{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,4]],"date-time":"2026-05-04T19:49:24Z","timestamp":1777924164384,"version":"3.51.4"},"reference-count":33,"publisher":"Walter de Gruyter GmbH","issue":"2","funder":[{"name":"Academie de Recherche et D\u2019Enseignement Superieur of Belgique","award":["2016-157E"],"award-info":[{"award-number":["2016-157E"]}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2021,7,20]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec id=\"j_hmbci-2020-0076_abs_001_w2aab3b7c45b1b6b1aab1c16b1Aa\">\n                    <jats:title>Objectives<\/jats:title>\n                    <jats:p>\n                      Reduced gene expression of\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      in subjects with insulin resistance (IR) has been reported. Insulin resistance occurs early on the course of Turner syndrome (TS). The main objective of this study was to evaluate the relationship between\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      promoter DNA methylation status in lymphocytes and insulin sensitivity and secretion in Ecuadorian females with TS.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_hmbci-2020-0076_abs_002_w2aab3b7c45b1b6b1aab1c16b2Aa\">\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We examined a cohort of 34 Ecuadorian patients with TS along with a sex-, age- and BMI-matched reference group. All subjects received a standard 75\u00a0g oral glucose tolerance test. Insulin resistance and secretion indices were calculated. The\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      methylated DNA\/unmethylated DNA ratio and mitochondrial content (mtDNA\/nDNA ratio) were further determined.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_hmbci-2020-0076_abs_003_w2aab3b7c45b1b6b1aab1c16b3Aa\">\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Notably, the\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      DNA methylation level was significantly higher in TS subjects than the reference group and correlated with IR indices. Conversely, mitochondrial content was significantly lower in the study group than healthy controls and negatively correlated with the\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      methylated DNA\/unmethylated DNA ratio in TS individuals.\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      promoter DNA methylation status contributed to 20% of the total variability in Homeostasis Model Assessment for Insulin Resistance (HOMA-IR) independently of BMI or age in TS subjects.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec id=\"j_hmbci-2020-0076_abs_004_w2aab3b7c45b1b6b1aab1c16b4Aa\">\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our collective findings suggest that expression of\n                      <jats:italic>PPARGC1A<\/jats:italic>\n                      and lower mitochondrial number affect the metabolic phenotype in TS subjects.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1515\/hmbci-2020-0076","type":"journal-article","created":{"date-parts":[[2020,12,22]],"date-time":"2020-12-22T09:35:07Z","timestamp":1608629707000},"page":"159-165","source":"Crossref","is-referenced-by-count":4,"title":["<i>PPARGC1A<\/i>\n                    promoter DNA-methylation level and glucose metabolism in Ecuadorian women with Turner syndrome"],"prefix":"10.1515","volume":"42","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-4673-3643","authenticated-orcid":false,"given":"Francisco","family":"\u00c1lvarez-Nava","sequence":"first","affiliation":[{"name":"Biological Sciences School, Faculty of Biological Sciences , Central University of Ecuador , Quito Ecuador"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marco","family":"Salinas","sequence":"additional","affiliation":[{"name":"Institute of Biomedicine Research , Central University of Ecuador , Quito , Ecuador"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Daniela","family":"Bastidas","sequence":"additional","affiliation":[{"name":"Biological Sciences School, Faculty of Biological Sciences , Central University of Ecuador , Quito Ecuador"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Yosselin","family":"Vicu\u00f1a","sequence":"additional","affiliation":[{"name":"Institute of Biomedicine Research , Central University of Ecuador , Quito , Ecuador"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marcia","family":"Racines-Orbe","sequence":"additional","affiliation":[{"name":"Institute of Biomedicine Research , Central University of Ecuador , Quito , Ecuador"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"374","published-online":{"date-parts":[[2020,12,22]]},"reference":[{"key":"2025121207185831155_j_hmbci-2020-0076_ref_001_w2aab3b7c45b1b6b1ab2b2b1Aa","doi-asserted-by":"crossref","unstructured":"Gravholt, CH, Andersen, NH, Conway, GS, Dekkers, OM, Geffner, ME, Klein, KO, et al.. Clinical practice guidelines for the care of girls and women with Turner syndrome: proceedings from the 2016 cincinnati international Turner syndrome meeting. Eur J Endocrinol 2017;177:G1\u201370. https:\/\/doi.org\/10.1530\/EJE-17-0430.","DOI":"10.1530\/EJE-17-0430"},{"key":"2025121207185831155_j_hmbci-2020-0076_ref_002_w2aab3b7c45b1b6b1ab2b2b2Aa","doi-asserted-by":"crossref","unstructured":"Lebenthal, Y, Levy, S, Sofrin-Drucker, E, Nagelberg, N, Weintrob, N, Shalitin, S, et al.. The natural history of metabolic comorbidities in Turner syndrome from childhood to early adulthood: comparison between 45,X monosomy and other karyotypes. Front Endocrinol 2018;9:27. https:\/\/doi.org\/10.3389\/fendo.2018.00027.","DOI":"10.3389\/fendo.2018.00027"},{"key":"2025121207185831155_j_hmbci-2020-0076_ref_003_w2aab3b7c45b1b6b1ab2b2b3Aa","doi-asserted-by":"crossref","unstructured":"Mortensen, KH, Andersen, NH, Gravholt, CH. 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