Evidence map›Paper›PMID 42728312›Full record

ArticlePediatric research2026

Kidney mitochondrial complex I dysfunction in a juvenile rat model of diabetic ketoacidosis.

Scott L Weiss, Sumera Farooqi, Subir Kumar Roy Chowdhury, Marian Cabrera-Ayala, Luis Fernandez, Steven Chu, Martha E O'Donnell, Nathan Kuppermann, Nicole S Glaser

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Article in Pediatric research, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

9 authors.

Scott L WeissCritical Care Mitochondrial Unit, Nemours Biomedical Research, Wilmington, DE, USA. scott.weiss@nemours.org.
Sumera FarooqiCritical Care Mitochondrial Unit, Nemours Biomedical Research, Wilmington, DE, USA.
Subir Kumar Roy ChowdhuryCritical Care Mitochondrial Unit, Nemours Biomedical Research, Wilmington, DE, USA.
Marian Cabrera-AyalaCritical Care Mitochondrial Unit, Nemours Biomedical Research, Wilmington, DE, USA.
Luis FernandezDepartment of Physiology and Membrane Biology, University of California, Davis School of Medicine, Sacramento, CA, USA.
Steven ChuDepartment of Physiology and Membrane Biology, University of California, Davis School of Medicine, Sacramento, CA, USA.
Martha E O'DonnellDepartment of Physiology and Membrane Biology, University of California, Davis School of Medicine, Sacramento, CA, USA.
Nathan KuppermannDepartments of Pediatrics and Emergency Medicine, George Washington School of Medicine and Health Sciences, and Children's National Hospital, Washington, DC, USA.
Nicole S GlaserDepartment of Pediatrics, University of California, Davis, School of Medicine, Sacramento, CA, USA.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundThe pathobiology of acute kidney injury during diabetic ketoacidosis (DKA) is not completely understood. We hypothesized that mitochondrial function is impaired during DKA as a mechanism of acute kidney injury.

methodsWe isolated kidney samples from 4 to 5 week-old rats with normoglycemia (NG, controls; n = 7), hyperglycemia (HG; n = 5), acute DKA (DKA; n = 5), and after 24 h of DKA treatment (DKA-24; n = 5). Kidney tissue homogenates were prepared from frozen tissue for measurement of mitochondrial electron transport system (ETS) complex I + III, II + III, and IV activity and citrate synthase activity using spectrophotometry and ETS complex protein expression using Western blots.

resultsMitochondrial ETS complex I + III activity (mean ± SD) exhibited a stepwise decrease from HG (113 ± 54 nmol/min/mg tissue protein) to DKA (64 ± 32; p < 0.05 compared to NG) and trended toward NG control levels (143 ± 37) in DKA-24 (135 ± 39). Mitochondrial content, including citrate synthase activity and ETS complex proteins I, II, IV, and V, did not differ between groups, except that ETS complex III increased in HG and DKA and subsequently decreased in DKA-24.

conclusionsIn a juvenile rat model of DKA, increasing glycemic stress caused a reversible change in kidney mitochondrial complex I function and complex III expression. IMPACT: Acute kidney injury during diabetic ketoacidosis (DKA) increases risk of future diabetic kidney disease, but the underlying pathobiology is not understood. In a juvenile rat model of DKA, we found that increasing glycemic stress caused a reversible change in kidney mitochondrial complex I function and complex III expression. These data support further investigation to determine if mitochondrial dysfunction may contribute to DKA-related acute kidney injury.

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PMID42728312

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