<?xml version="1.0" encoding="UTF-8"?>
<!DOCTYPE article PUBLIC "-//NLM//DTD JATS (Z39.96) Journal Publishing DTD v1.3 20210610//EN" "JATS-journalpublishing1-3.dtd">
<article article-type="research-article" dtd-version="1.3" xmlns:mml="http://www.w3.org/1998/Math/MathML" xmlns:xlink="http://www.w3.org/1999/xlink" xmlns:xsi="http://www.w3.org/2001/XMLSchema-instance" xml:lang="ru"><front><journal-meta><journal-id journal-id-type="publisher-id">medsovet</journal-id><journal-title-group><journal-title xml:lang="ru">Медицинский Совет</journal-title><trans-title-group xml:lang="en"><trans-title>Meditsinskiy sovet = Medical Council</trans-title></trans-title-group></journal-title-group><issn pub-type="ppub">2079-701X</issn><issn pub-type="epub">2658-5790</issn><publisher><publisher-name>REMEDIUM GROUP Ltd.</publisher-name></publisher></journal-meta><article-meta><article-id pub-id-type="doi">10.21518/2079-701X-2015-8-82-85</article-id><article-id custom-type="elpub" pub-id-type="custom">medsovet-233</article-id><article-categories><subj-group subj-group-type="heading"><subject>Research Article</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="ru"><subject>Эндокринология</subject></subj-group><subj-group subj-group-type="section-heading" xml:lang="en"><subject>Endocrinology</subject></subj-group></article-categories><title-group><article-title>Фармакогенетические аспекты пероральной сахароснижающей терапии. Фенотипы «ответа» и «провала»</article-title><trans-title-group xml:lang="en"><trans-title>Pharmacogenetic aspects of oral hypoglycemic therapy. Response and failure phenotypes</trans-title></trans-title-group></title-group><contrib-group><contrib contrib-type="author" corresp="yes"><name-alternatives><name name-style="eastern" xml:lang="ru"><surname>Сорокина</surname><given-names>Ю. А.</given-names></name><name name-style="western" xml:lang="en"><surname>Sorokina</surname><given-names>Y. A.</given-names></name></name-alternatives><email xlink:type="simple">noemail@neicon.ru</email><xref ref-type="aff" rid="aff-1"/></contrib></contrib-group><aff-alternatives id="aff-1"><aff xml:lang="ru">Нижегородская государственная медицинская академия Минздрава России<country>Россия</country></aff><aff xml:lang="en">Nizhniy Novgorod State Medical Academy, Russia's Ministry of Health<country>Russian Federation</country></aff></aff-alternatives><pub-date pub-type="collection"><year>2015</year></pub-date><pub-date pub-type="epub"><day>30</day><month>12</month><year>2015</year></pub-date><volume>0</volume><issue>8</issue><fpage>82</fpage><lpage>85</lpage><permissions><copyright-statement>Copyright &amp;#x00A9; Сорокина Ю.А., 2015</copyright-statement><copyright-year>2015</copyright-year><copyright-holder xml:lang="ru">Сорокина Ю.А.</copyright-holder><copyright-holder xml:lang="en">Sorokina Y.A.</copyright-holder><license license-type="creative-commons-attribution" xlink:href="https://creativecommons.org/licenses/by/4.0/" xlink:type="simple"><license-p>This work is licensed under a Creative Commons Attribution 4.0 License.</license-p></license></permissions><self-uri xlink:href="https://www.med-sovet.pro/jour/article/view/233">https://www.med-sovet.pro/jour/article/view/233</self-uri><abstract><p>В данной работе была сделана попытка ответить на вопрос о возможности эффективной персонифицированной сахароснижающей терапии, в частности метформином, у пациентов c сахарным диабетом 2-го типа с учетом однонуклеотидного полиморфизма трех генов (эндотелиальная синтаза оксида азота, 8-оксогуанин-ДНК-гликозилаза, блок р53). Предполагается, что эффективность использования метформина зависит, в частности, от наличия полиморфизма данных генов.</p></abstract><trans-abstract xml:lang="en"><p>The research work attempted to answer the question whether an effective personalized glucose-lowering therapy, particularly with metformin, is possible in patients with type 2 diabetes based on single nucleotide polymorphism of the three genes (endothelial nitric oxide synthase, 8-oxoguanine DNA glycosylase and p53). Metformin efficacy could depend, in particular, on the presence of polymorphism in these genes.</p></trans-abstract><kwd-group xml:lang="ru"><kwd>фармакогенетика</kwd><kwd>метформин фенотип «провала»</kwd><kwd>фенотип «ответа»</kwd><kwd>персонифицированная медицина</kwd><kwd>pharmacogenetics</kwd><kwd>metformin</kwd><kwd>failure phenotype</kwd><kwd>response phenotype</kwd><kwd>personalized medicine</kwd></kwd-group></article-meta></front><back><ref-list><title>References</title><ref id="cit1"><label>1</label><citation-alternatives><mixed-citation xml:lang="ru">Алгоритмы специализированной медицинской помощи больным сахарным диабетом. Под редакцией И.И. Дедова, М.В. Шестаковой. Издание шестое. М.: ФГБУ ЭНЦ, 2013: 120.</mixed-citation><mixed-citation xml:lang="en">Алгоритмы специализированной медицинской помощи больным сахарным диабетом. Под редакцией И.И. Дедова, М.В. Шестаковой. Издание шестое. М.: ФГБУ ЭНЦ, 2013: 120.</mixed-citation></citation-alternatives></ref><ref id="cit2"><label>2</label><citation-alternatives><mixed-citation xml:lang="ru">Кравчук Е.Н. Применение метформина при сочетании ишемической болезни сердца и сахарного диабета 2-го типа: механизмы действия и клиническая эффективность. Е.Н. Кравчук, М.М. Галагудза. Сахарный диабет, 2013, 1: 5-14.</mixed-citation><mixed-citation xml:lang="en">Кравчук Е.Н. Применение метформина при сочетании ишемической болезни сердца и сахарного диабета 2-го типа: механизмы действия и клиническая эффективность. Е.Н. Кравчук, М.М. Галагудза. Сахарный диабет, 2013, 1: 5-14.</mixed-citation></citation-alternatives></ref><ref id="cit3"><label>3</label><citation-alternatives><mixed-citation xml:lang="ru">HeritabiLity of variation in glycaemic response to metformin: a genome-wide complex trait analysis. Zhou K., Donnelly L., Yang J. et al. The Lancet. Diabetes and Endocrinology, 2014, 2(6): 481-487. doi: 10.1016/S2213-8587(14)70050-6. Epub 2014 Mar 19.</mixed-citation><mixed-citation xml:lang="en">HeritabiLity of variation in glycaemic response to metformin: a genome-wide complex trait analysis. Zhou K., Donnelly L., Yang J. et al. The Lancet. Diabetes and Endocrinology, 2014, 2(6): 481-487. doi: 10.1016/S2213-8587(14)70050-6. Epub 2014 Mar 19.</mixed-citation></citation-alternatives></ref><ref id="cit4"><label>4</label><citation-alternatives><mixed-citation xml:lang="ru">Genetic variants in transcription factors are associated with the pharmacokinetics and pharmacodynamics of metformin. Goswami S at al. Clin Pharmacol Ther., 2014, 96(3): P. 370379. doi: 10.1038/clpt.2014.109. Epub 2014 May 22.</mixed-citation><mixed-citation xml:lang="en">Genetic variants in transcription factors are associated with the pharmacokinetics and pharmacodynamics of metformin. Goswami S at al. Clin Pharmacol Ther., 2014, 96(3): P. 370379. doi: 10.1038/clpt.2014.109. Epub 2014 May 22.</mixed-citation></citation-alternatives></ref><ref id="cit5"><label>5</label><citation-alternatives><mixed-citation xml:lang="ru">Stratified medicine for the use of antidiabetic medication in treatment of type II diabetes and cancer: where do we go from here? (Review). Emami-Riedmaier A. [et al.]. J Intern Med., 2015, 277: 235-247.</mixed-citation><mixed-citation xml:lang="en">Stratified medicine for the use of antidiabetic medication in treatment of type II diabetes and cancer: where do we go from here? (Review). Emami-Riedmaier A. [et al.]. J Intern Med., 2015, 277: 235-247.</mixed-citation></citation-alternatives></ref><ref id="cit6"><label>6</label><citation-alternatives><mixed-citation xml:lang="ru">Wang XL, Mahaney MC, Sim AS et al. Genetic contribution of the endothelial constitutive nitric oxide synthase gene to plasma nitric oxide levels. Arterioscler. Thromb. Vasc. Biol, 1997, 17: 3147-3153.</mixed-citation><mixed-citation xml:lang="en">Wang XL, Mahaney MC, Sim AS et al. Genetic contribution of the endothelial constitutive nitric oxide synthase gene to plasma nitric oxide levels. Arterioscler. Thromb. Vasc. Biol, 1997, 17: 3147-3153.</mixed-citation></citation-alternatives></ref><ref id="cit7"><label>7</label><citation-alternatives><mixed-citation xml:lang="ru">Nakayama M, Yasue H, Yoshimura M et al. T-786 C mutation in the 5'-flanking region of the endothelial nitric oxide synthase gene is associated with coronary spasm. Circulation, 1999, 99: 2864-2870.</mixed-citation><mixed-citation xml:lang="en">Nakayama M, Yasue H, Yoshimura M et al. T-786 C mutation in the 5'-flanking region of the endothelial nitric oxide synthase gene is associated with coronary spasm. Circulation, 1999, 99: 2864-2870.</mixed-citation></citation-alternatives></ref><ref id="cit8"><label>8</label><citation-alternatives><mixed-citation xml:lang="ru">T(-786)^C polymorphism of the endothelial nitric oxide synthase gene is associated with insulin resistance in patients with ischemic or non ischemic cardiomyopathy. C. Vecoli, M.G. Andreassi, R. Liga [et al.]. BMC Med Genet., 2012, 2(13): 92. doi: 10.1186/1471-2350-13-92.</mixed-citation><mixed-citation xml:lang="en">T(-786)^C polymorphism of the endothelial nitric oxide synthase gene is associated with insulin resistance in patients with ischemic or non ischemic cardiomyopathy. C. Vecoli, M.G. Andreassi, R. Liga [et al.]. BMC Med Genet., 2012, 2(13): 92. doi: 10.1186/1471-2350-13-92.</mixed-citation></citation-alternatives></ref><ref id="cit9"><label>9</label><citation-alternatives><mixed-citation xml:lang="ru">eNOS polymorphism associated with metabolic syndrome in children and adolescents. J.A. Miranda, V.A. Belo, D.C. Souza-Costa. Mol Cell Biochem., 2013, 372(1-2): 155-60. doi: 10.1007/ s11010-012-1456-y.</mixed-citation><mixed-citation xml:lang="en">eNOS polymorphism associated with metabolic syndrome in children and adolescents. J.A. Miranda, V.A. Belo, D.C. Souza-Costa. Mol Cell Biochem., 2013, 372(1-2): 155-60. doi: 10.1007/ s11010-012-1456-y.</mixed-citation></citation-alternatives></ref><ref id="cit10"><label>10</label><citation-alternatives><mixed-citation xml:lang="ru">Roy D, Perreault M and Marette A. Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent. AJP-Endocrinology and Metabolism, 1998, 274(4): 692-699.</mixed-citation><mixed-citation xml:lang="en">Roy D, Perreault M and Marette A. Insulin stimulation of glucose uptake in skeletal muscles and adipose tissues in vivo is NO dependent. AJP-Endocrinology and Metabolism, 1998, 274(4): 692-699.</mixed-citation></citation-alternatives></ref><ref id="cit11"><label>11</label><citation-alternatives><mixed-citation xml:lang="ru">Variants of endothelial nitric oxide synthase gene are associated with components of metabolic syndrome in an Arab population. K.M. Alkharfy, N.M. Al-Daghri, O.S. Al-Attas et al. Endocr J., 2012, 59(3): 253-263. Epub 2012 Jan 12.</mixed-citation><mixed-citation xml:lang="en">Variants of endothelial nitric oxide synthase gene are associated with components of metabolic syndrome in an Arab population. K.M. Alkharfy, N.M. Al-Daghri, O.S. Al-Attas et al. Endocr J., 2012, 59(3): 253-263. Epub 2012 Jan 12.</mixed-citation></citation-alternatives></ref><ref id="cit12"><label>12</label><citation-alternatives><mixed-citation xml:lang="ru">Tallapragada DS. Long standing partnership between insulin resistance and endothelial dysfunction: Role of metabolic memory. D.S. Tallapragada, P.A. Karpe, K.Tikoo. Br J Pharmacol., 2015, Mar 30. doi: 10.1111/ bph.13145. [Epub ahead of print].</mixed-citation><mixed-citation xml:lang="en">Tallapragada DS. Long standing partnership between insulin resistance and endothelial dysfunction: Role of metabolic memory. D.S. Tallapragada, P.A. Karpe, K.Tikoo. Br J Pharmacol., 2015, Mar 30. doi: 10.1111/ bph.13145. [Epub ahead of print].</mixed-citation></citation-alternatives></ref><ref id="cit13"><label>13</label><citation-alternatives><mixed-citation xml:lang="ru">Alteration of mitochondrial function and insulin sensitivity in primary mouse skeletal muscle cells isolated from transgenic and knockout mice: role of OGG1. L.V. Yuzefovych, A.M. Schuler, J. Chen et al. Endocrinology, 2013, 154(8): 2640-2649. doi: 10.1210/en.2013-1076.</mixed-citation><mixed-citation xml:lang="en">Alteration of mitochondrial function and insulin sensitivity in primary mouse skeletal muscle cells isolated from transgenic and knockout mice: role of OGG1. L.V. Yuzefovych, A.M. Schuler, J. Chen et al. Endocrinology, 2013, 154(8): 2640-2649. doi: 10.1210/en.2013-1076.</mixed-citation></citation-alternatives></ref><ref id="cit14"><label>14</label><citation-alternatives><mixed-citation xml:lang="ru">The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance. C.L. Wang, M.C. Hsieh, S.C. Hsin. Journal of Human Genetics, 2006, 51(2): 124-128. Epub 2005 Dec 7,</mixed-citation><mixed-citation xml:lang="en">The hOGG1 Ser326Cys gene polymorphism is associated with decreased insulin sensitivity in subjects with normal glucose tolerance. C.L. Wang, M.C. Hsieh, S.C. Hsin. Journal of Human Genetics, 2006, 51(2): 124-128. Epub 2005 Dec 7,</mixed-citation></citation-alternatives></ref><ref id="cit15"><label>15</label><citation-alternatives><mixed-citation xml:lang="ru">Associations between hOGG1 Ser326Cys polymorphism and increased body mass index and fasting glucose level in the Japanese general population. M. Hara, K. Nakamura, H. Nanri [et al.]. Journal of Epidemiology, 2014, 24(5): 379-384.</mixed-citation><mixed-citation xml:lang="en">Associations between hOGG1 Ser326Cys polymorphism and increased body mass index and fasting glucose level in the Japanese general population. M. Hara, K. Nakamura, H. Nanri [et al.]. Journal of Epidemiology, 2014, 24(5): 379-384.</mixed-citation></citation-alternatives></ref><ref id="cit16"><label>16</label><citation-alternatives><mixed-citation xml:lang="ru">Гормонально-метаболические и генетические маркеры чувствительности к метформину при диабете и раке: предсказание и реальность. Берштейн Л.М., Васильев Д.А., Иевлева А.Г. и др. Сахарный диабет, 2014, 1: 21-28.</mixed-citation><mixed-citation xml:lang="en">Гормонально-метаболические и генетические маркеры чувствительности к метформину при диабете и раке: предсказание и реальность. Берштейн Л.М., Васильев Д.А., Иевлева А.Г. и др. Сахарный диабет, 2014, 1: 21-28.</mixed-citation></citation-alternatives></ref><ref id="cit17"><label>17</label><citation-alternatives><mixed-citation xml:lang="ru">Bonfigli AR. The p53 codon 72 (Arg72Pro) polymorphism is associated with the degree of insulin resistance in type 2 diabetic subjects: a cross-sectional study. A.R. Bonfigli. Acta Diabetologia, 2013, 50(3): 429-436.</mixed-citation><mixed-citation xml:lang="en">Bonfigli AR. The p53 codon 72 (Arg72Pro) polymorphism is associated with the degree of insulin resistance in type 2 diabetic subjects: a cross-sectional study. A.R. Bonfigli. Acta Diabetologia, 2013, 50(3): 429-436.</mixed-citation></citation-alternatives></ref><ref id="cit18"><label>18</label><citation-alternatives><mixed-citation xml:lang="ru">Burgdorf KS. Studies of the association of Arg72Pro of tumor suppressor protein p53 with type 2 diabetes in a combined analysis of 55,521 Europeans. K.S. Burgdorf. PLoS One, 2011, 20(6): e15813. doi: 10.1371/journal. pone.0015813 [Электронный ресурс]. -Режим доступа: http//www.ncbi.nlm.nih.gov/ pmc/articles/PMC3024396/ (дата обращения 20.11.2013).</mixed-citation><mixed-citation xml:lang="en">Burgdorf KS. Studies of the association of Arg72Pro of tumor suppressor protein p53 with type 2 diabetes in a combined analysis of 55,521 Europeans. K.S. Burgdorf. PLoS One, 2011, 20(6): e15813. doi: 10.1371/journal. pone.0015813 [Электронный ресурс]. -Режим доступа: http//www.ncbi.nlm.nih.gov/ pmc/articles/PMC3024396/ (дата обращения 20.11.2013).</mixed-citation></citation-alternatives></ref><ref id="cit19"><label>19</label><citation-alternatives><mixed-citation xml:lang="ru">Gaulton KJ. Comprehensive association study of type 2 diabetes and related quantitative traits with 222 candidate genes. K.J. Gaulton. Diabetes., 2008, 11: 3136-3144.</mixed-citation><mixed-citation xml:lang="en">Gaulton KJ. Comprehensive association study of type 2 diabetes and related quantitative traits with 222 candidate genes. K.J. Gaulton. Diabetes., 2008, 11: 3136-3144.</mixed-citation></citation-alternatives></ref><ref id="cit20"><label>20</label><citation-alternatives><mixed-citation xml:lang="ru">Gloria-Bottini F. Is there a role of p53 codon 72 polymorphism in the susceptibility to type 2 diabetes in overweight subjects? A study in patients with cardiovascular diseases. F. Gloria-Bottini. Diabetes Research and Clinical Practice, 2011, 3: P. 4-7.</mixed-citation><mixed-citation xml:lang="en">Gloria-Bottini F. Is there a role of p53 codon 72 polymorphism in the susceptibility to type 2 diabetes in overweight subjects? A study in patients with cardiovascular diseases. F. Gloria-Bottini. Diabetes Research and Clinical Practice, 2011, 3: P. 4-7.</mixed-citation></citation-alternatives></ref><ref id="cit21"><label>21</label><citation-alternatives><mixed-citation xml:lang="ru">Tornovsky-Babeay S. Type 2 diabetes and congenital hyperinsulinism cause DNA double-strand breaks and p53 activity in p cells. S. Tornovsky-Babeay et al. Cell metabolism., 2014, 19(1): 109-121.</mixed-citation><mixed-citation xml:lang="en">Tornovsky-Babeay S. Type 2 diabetes and congenital hyperinsulinism cause DNA double-strand breaks and p53 activity in p cells. S. Tornovsky-Babeay et al. Cell metabolism., 2014, 19(1): 109-121.</mixed-citation></citation-alternatives></ref><ref id="cit22"><label>22</label><citation-alternatives><mixed-citation xml:lang="ru">Ou L. Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population. L. Ou et al. Diabetes Research and Clinical Practice, 2011, 91(2): 171-176.</mixed-citation><mixed-citation xml:lang="en">Ou L. Association between polymorphisms in RAPGEF1, TP53, NRF1 and type 2 diabetes in Chinese Han population. L. Ou et al. Diabetes Research and Clinical Practice, 2011, 91(2): 171-176.</mixed-citation></citation-alternatives></ref><ref id="cit23"><label>23</label><citation-alternatives><mixed-citation xml:lang="ru">Luo Z, Zang M, Guo W. AMPK as a metabolic tumor suppressor: control of metabolism and cell growth. Z. Luo, M. Zang, W.Guo. Future Oncology, 2010, 6(3). Vol. 457-470. doi: 10.2217/ fon.09.174.</mixed-citation><mixed-citation xml:lang="en">Luo Z, Zang M, Guo W. AMPK as a metabolic tumor suppressor: control of metabolism and cell growth. Z. Luo, M. Zang, W.Guo. Future Oncology, 2010, 6(3). Vol. 457-470. doi: 10.2217/ fon.09.174.</mixed-citation></citation-alternatives></ref><ref id="cit24"><label>24</label><citation-alternatives><mixed-citation xml:lang="ru">Dincer Y. Serum levels of p53 and cytochrome c in subjects with type 2 diabetes and impaired glucose tolerance. Y Dincer. Clin Invest Med., 2009, 32(4): 266-270.</mixed-citation><mixed-citation xml:lang="en">Dincer Y. Serum levels of p53 and cytochrome c in subjects with type 2 diabetes and impaired glucose tolerance. Y Dincer. Clin Invest Med., 2009, 32(4): 266-270.</mixed-citation></citation-alternatives></ref><ref id="cit25"><label>25</label><citation-alternatives><mixed-citation xml:lang="ru">Minamino T. A crucial role for adipose tissue p53 in the regulation of insulin resistance. T. Minamino et al. Nature Med., 2009, 15(9): 1082-1087.</mixed-citation><mixed-citation xml:lang="en">Minamino T. A crucial role for adipose tissue p53 in the regulation of insulin resistance. T. Minamino et al. Nature Med., 2009, 15(9): 1082-1087.</mixed-citation></citation-alternatives></ref></ref-list><fn-group><fn fn-type="conflict"><p>The authors declare that there are no conflicts of interest present.</p></fn></fn-group></back></article>
