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During the congress, E-Posters will be accessible to all participants on the congress website 24/7, as well as in the E-poster stations in the congress center.
Preparing your E-Poster
Please review the E-Poster format requirements carefully when preparing your E-Poster. Should your E-Poster not meet the mentioned requirements, it may not be displayed as described above.
E-Poster Submission Deadline
Please prepare and upload your E-Poster no later than March 14, 2026 11.59PM CET. After this date, you will no longer be able to prepare and upload your E-poster and it will not be displayed and accessible on the congress website.
Please follow the instructions below to input your abstract title.
Abstract titles should be brief and reflect the content of the abstract.
Renal cortical mitochondria are damaged by oxidative stress even during the normoalbuminuric stage of type 1 diabetes mellitus (DM) (Clin Sci 124:543-52, 2013). Damaged mitochondria are known to be removed via multiple mechanisms including mitochondrial autophagy (mitophagy). However, the changes of β-oxidation and glucose metabolism associated with mitophagy in the renal cortex remain poorly understood. The objective of this research is to investigate fatty acids related to β-oxidation, which is responsible for energy production in mitochondria, the dynamics of carnitine that transports these fatty acids, and glucose metabolism in the renal cortex.
Four groups of rats (n=5 per group) received one of the following treatments: 1) streptozotocin (STZ) group: rats with DM induced by STZ injection (STZ, 65 mg/kg, i.v.); 2) Sham group: rats receiving the STZ vehicle; 3) STZ+TLM group: STZ rats treated with telmisartan (TLM, an angiotensin receptor blocker; 10 mg/kg/day in chow); and 4) Sham+TLM group: TLM-treated Sham rats. Two weeks later, blood glucose levels, blood pressure, glomerular filtration rate (GFR), and urinary excretion of albumin and N-acetyl-β-D-glucosaminidase (NAG) were measured in each rat. Renal cortex homogenates were assayed for 3-nitrotyrosine (3-NT, an oxidative stress marker measured by HPLC), and Western blotting was used to quantify proteins related to mitophagy (LC3-II, p62, PINK1, BNIP3), β-oxidation (CPT2, ACADVL, HADHA), and glucose metabolism (HK2, PCK1). Furthermore, carnitine and acylcarnitine in the renal cortex and plasma, as well as ω-3 fatty acids (α-linolenic acid, EPA, DHA), and ω-6 fatty acids (linoleic acid, arachidonic acid) were evaluated.
Blood glucose levels and GFR were higher in STZ rats than in Sham rats (P<0.05) and were not affected by TLM. Blood pressure, urinary albumin excretion, and urinary NAG excretion were unaltered by STZ or TLM. Renal cortical 3-NT levels were increased in STZ rats (P<0.05), and this change was prevented by TLM (P<0.05). STZ rats had increased renal cortical LC3-II and PINK1 protein levels compared with Sham rats (P<0.05), with these effects prevented by TLM (P<0.05). STZ rats had increased renal cortical HADHA and PCK1 protein levels compared with Sham rats (P<0.05). p62, BNIP3, CPT2, ACADVL, and HK2 did not differ among groups.
In the renal cortex, DM-induced mitophagy was associated with a metabolic shift from ω-6 to ω-3 fatty acids, increased acylcarnitine levels, enhanced β-oxidation, and gluconeogenesis. These were blunted by the antioxidant effects of TLM, suggesting that they may be closely related mitochondrial quality control mechanisms triggered by oxidative damage during the normoalbuminuric stage of DM.
