A word of caution concerning the use of Nnt-mutated C57BL/6 mice substrains as experimental models to study metabolism and mitochondrial pathophysiology

Experimental Physiology

Volumn 98, Issue 11, 2013, Pages 1643-1643

  Figueira, Tiago R ^a  

^a UNIVERSITY OF CAMPINAS   (Brazil)

Author keywords

[No Author keywords available]

Indexed keywords

NICOTINAMIDE ADENINE DINUCLEOTIDE (PHOSPHATE) TRANSHYDROGENASE;

C57BL 6 MOUSE; EXPERIMENTAL MODEL; GENE; GENE MUTATION; HUMAN; LETTER; METABOLISM; MITOCHONDRION; NNT GENE; NONHUMAN; PATHOPHYSIOLOGY;

ANIMALS; HUMANS; MITOCHONDRIA, MUSCLE; MUSCLE, SKELETAL; OXYGEN CONSUMPTION;

EID: 84885953535     PISSN: 09580670     EISSN: 1469445X     Source Type: Journal    
DOI: 10.1113/expphysiol.2013.074682     Document Type: Letter

References (5)

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2. Jacobs RA, Díaz V, Meinild AK, Gassmann M & Lundby C (2013). The C57Bl/6 mouse serves as a suitable model of human skeletal muscle mitochondrial function. Exp Physiol 98, 908-921.
3. Ronchi JA, Figueira TR, Ravagnani FG, Oliveira HC, Vercesi AE & Castilho RF (2013). A spontaneous mutation in the nicotinamide nucleotide transhydrogenase gene of C57BL/6 J mice results in mitochondrial redox abnormalities. Free Radic Biol Med 63, 446-456.
4. Rydström J (2006). Mitochondrial NADPH, transhydrogenase and disease. Biochim Biophys Acta 1757, 721-726.
5. Toye AA, Lippiat JD, Proks P, Shimomura K, Bentley L, Hugill A, Mijat V, Goldsworthy M, Moir L, Haynes A, Quarterman J, Freeman HC, Ashcroft FM & Cox RD. (2005). A genetic and physiological study of impaired glucose homeostasis control in C57BL/6J mice. Diabetologia 48, 675-686.