{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,26]],"date-time":"2026-09-26T14:48:36Z","timestamp":1790434116986,"version":"4.1.0"},"reference-count":53,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"12","funder":[{"DOI":"10.13039\/501100000654","name":"Marie Curie","doi-asserted-by":"publisher","award":["PIOF-GA-2012-332395"],"award-info":[{"award-number":["PIOF-GA-2012-332395"]}],"id":[{"id":"10.13039\/501100000654","id-type":"DOI","asserted-by":"publisher"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["JASN"],"published-print":{"date-parts":[[2019,12]]},"abstract":"<jats:sec>\n                    <jats:title>Significance Statement<\/jats:title>\n                    <jats:p>\n                      Lithium causes nephrogenic diabetes insipidus and hypercalcemia in 20% and 10% of patients, respectively, and may lead to metabolic acidosis. To determine the potential role of genetic predisposition in these adverse effects, the authors fed mice from 29 genetically different inbred strains a normal or a lithium-supplemented diet. Some strains developed adverse effects, whereas others did not. Genome-wide association studies revealed eight loci containing different candidate genes that were associated with development of lithium-induced nephrogenic diabetes insipidus. Of these,\n                      <jats:italic toggle=\"yes\">Acer2<\/jats:italic>\n                      is specifically expressed in the collecting duct; mice lacking\n                      <jats:italic toggle=\"yes\">Acer2<\/jats:italic>\n                      were more likely to develop lithium-induced nephrogenic diabetes insipidus. These findings demonstrate the importance of genetic variation in susceptibility for lithium-induced adverse effects in mice, and the genes identified may facilitate subsequent identification of human susceptibility genes.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>Lithium, mainstay treatment for bipolar disorder, causes nephrogenic diabetes insipidus and hypercalcemia in about 20% and 10% of patients, respectively, and may lead to acidosis. These adverse effects develop in only a subset of patients treated with lithium, suggesting genetic factors play a role.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>To identify susceptibility genes for lithium-induced adverse effects, we performed a genome-wide association study in mice, which develop such effects faster than humans. On day 8 and 10 after assigning female mice from 29 different inbred strains to normal chow or lithium diet (40 mmol\/kg), we housed the animals for 48 hours in metabolic cages for urine collection. We also collected blood samples.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      In 17 strains, lithium treatment significantly elevated urine production, whereas the other 12 strains were not affected. Increased urine production strongly correlated with lower urine osmolality and elevated water intake. Lithium caused acidosis only in one mouse strain, whereas hypercalcemia was found in four strains. Lithium effects on blood pH or ionized calcium did not correlate with effects on urine production. Using genome-wide association analyses, we identified eight gene-containing loci, including a locus containing\n                      <jats:italic toggle=\"yes\">Acer2<\/jats:italic>\n                      , which encodes a ceramidase and is specifically expressed in the collecting duct. Knockout of\n                      <jats:italic toggle=\"yes\">Acer2<\/jats:italic>\n                      led to increased susceptibility for lithium-induced diabetes insipidus development.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      We demonstrate that genome-wide association studies in mice can be used successfully to identify susceptibility genes for development of lithium-induced adverse effects. We identified\n                      <jats:italic toggle=\"yes\">Acer2<\/jats:italic>\n                      as a first susceptibility gene for lithium-induced diabetes insipidus in mice.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1681\/asn.2018050549","type":"journal-article","created":{"date-parts":[[2019,9,26]],"date-time":"2019-09-26T16:24:08Z","timestamp":1569515048000},"page":"2322-2336","source":"Crossref","is-referenced-by-count":12,"title":["Identification of Acer2 as a First Susceptibility Gene for Lithium-Induced Nephrogenic Diabetes Insipidus in Mice"],"prefix":"10.1681","volume":"30","author":[{"given":"Theun","family":"de Groot","sequence":"first","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, Maine;"},{"name":"Physiology,"},{"name":"Department of Medical Microbiology and Infectious Diseases, Canisius Wilhelmina Hospital, Nijmegen, The Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Lena 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University, Pierre and Marie Curie University Paris 06, INSERM (Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale), Paris Descartes University, Sorbonne Paris Cit\u00e9, UMR_S (Unit\u00e9 Mixte de Recherche en Sciences) 1138, Paris, France;"},{"name":"Physiology of Renal and Tubulopathies, CNRS (Centre National de la Recherche Scientifique) ERL 8228, Cordeliers Research Center, INSERM, Sorbonne University, Sorbonne Paris Cit\u00e9 University, Paris Descartes University, Paris Diderot University, Paris, France;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alain","family":"Doucet","sequence":"additional","affiliation":[{"name":"Cordeliers Research Center, Sorbonne University, Pierre and Marie Curie University Paris 06, INSERM (Institut National de la Sant\u00e9 et de la Recherche M\u00e9dicale), Paris Descartes University, Sorbonne Paris Cit\u00e9, UMR_S (Unit\u00e9 Mixte de Recherche en Sciences) 1138, Paris, France;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cungui","family":"Mao","sequence":"additional","affiliation":[{"name":"Department of Medicine, Stony Brook University, Stony Brook, New York;"},{"name":"Stony Brook Cancer Center, Stony Brook, New York;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Ruben","family":"Baumgarten","sequence":"additional","affiliation":[{"name":"Reinier-Haga Medical Diagnostic Center, Delft, The Netherlands;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Benjamin E.","family":"Low","sequence":"additional","affiliation":[{"name":"The Jackson Laboratory, Bar Harbor, Maine;"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Roger","family":"Sandhoff","sequence":"additional","affiliation":[{"name":"Lipid Pathobiochemistry Group, Department of Cellular and Molecular Pathology, German Cancer Research Center (DKFZ), Heidelberg, Germany; and"},{"name":"Centre for Applied Sciences at Technical 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