<HashMap><database>biostudies-literature</database><scores/><additional><omics_type>Unknown</omics_type><volume>11(1)</volume><submitter>Canta A</submitter><funding>Regione Lombardia “NanoCosPha” grant</funding><pubmed_abstract>The development and progression of diabetic polyneuropathy (DPN) are due to multiple mechanisms. The creation of reliable animal models of DPN has been challenging and this issue has not yet been solved. However, despite some recognized differences from humans, most of the current knowledge on the pathogenesis of DPN relies on results achieved using rodent animal models. The simplest experimental DPN model reproduces type 1 diabetes, induced by massive chemical destruction of pancreatic beta cells with streptozotocin (STZ). Spontaneous/transgenic models of diabetes are less frequently used, mostly because they are less predictable in clinical course, more expensive, and require a variable time to achieve homogeneous metabolic conditions. Among them, Zucker diabetic fatty (ZDF) rats represe</pubmed_abstract><journal>Biomedicines</journal><pagination>20</pagination><full_dataset_link>https://www.ebi.ac.uk/biostudies/studies/S-EPMC9855818</full_dataset_link><repository>biostudies-literature</repository><pubmed_title>Multimodal Comparison of Diabetic Neuropathy in Aged Streptozotocin-Treated Sprague-Dawley and Zucker Diabetic Fatty Rats.</pubmed_title><pmcid>PMC9855818</pmcid><pubmed_authors>Meregalli C</pubmed_authors><pubmed_authors>Carozzi VA</pubmed_authors><pubmed_authors>Oggioni N</pubmed_authors><pubmed_authors>Rodriguez-Menendez V</pubmed_authors><pubmed_authors>Sala B</pubmed_authors><pubmed_authors>Melcangi RC</pubmed_authors><pubmed_authors>Chiorazzi A</pubmed_authors><pubmed_authors>Cavaletti G</pubmed_authors><pubmed_authors>Canta A</pubmed_authors><pubmed_authors>Bianchi R</pubmed_authors><pubmed_authors>Lombardi R</pubmed_authors><pubmed_authors>Marmiroli P</pubmed_authors><pubmed_authors>Giatti S</pubmed_authors></additional><is_claimable>false</is_claimable><name>Multimodal Comparison of Diabetic Neuropathy in Aged Streptozotocin-Treated Sprague-Dawley and Zucker Diabetic Fatty Rats.</name><description>The development and progression of diabetic polyneuropathy (DPN) are due to multiple mechanisms. The creation of reliable animal models of DPN has been challenging and this issue has not yet been solved. However, despite some recognized differences from humans, most of the current knowledge on the pathogenesis of DPN relies on results achieved using rodent animal models. The simplest experimental DPN model reproduces type 1 diabetes, induced by massive chemical destruction of pancreatic beta cells with streptozotocin (STZ). Spontaneous/transgenic models of diabetes are less frequently used, mostly because they are less predictable in clinical course, more expensive, and require a variable time to achieve homogeneous metabolic conditions. Among them, Zucker diabetic fatty (ZDF) rats represe</description><dates><release>2022-01-01T00:00:00Z</release><publication>2022 Dec</publication><modification>2025-08-15T03:05:34.276Z</modification><creation>2025-04-05T19:50:34.697Z</creation></dates><accession>S-EPMC9855818</accession><cross_references><pubmed>36672528</pubmed><doi>10.3390/biomedicines11010020</doi></cross_references></HashMap>