> <span style="fixed-case">ACE</span>2 </i> G8790A between the T2 <span style="fixed-case">DM</span> and the control groups. The A allele may increase the risk of <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span> combined with <span style="fixed-case">CS</span>. The <span style="fixed-case">AA</span> genotype may also increase the risk of <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span> combined with <span style="fixed-case">CS</span> ( <span style="fixed-case">OR</span> = 3.733, 95% <span style="fixed-case">CI</span> = 2.069–6.738; <span style="fixed-case">OR</span> = 3.597, 95% <span style="fixed-case">CI</span> = 1.884–6.867). Serum <span style="fixed-case">ACE</span>2 levels showed statistically significant differences among the groups. Systolic pressure and diastolic pressure were protective factors of T2 <span style="fixed-case">DM</span> combined with <span style="fixed-case">CS</span>. </p> </div><div class="section"> <a class="named-anchor" id="jcla22033-sec-0004"> <!-- named anchor --> </a> <h5 class="section-title" id="d1200685e323">Conclusion</h5> <p id="d1200685e325">The <i> <span style="fixed-case">ACE</span>2 </i> G8790A polymorphism in <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span> patients was correlated with <span style="fixed-case">CS</span>, and the <span style="fixed-case">A</span> allele might be a risk factor of <span style="fixed-case">T</span>2 <span style="fixed-case">DM</span> combined with <span style="fixed-case">CS</span>. </p> </div>

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          Current views on type 2 diabetes.

          Type 2 diabetes mellitus (T2DM) affects a large population worldwide. T2DM is a complex heterogeneous group of metabolic disorders including hyperglycemia and impaired insulin action and/or insulin secretion. T2DM causes dysfunctions in multiple organs or tissues. Current theories of T2DM include a defect in insulin-mediated glucose uptake in muscle, a dysfunction of the pancreatic beta-cells, a disruption of secretory function of adipocytes, and an impaired insulin action in liver. The etiology of human T2DM is multifactorial, with genetic background and physical inactivity as two critical components. The pathogenesis of T2DM is not fully understood. Animal models of T2DM have been proved to be useful to study the pathogenesis of, and to find a new therapy for, the disease. Although different animal models share similar characteristics, each mimics a specific aspect of genetic, endocrine, metabolic, and morphologic changes that occur in human T2DM. The purpose of this review is to provide the recent progress and current theories in T2DM and to summarize animal models for studying the pathogenesis of the disease.
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            Risk Assessment Tools for Identifying Individuals at Risk of Developing Type 2 Diabetes

            Trials have demonstrated the preventability of type 2 diabetes through lifestyle modifications or drugs in people with impaired glucose tolerance. However, alternative ways of identifying people at risk of developing diabetes are required. Multivariate risk scores have been developed for this purpose. This article examines the evidence for performance of diabetes risk scores in adults by 1) systematically reviewing the literature on available scores and 2) their validation in external populations; and 3) exploring methodological issues surrounding the development, validation, and comparison of risk scores. Risk scores show overall good discriminatory ability in populations for whom they were developed. However, discriminatory performance is more heterogeneous and generally weaker in external populations, which suggests that risk scores may need to be validated within the population in which they are intended to be used. Whether risk scores enable accurate estimation of absolute risk remains unknown; thus, care is needed when using scores to communicate absolute diabetes risk to individuals. Several risk scores predict diabetes risk based on routine noninvasive measures or on data from questionnaires. Biochemical measures, in particular fasting plasma glucose, can improve prediction of such models. On the other hand, usefulness of genetic profiling currently appears limited.
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              From gene to protein—experimental and clinical studies of ACE2 in blood pressure control and arterial hypertension

              Hypertension is a major risk factor for stroke, coronary events, heart and renal failure, and the renin-angiotensin system (RAS) plays a major role in its pathogenesis. Within the RAS, angiotensin converting enzyme (ACE) converts angiotensin (Ang) I into the vasoconstrictor Ang II. An “alternate” arm of the RAS now exists in which ACE2 counterbalances the effects of the classic RAS through degradation of Ang II, and generation of the vasodilator Ang 1-7. ACE2 is highly expressed in the heart, blood vessels, and kidney. The catalytically active ectodomain of ACE2 undergoes shedding, resulting in ACE2 in the circulation. The ACE2 gene maps to a quantitative trait locus on the X chromosome in three strains of genetically hypertensive rats, suggesting that ACE2 may be a candidate gene for hypertension. It is hypothesized that disruption of tissue ACE/ACE2 balance results in changes in blood pressure, with increased ACE2 expression protecting against increased blood pressure, and ACE2 deficiency contributing to hypertension. Experimental hypertension studies have measured ACE2 in either the heart or kidney and/or plasma, and have reported that deletion or inhibition of ACE2 leads to hypertension, whilst enhancing ACE2 protects against the development of hypertension, hence increasing ACE2 may be a therapeutic option for the management of high blood pressure in man. There have been relatively few studies of ACE2, either at the gene or the circulating level in patients with hypertension. Plasma ACE2 activity is low in healthy subjects, but elevated in patients with cardiovascular risk factors or cardiovascular disease. Genetic studies have investigated ACE2 gene polymorphisms with either hypertension or blood pressure, and have produced largely inconsistent findings. This review discusses the evidence regarding ACE2 in experimental hypertension models and the association between circulating ACE2 activity and ACE2 polymorphisms with blood pressure and arterial hypertension in man.
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                Author and article information

                Journal
                Journal of Clinical Laboratory Analysis
                J. Clin. Lab. Anal.
                Wiley
                08878013
                March 2017
                March 2017
                August 08 2016
                : 31
                : 2
                : e22033
                Affiliations
                [1 ]Department of Endocrinology; The Second Affiliated Hospital of Harbin Medical University; Harbin China
                Article
                10.1002/jcla.22033
                6817163
                27500554
                e8cd1313-8782-4eaa-9fe5-1b298e05f037
                © 2016

                http://doi.wiley.com/10.1002/tdm_license_1

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