The DOI matches its Crossref record; 29 of the 29 references it cites were found in a registry or an index.
Diabetes-induced up-regulation of uncoupling protein-2 results in increased mitochondrial uncoupling in kidney proximal tubular cells
Open accessAbstract
We have previously reported increased O(2) consumption unrelated to active transport by tubular cells and up-regulated mitochondrial uncoupling protein (UCP)-2 expressions in diabetic kidneys. It is presently unknown if the increased UCP-2 levels in the diabetic kidney results in mitochondrial uncoupling and increased O(2) consumption, which we therefore investigated in this study. The presence of UCP-2 in proximal tubular cells was confirmed by immunohistochemistry and found to be increased (western blot) in homogenized tissue and isolated mitochondria from kidney cortex of diabetic rats. Isolated proximal tubular cells had increased total and ouabain-insensitive O(2) consumption compared to controls. Isolated mitochondria from diabetic animals displayed increased glutamate-stimulated O(2) consumption (in the absence of ADP and during inhibition of the ATP-synthase by oligomycin) compared to controls. Guanosine diphosphate, an UCP inhibitor, and bovine serum albumin which removes fatty acids that are essential for UCP-2 uncoupling activity, independently prevented the increased glutamate-stimulated O(2) consumption in mitochondria from diabetic animals. In conclusion, diabetic rats have increased mitochondrial UCP-2 expression in renal proximal tubular cells, which results in mitochondrial uncoupling and increased O(2) consumption. This mechanism may be protective against diabetes-induced oxidative stress, but will increase O(2) usage. The subsequently reduced O(2) availability may contribute to diabetes-induced progressive kidney damage.
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“Recent immunohistochemical studies revealed an increase in proximal tubular UCP2 expression in STZ diabetic rats (108).”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [108]
In the citing paper
“Friederich et al. (108) showed that diabetic rats express increased mitochondrial UCP-2 in proximal tubular cells associated with increased oxygen use and suggested that the increase in UCP2 was protective against oxidative stress.”
From Mitochondrial Dysfunction in Diabetes: From Molecular Mechanisms to Functional Significance and Therapeutic Opportunities (2010) · cites this paper as [108]
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Liu, C. (2012) · TSpace (University of Toronto)
Mitochondria and Oxidative Stress in Diabetes
Sivitz, W. I. (2014) · Oxidative stress in applied basic research and clinical practice · doi:10.1007/978-1-4899-8035-9_5
Erythrocyte metabolism, oxygen delivery, and hypertensive kidney disease
Limper, U., Tank, J., & Jordan, J. (2020) · International Journal of Cardiology Hypertension · doi:10.1016/j.ijchy.2020.100049
Gustafsson, J. (2013) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
(2008) · Current Opinion in Nephrology & Hypertension · doi:10.1097/mnh.0b013e32831fd875
Persson, P. (2024) · Upsala Journal of Medical Sciences · doi:10.48101/ujms.v129.10791
Ahmad, M. (2010) · KTH Publication Database DiVA (KTH Royal Institute of Technology)
Pathophysiology and pathogenesis of diabetic kidney disease
Cooper, M. E., & Thomas, M. C. (2026) · Elsevier eBooks · doi:10.1016/b978-0-12-815389-5.00042-3
The Role of Uncoupling Protein 2 in Renal Adaptation to Hypertension: Mechanistic Insights
Sperhake, J., Schreckenberg, R., Sato, T., & Schlüter, K. (2026) · Biomedicines · doi:10.3390/biomedicines14102367
Metadata
- Authors
- Friederich, M., Fasching, A., Hansell, P., Nordquist, L., & Palm, F.
- Affiliations
- Uppsala University (SE)
- Corresponding author
- Palm, Fredrik
- Venue
- Biochimica et Biophysica Acta (BBA) - Bioenergetics
- Publisher
- Elsevier BV
- Published
- 2008-07
- Volume
- 1777
- Issue
- 7-8
- Pages
- 935-940
- ISSN
- 0005-2728 (ISSN-L)
- OpenAlex
- W2084502320
- Cited by
- 111
- References
- 29
- Citations by year
- 2026: 3 · 2025: 1 · 2024: 4 · 2023: 6 · 2022: 5 · 2021: 6 · 2020: 9 · 2019: 7 · 2018: 9 · 2017: 7 · 2016: 6 · 2015: 4 · 2014: 11 · 2013: 5 · 2012: 12
- FWCI
- 2.20
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Biochimica et Biophysica Acta (BBA) - Bioenergetics (publishedVersion)
- PubMed (publishedVersion)
- Funders
- Fondation pour la Recherche Médicale
- Svenska Sällskapet för Medicinsk Forskning
- Stiftelsen Familjen Ernfors Fond
- Marcus och Amalia Wallenbergs minnesfond
- National Institutes of Health
- National Institute of Diabetes and Digestive and Kidney Diseases (K99DK077858)
- Topics
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Metabolism, Diabetes, and Cancer
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cell Biology › Autophagy in Disease and Therapy
- Keywords
- UCP2, mitochondrial uncoupling, diabetes mellitus, diabetic kidney, proximal tubular epithelial cells, oxygen consumption, oxidative stress, kidney injury, guanosine diphosphate, fatty acids
- MeSH terms
- Uncoupling Protein 2, Animals, Diabetes Mellitus, Experimental, Hyperglycemia, Insulin, Ion Channels, Kidney Tubules, Proximal, Male, Mitochondria, Oxygen Consumption, Rats, Inbred WF, Up-Regulation, Mitochondrial Proteins, Rats
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