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We examined the effect of type 1 diabetes in wild\u2010type (<jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content>) mice and mice lacking the \u03b21 subunit of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> (<jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> \u03b21<jats:sup>\u2212\/\u2212<\/jats:sup> mice), which have reduced <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> activity in kidneys and other organs. Diabetes was induced using streptozotocin (<jats:styled-content style=\"fixed-case\">STZ<\/jats:styled-content>) and the animals followed up for 4\u00a0weeks. Hyperglycaemia was more severe in diabetic <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> \u03b21<jats:sup>\u2212\/\u2212<\/jats:sup> mice, despite the absence of any difference in serum levels of insulin, adiponectin and leptin. There was no change in <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> activity in the kidneys of diabetic <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice by <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> activity assay, or phosphorylation of either the \u03b1T172 activation site on the \u03b1 catalytic subunit of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> or the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content>\u2010specific phosphosite S79 on acetyl CoA carboxylase 1 (<jats:styled-content style=\"fixed-case\">ACC<\/jats:styled-content>1). Phosphorylation of the inhibitory \u03b1S485 site on the \u03b1 subunit of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> was significantly increased in the <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> diabetic mice compared to non\u2010diabetic controls. Despite increased plasma glucose levels in the diabetic <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> \u03b21<jats:sup>\u2212\/\u2212<\/jats:sup> mice, there were fewer myofibroblasts in the kidneys compared to diabetic <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice, as evidenced by reduced \u03b1\u2010smooth muscle actin (\u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>) protein by Western blot, <jats:styled-content style=\"fixed-case\">mRNA<\/jats:styled-content> by <jats:styled-content style=\"fixed-case\">qRT<\/jats:styled-content>\u2010<jats:styled-content style=\"fixed-case\">PCR<\/jats:styled-content> and fewer \u03b1\u2010<jats:styled-content style=\"fixed-case\">SMA<\/jats:styled-content>\u2010positive cells by immunohistochemical staining. Albuminuria was also reduced in the <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> \u03b21<jats:sup>\u2212\/\u2212<\/jats:sup> mice. In contrast to previous studies, therefore, myofibroblasts were reduced in the kidneys of <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> \u03b21<jats:sup>\u2212\/\u2212<\/jats:sup> diabetic mice compared to diabetic <jats:styled-content style=\"fixed-case\">WT<\/jats:styled-content> mice, despite increased circulating glucose, suggesting that <jats:styled-content style=\"fixed-case\">AMPK<\/jats:styled-content> can worsen renal fibrosis in type 1 diabetes.<\/jats:p>","DOI":"10.1111\/iep.12313","type":"journal-article","created":{"date-parts":[[2019,4,26]],"date-time":"2019-04-26T09:32:00Z","timestamp":1556271120000},"page":"114-122","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":2,"title":["Absence of the \u03b21 subunit of <scp>AMP<\/scp>\u2010activated protein kinase reduces myofibroblast infiltration of the kidneys in early diabetes"],"prefix":"10.1111","volume":"100","author":[{"given":"Suet\u2010Wan","family":"Choy","sequence":"first","affiliation":[{"name":"Kidney Laboratory Institute for Breathing and Sleep University of Melbourne  Heidelberg Victoria Australia"},{"name":"Department of Nephrology University of Melbourne  Heidelberg Victoria Australia"},{"name":"Department of Medicine University of Melbourne Austin Health and St. Vincent's Hospital  Heidelberg Victoria Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Scott A.","family":"Fraser","sequence":"additional","affiliation":[{"name":"Kidney Laboratory Institute for Breathing and Sleep University of Melbourne  Heidelberg Victoria Australia"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Marina","family":"Katerelos","sequence":"additional","affiliation":[{"name":"Kidney Laboratory Institute for Breathing and Sleep University of Melbourne  Heidelberg Victoria 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