{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,27]],"date-time":"2026-09-27T03:42:38Z","timestamp":1790480558997,"version":"4.1.0"},"reference-count":33,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"8","funder":[{"DOI":"10.13039\/501100002738","name":"Assistance Publique des H\u00f4pitaux de Paris","doi-asserted-by":"publisher","award":["PHRC AOM 12-074"],"award-info":[{"award-number":["PHRC AOM 12-074"]}],"id":[{"id":"10.13039\/501100002738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002738","name":"Assistance Publique des H\u00f4pitaux de Paris","doi-asserted-by":"publisher","award":["FP7EUNEFRON 201590"],"award-info":[{"award-number":["FP7EUNEFRON 201590"]}],"id":[{"id":"10.13039\/501100002738","id-type":"DOI","asserted-by":"publisher"}]},{"DOI":"10.13039\/501100002738","name":"Assistance Publique des H\u00f4pitaux de Paris","doi-asserted-by":"publisher","award":["2012-305608"],"award-info":[{"award-number":["2012-305608"]}],"id":[{"id":"10.13039\/501100002738","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2019,8]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      About 1% of the population is heterozygous for loss-of-function variants in\n                      <jats:italic toggle=\"yes\">SLC12A3<\/jats:italic>\n                      , which encodes the thiazide-sensitive sodium-chloride cotransporter. Biallelic\n                      <jats:italic toggle=\"yes\">SLC12A3<\/jats:italic>\n                      mutations are responsible for Gitelman syndrome, a salt-losing tubulopathy. In a cross-sectional study of 81 heterozygous carriers, 82 healthy noncarriers, and 79 patients with Gitelman syndrome of similar age, body mass index, and sex ratio, the authors assessed findings from home BP monitoring, oral glucose tolerance testing, and assays of plasma and urine electrolyte and hormone levels. They found evidence for a subtle intermediate phenotype in heterozygous carriers and demonstrated a resistance to insulin in the patients with Gitelman syndrome. These findings indicate that counseling of such patients is warranted to reduce their risk of type 2 diabetes and to reassure them about the health of their heterozygous relatives.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      Gitelman syndrome is a salt-losing tubulopathy caused by mutations in the\n                      <jats:italic toggle=\"yes\">SLC12A3<\/jats:italic>\n                      gene, which encodes the thiazide-sensitive sodium-chloride cotransporter. Previous studies suggested an intermediate phenotype for heterozygous carriers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      To evaluate the phenotype of heterozygous carriers of pathogenic\n                      <jats:italic toggle=\"yes\">SLC12A3<\/jats:italic>\n                      mutations, we performed a cross-sectional study of patients with Gitelman syndrome, heterozygous carriers, and healthy noncarriers. Participants measured their BP at home for three consecutive days before hospital admission for blood and urine sampling and an oral glucose tolerance test.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      We enrolled 242 participants, aged 18\u201375 years, including 81 heterozygous carriers, 82 healthy noncarriers, and 79 patients with Gitelman syndrome. The three groups had similar age, sex ratio, and body mass index. Compared with healthy noncarriers, heterozygous carriers showed significantly higher serum calcium concentration (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.01) and a trend for higher plasma aldosterone (\n                      <jats:italic toggle=\"yes\">P<\/jats:italic>\n                      =0.06), but measures of home BP, plasma and urine electrolytes, renin, parathyroid hormone, vitamin D, and response to oral glucose tolerance testing were similar. Patients with Gitelman syndrome had lower systolic BP and higher heart rate than noncarriers and heterozygote carriers; they also had significantly higher fasting serum glucose concentration, higher levels of markers of insulin resistance, and a three-fold higher sensitivity to overweight. According to oral glucose tolerance testing, approximately 14% of patients with Gitelman syndrome were prediabetic, compared with 5% of heterozygous carriers and 4% of healthy noncarriers.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Heterozygous carriers had a weak intermediate phenotype, between that of healthy noncarriers and patients with Gitelman syndrome. Moreover, the latter are at risk for development of type 2 diabetes, indicating the heightened importance of body weight control in these patients.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2019010031","type":"journal-article","created":{"date-parts":[[2019,7,8]],"date-time":"2019-07-08T15:55:31Z","timestamp":1562601331000},"page":"1534-1545","source":"Crossref","is-referenced-by-count":49,"title":["Resistance to Insulin in Patients with Gitelman Syndrome and a Subtle Intermediate Phenotype in Heterozygous Carriers: A Cross-Sectional Study"],"prefix":"10.1681","volume":"30","clinical-trial-number":[{"clinical-trial-number":"nct02035046","registry":"10.18810\/clinical-trials-gov"}],"author":[{"given":"Anne","family":"Blanchard","sequence":"first","affiliation":[{"name":"Clinical Investigations Center,"},{"name":"Faculty of Medicine, Paris Descartes Universit\u00e9, Sorbonne Paris Cit\u00e9, Paris, France;"},{"name":"Clinical Investigations Center-1418, Institut 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France;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Julien","family":"Allard","sequence":"additional","affiliation":[{"name":"Department of Nephrology, H\u00f4pital Dupuytren, Centre Hospitalier Universitaire de Limoges, Limoges, France;"},{"name":"Clinical Investigations Center-1435, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Limoges, France;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jean-Philippe","family":"Haymann","sequence":"additional","affiliation":[{"name":"Department of Physiological Functional Investigations, H\u00f4pital Tenon, Assistance Publique H\u00f4pitaux des H\u00f4pitaux de Paris, Paris, France;"},{"name":"Faculty of Medicine, Universit\u00e9 Pierre et Marie Curie, Paris, France;"},{"name":"Unit\u00e9 Mixte de Recherche_S 1155, Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale, Paris, France;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Renaud","family":"de la 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