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Simultaneous Measurement of Superoxide/Hydrogen Peroxide and NADH Production by Flavin-containing Mitochondrial Dehydrogenases
Published on: February 24, 2018
Mitochondrial reactive oxygen species are required for hypothalamic glucose sensing
Corinne Leloup1, Christophe Magnan, Alexandre Benani
1UMR 5018-CNRS UPS, Institut L. Bugnard, IFR31, BP 84432, 31 432 Toulouse cedex 4, France. coleloup@toulouse.inserm.fr
Diabetes
|June 29, 2006
Summary
Mitochondrial reactive oxygen species (mROS) act as key signaling molecules in the brain
Area of Science:
- Neuroscience
- Metabolic Signaling
- Cellular Physiology
Background:
- The precise mechanisms linking glucose sensing to hypothalamic electrical activity remain debated.
- While ATP production was a primary suspect, glucose-stimulated neuronal signaling is not solely dependent on it.
Purpose of the Study:
- To investigate the role of mitochondrial reactive oxygen species (mROS) as physiological sensors in brain glucose sensing.
- To determine if mROS mediate the link between glucose levels and neuronal activity in the hypothalamus.
Main Methods:
- Ex vivo experiments using hypothalamic slices to measure ROS generation in response to glucose.
- In vivo studies in mice examining neuronal activity and insulin release.
- Pharmacological manipulation using mitochondrial complex blockers (antimycin, rotenone), antioxidants (trolox, catalase), and uncouplers (carbonyl cyanide m-chlorophenylhydrazone).
Main Results:
- Increased glucose levels stimulated ROS generation in hypothalamic slices, which was reversible with antioxidants.
- Mitochondrial complex blockers, known mROS generators, mimicked glucose-induced neuronal activity and insulin release.
- Antioxidants or uncouplers abolished glucose-induced neuronal activity and insulin release, indicating mROS dependence.
Conclusions:
- Brain glucose-sensing mechanisms involve mitochondrial reactive oxygen species (mROS) signaling.
- mROS production plays a critical role in mediating brain metabolic signaling pathways.
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