Fisher-Wellman 2012 Trends Endocrinol Metab
Fisher-Wellman KH, Neufer PD (2012) Linking mitochondrial bioenergetics to insulin resistance via redox biology. Trends Endocrinol Metab 23:142-53. doi: 10.1016/j.tem.2011.12.008 |
Fisher-Wellman KH, Neufer PD (2012) Trends Endocrinol Metab
Abstract: Chronic overnutrition and physical inactivity are major risk factors for insulin resistance and type 2 diabetes. Recent research indicates that overnutrition generates an increase in hydrogen peroxide (H2O2) emission from mitochondria, serving as a release valve to relieve the reducing pressure created by fuel overload, as well as a primary signal that ultimately decreases insulin sensitivity. H(2)O(2) is a major input to cellular redox circuits that link to cysteine residues throughout the entire proteome to regulate cell function. Here we review the principles of mitochondrial bioenergetics and redox systems biology and offer new insight into how H(2)O(2) emission may be linked via redox biology to the etiology of insulin resistance.
β’ Bioblast editor: Gnaiger E
Correction: FADH2 and S-pathway
- A commonly found error on FADH2 in the S-pathway requires correction. For clarification, see page 48 in Gnaiger (2020)
- Quote (p 48): "The substrate of CII is succinate, which is oxidized forming fumarate while reducing flavin adenine dinucleotide FAD to FADH2, with further electron transfer to the quinone pool. Whereas reduced NADH is a substrate of Complex I linked to dehydrogenases of the TCA cycle and mt-matrix upstream of CI, reduced FADH2 is a product of Complex II with downstream electron flow from CII to Q."
- A commonly found error on FADH2 in the S-pathway requires correction. For clarification, see page 48 in Gnaiger (2020)
- Gnaiger E (2020) Mitochondrial pathways and respiratory control. An introduction to OXPHOS analysis. 5th ed. Bioenerg Commun 2020.2. https://doi.org/10.26124/bec:2020-0002
Labels:
Pathology: Diabetes, Obesity
Stress:Oxidative stress;RONS
Regulation: Redox state