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      Association of TRPC1 Gene Polymorphisms with Type 2 Diabetes and Diabetic Nephropathy in Han Chinese Population

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          Abstract

          The recent genome-wide association studies reveal that chromosome 3q resides within the linkage region for diabetic nephropathy (DN) in type 1 and type 2 diabetes mellitus (T1D and T2D). The TRPC1 gene is on chromosome 3q22-24, and it has been demonstrated that TRPC1 expression is reduced in the kidney of diabetic animal models. Genetic association of TRPC1 polymorphism with T1D and DN has been reported in European Americans. However, there are no studies reporting the association of TRPC1 genetic polymorphism with T2D with and without DN in Chinese population. This study aimed to demonstrate the genetic role of TRPC1 in the development of T2D with and without DN in Chinese Han population. A genetic association study of TRPC1 was performed in T2D cases and in nondiabetic controls from Han population located in Northern Chinese areas. Six tag single nucleotide polymorphism (SNP) markers derived from HapMap data were genotyped. Among the six SNPs, only rs7638459 was suspected as risk factor of T2D without DN, fitting the log-additive model. The adjusted odds ratio (OR) for the CC genotyping was 2.39 (95% confidence interval (CI) = 1.00–5.68), compared with the TT genotyping. In addition, rs953239 was found to be a protective factor of getting DN in T2D, also fitting the log-additive model. When compared with the AA genotyping for SNP rs953239, the adjusted OR for CC genotyping was 0.63 (95% CI = 0.44–0.99). To summarize, this study shows that TRPC1 genetic polymorphisms are associated with T2D and DN in T2D in the Han Chinese population.

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          Diabetic nephropathy: mechanisms of renal disease progression.

          Yashpal S Kanwar, Jun Wada, Lin Sun … (2008)
          Diabetic nephropathy is characterized by excessive amassing of extracellular matrix (ECM) with thickening of glomerular and tubular basement membranes and increased amount of mesangial matrix, which ultimately progress to glomerulosclerosis and tubulo-interstitial fibrosis. In view of this outcome, it would mean that all the kidney cellular elements, i.e., glomerular endothelia, mesangial cells, podocytes, and tubular epithelia, are targets of hyperglycemic injury. Conceivably, high glucose activates various pathways via similar mechanisms in different cell types of the kidney except for minor exceptions that are related to the selective expression of a given molecule in a particular renal compartment. To begin with, there is an obligatory excessive channeling of glucose intermediaries into various metabolic pathways with generation of advanced glycation products (AGEs), activation of protein kinase C (PKC), increased expression of transforming growth factor-beta (TGF-beta), GTP-binding proteins, and generation of reactive oxygen species (ROS). The ROS seem to be the common denominator in various pathways and are central to the pathogenesis of hyperglycemic injury. In addition, there are marked alterations in intraglomerular hemodynamics, i.e., hyperfiltration, and this along with metabolic derangements adversely compounds the hyperglycemia-induced injury. Here, the information compiled under various subtitles of this article is derived from an enormous amount of data summarized in several excellent literature reviews, and thus their further reading is suggested to gain in-depth knowledge of each of the subject matter.
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            Prevalence of diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults. The Third National Health and Nutrition Examination Survey, 1988-1994.

            Daniel Little, Brian D Byrd, Nathaniel Goldstein … (1998)
            To evaluate the prevalence and time trends for diagnosed and undiagnosed diabetes, impaired fasting glucose, and impaired glucose tolerance in U.S. adults by age, sex, and race or ethnic group, based on data from the Third National Health and Nutrition Examination Survey, 1988-1994 (NHANES III) and prior Health and Nutrition Examination Surveys (HANESs). NHANES III contained a probability sample of 18,825 U.S. adults > or = 20 years of age who were interviewed to ascertain a medical history of diagnosed diabetes, a subsample of 6,587 adults for whom fasting plasma glucose values were obtained, and a subsample of 2,844 adults between 40 and 74 years of age who received an oral glucose tolerance test. The Second National Health and Nutrition Examination Survey, 1976-1980, and Hispanic HANES used similar procedures to ascertain diabetes. Prevalence was calculated using the 1997 American Diabetes Association fasting plasma glucose criteria and the 1980-1985 World Health Organization (WHO) oral glucose tolerance test criteria. Prevalence of diagnosed diabetes in 1988-1994 was estimated to be 5.1% for U.S. adults > or = 20 years of age (10.2 million people when extrapolated to the 1997 U.S. population). Using American Diabetes Association criteria, the prevalence of undiagnosed diabetes (fasting plasma glucose > or = 126 mg/dl) was 2.7% (5.4 million), and the prevalence of impaired fasting glucose (110 to < 126 mg/dl) was 6.9% (13.4 million). There were similar rates of diabetes for men and women, but the rates for non-Hispanic blacks and Mexican-Americans were 1.6 and 1.9 times the rate for non-Hispanic whites. Based on American Diabetes Association criteria, prevalence of diabetes (diagnosed plus undiagnosed) in the total population of people who were 40-74 years of age increased from 8.9% in the period 1976-1980 to 12.3% by 1988-1994. A similar increase was found when WHO criteria were applied (11.4 and 14.3%). The high rates of abnormal fasting and postchallenge glucose found in NHANES III, together with the increasing frequency of obesity and sedentary lifestyles in the population, make it likely that diabetes will continue to be a major health problem in the U.S.
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              TRPC1, a human homolog of a Drosophila store-operated channel.

              A Jeromin, G Stetten, J Chevesich … (1995)
              In many vertebrate and invertebrate cells, inositol 1,4,5-trisphospate production induces a biphasic Ca2+ signal. Mobilization of Ca2+ from internal stores drives the initial burst. The second phase, referred to as store-operated Ca2+ entry (formerly capacitative Ca2+ entry), occurs when depletion of intracellular Ca2+ pools activates a non-voltage-sensitive plasma membrane Ca2+ conductance. Despite the prevalence of store-operated Ca2+ entry, no vertebrate channel responsible for store-operated Ca2+ entry has been reported. trp (transient receptor potential), a Drosophila gene required in phototransduction, encodes the only known candidate for such a channel throughout phylogeny. In this report, we describe the molecular characterization of a human homolog of trp, TRPC1. TRPC1 (transient receptor potential channel-related protein 1) was 40% identical to Drosophila TRP over most of the protein and lacked the charged residues in the S4 transmembrane region proposed to be required for the voltage sensor in many voltage-gated ion channels. TRPC1 was expressed at the highest levels in the fetal brain and in the adult heart, brain, testis, and ovaries. Evidence is also presented that TRPC1 represents the archetype of a family of related human proteins.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Endocr Res
                Journal ID (iso-abbrev): Endocr. Res
                Journal ID (publisher-id): ERC
                Title: Endocrine Research
                Publisher: Informa Healthcare
                ISSN (Print): 0743-5800
                ISSN (Electronic): 1532-4206
                Publication date (Print): May 2013
                Publication date (Electronic): 01 April 2013
                Volume: 38
                Issue: 2
                Pages: 59-68
                Affiliations
                1Departmentof Endocrinology and Metabolism, The Second Affiliated Hospital of Harbin Medical University , Harbin, China
                2Department of Endocrinology and Metabolism, Daqing Oil Field General Hospital , Daqing, China
                Author notes
                Address correspondence to Qiang Li, Department of Endocrinology and Metabolism, The Second Affiliated Hospital of Harbin Medical University , Harbin, China. E-mail: qiangli2000@ 123456hotmail.com
                Article
                DOI: 10.3109/07435800.2012.681824
                PMC ID: 3619450
                PubMed ID: 23544998
                SO-VID: 4e67b8ce-51a7-4eaf-afdf-76fdb1816ae9
                Copyright © © Informa Healthcare USA, Inc.
                License:

                This is an open-access article distributed under the terms of the Creative Commons Attribution Noncommercial License which permits any noncommercial use, distribution, and reproduction in any medium, provided the source is credited.

                History
                Date received : 31 July 2011
                Date accepted : 26 March 2012
                Page count
                Tables: 5, References: 43, Pages: 10
                Categories
                Subject: Research Article

                Keywords: trpc1,single nucleotide polymorphism,type 2 diabetes mellitus,diabetic nephropathy
                Data availability:
                Keywords: trpc1, single nucleotide polymorphism, type 2 diabetes mellitus, diabetic nephropathy

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