{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,23]],"date-time":"2026-09-23T21:32:38Z","timestamp":1790199158025,"version":"4.1.0"},"reference-count":38,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2013,5,21]],"date-time":"2013-05-21T00:00:00Z","timestamp":1369094400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Clinical Exper Ophthalmology"],"published-print":{"date-parts":[[2013,8]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Background<\/jats:title>\n                    <jats:p>\n                      The\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      mouse has been reported to display retinal pathology degeneration associated with advanced diabetic retinopathy. In the present study, we monitored retinal changes in these mice to establish if this model displays clinical features associated with advanced diabetic retinopathy in human patients.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      mice (\n                      <jats:italic>\n                        <jats:styled-content style=\"fixed-case\">n<\/jats:styled-content>\n                      <\/jats:italic>\n                      \u2009=\u200955) on a\n                      <jats:styled-content style=\"fixed-case\">C57Bl<\/jats:styled-content>\n                      \/\n                      <jats:styled-content style=\"fixed-case\">6J<\/jats:styled-content>\n                      background were monitored clinically from 9 to 25 weeks of age using a combination of scanning laser ophthalmoscopy, fluorescein angiography and optical coherence tomography. After clinical imaging, eyes were processed for immunostaining to examine microglial, astroglial and\n                      <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>\n                      uller glial responses to hyperglycaemia. To complement our optical coherence tomography imaging, retinal morphology and thicknesses were examined in high\u2010quality semi\u2010thin sections.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      No retinal thinning or disruption of retinal architecture was observed by optical coherence tomography or resin histology in\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      mice up to 6 months of age. In addition, no vascular changes were detected by fluorescein angiography or by scanning laser ophthalmoscopy. With the exception of microglial activation, reduced glial fibrillary acid protein expression in astrocytes and an increase in glial fibrillary acid protein expression by\n                      <jats:styled-content style=\"fixed-case\">M<\/jats:styled-content>\n                      uller cells, no other changes were observed in the\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      retina.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>\n                      Our results indicate that the classical clinical correlates of human diabetic retinopathy are absent in\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      mice up to 6 months of age suggesting that either the histopathological processes underlying the development of diabetic retinopathy in this model require longer than 5 months of hyperglycaemia to result in disruption of retinal architecture or that advanced diabetic retinopathy is not a feature of the\n                      <jats:styled-content style=\"fixed-case\">\n                        <jats:italic>\n                          Ins2\n                          <jats:sup>Akita<\/jats:sup>\n                        <\/jats:italic>\n                      <\/jats:styled-content>\n                      diabetic mouse.\n                    <\/jats:p>\n                  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