Difference between revisions of "Benani 2007 Diabetes"
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{{Publication | {{Publication | ||
|title=Benani A, Troy S, Carmona | |title=Benani A, Troy S, Carmona OMC, Fioramonti X, Lorsignol A, Leloup C, Casteilla L, Pénicaud L (2012) Role for mitochondrial reactive oxygen species in brain lipid sensing: redox regulation of food intake. Diabetes 56:152-60. | ||
|info=[http://www.ncbi.nlm.nih.gov/pubmed/17192477 PMID:17192477] | |info=[http://www.ncbi.nlm.nih.gov/pubmed/17192477 PMID:17192477] | ||
|authors=Benani A, Troy S, Carmona | |authors=Benani A, Troy S, Carmona OMC, Fioramonti X, Lorsignol A, Leloup C, Casteilla L, Penicaud L | ||
|year=2007 | |year=2007 | ||
|journal=Diabetes | |journal=Diabetes | ||
|abstract=The ability for the brain to sense peripheral fuel availability is mainly accomplished within the hypothalamus, which detects ongoing systemic nutrients and adjusts food intake and peripheral metabolism as needed. Here, we hypothesized that mitochondrial reactive oxygen species (ROS) could trigger sensing of nutrients within the hypothalamus. For this purpose, we induced acute hypertriglyceridemia in rats and examined the function of mitochondria in the hypothalamus. Hypertriglyceridemia led to a rapid increase in the mitochondrial respiration in the ventral hypothalamus together with a transient production of ROS. Cerebral inhibition of fatty acids-CoA mitochondrial uptake prevented the hypertriglyceridemia-stimulated ROS production, indicating that ROS derived from mitochondrial metabolism. The hypertriglyceridemia-stimulated ROS production was associated with change in the intracellular redox state without any noxious cytotoxic effects, suggesting that ROS function acutely as signaling molecules. Moreover, cerebral inhibition of hypertriglyceridemia-stimulated ROS production fully abolished the satiety related to the hypertriglyceridemia, suggesting that hypothalamic ROS production was required to restrain food intake during hypertriglyceridemia. Finally, we found that fasting disrupted the hypertriglyceridemia-stimulated ROS production, indicating that the redox mechanism of brain nutrient sensing could be modulated under physiological conditions. Altogether, these findings support the role of mitochondrial ROS as molecular actors implied in brain nutrient sensing. | |abstract=The ability for the brain to sense peripheral fuel availability is mainly accomplished within the hypothalamus, which detects ongoing systemic nutrients and adjusts food intake and peripheral metabolism as needed. Here, we hypothesized that mitochondrial reactive oxygen species (ROS) could trigger sensing of nutrients within the hypothalamus. For this purpose, we induced acute hypertriglyceridemia in rats and examined the function of mitochondria in the hypothalamus. Hypertriglyceridemia led to a rapid increase in the mitochondrial respiration in the ventral hypothalamus together with a transient production of ROS. Cerebral inhibition of fatty acids-CoA mitochondrial uptake prevented the hypertriglyceridemia-stimulated ROS production, indicating that ROS derived from mitochondrial metabolism. The hypertriglyceridemia-stimulated ROS production was associated with change in the intracellular redox state without any noxious cytotoxic effects, suggesting that ROS function acutely as signaling molecules. Moreover, cerebral inhibition of hypertriglyceridemia-stimulated ROS production fully abolished the satiety related to the hypertriglyceridemia, suggesting that hypothalamic ROS production was required to restrain food intake during hypertriglyceridemia. Finally, we found that fasting disrupted the hypertriglyceridemia-stimulated ROS production, indicating that the redox mechanism of brain nutrient sensing could be modulated under physiological conditions. Altogether, these findings support the role of mitochondrial ROS as molecular actors implied in brain nutrient sensing. | ||
|keywords=Hypertriglyceridemia, ROS production | |keywords=Hypertriglyceridemia, ROS production | ||
|mipnetlab=FR Toulouse Casteilla L | |mipnetlab=FR Toulouse Casteilla L, FR Dijon Leloup C | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|diseases=Diabetes | |diseases=Diabetes | ||
|injuries=Oxidative stress;RONS | |||
|organism=Rat | |organism=Rat | ||
|tissues=Nervous system | |tissues=Nervous system | ||
|instruments=Oxygraph-2k | |||
}} | }} | ||
Latest revision as of 16:33, 26 March 2018
| Benani A, Troy S, Carmona OMC, Fioramonti X, Lorsignol A, Leloup C, Casteilla L, Pénicaud L (2012) Role for mitochondrial reactive oxygen species in brain lipid sensing: redox regulation of food intake. Diabetes 56:152-60. |
Benani A, Troy S, Carmona OMC, Fioramonti X, Lorsignol A, Leloup C, Casteilla L, Penicaud L (2007) Diabetes
Abstract: The ability for the brain to sense peripheral fuel availability is mainly accomplished within the hypothalamus, which detects ongoing systemic nutrients and adjusts food intake and peripheral metabolism as needed. Here, we hypothesized that mitochondrial reactive oxygen species (ROS) could trigger sensing of nutrients within the hypothalamus. For this purpose, we induced acute hypertriglyceridemia in rats and examined the function of mitochondria in the hypothalamus. Hypertriglyceridemia led to a rapid increase in the mitochondrial respiration in the ventral hypothalamus together with a transient production of ROS. Cerebral inhibition of fatty acids-CoA mitochondrial uptake prevented the hypertriglyceridemia-stimulated ROS production, indicating that ROS derived from mitochondrial metabolism. The hypertriglyceridemia-stimulated ROS production was associated with change in the intracellular redox state without any noxious cytotoxic effects, suggesting that ROS function acutely as signaling molecules. Moreover, cerebral inhibition of hypertriglyceridemia-stimulated ROS production fully abolished the satiety related to the hypertriglyceridemia, suggesting that hypothalamic ROS production was required to restrain food intake during hypertriglyceridemia. Finally, we found that fasting disrupted the hypertriglyceridemia-stimulated ROS production, indicating that the redox mechanism of brain nutrient sensing could be modulated under physiological conditions. Altogether, these findings support the role of mitochondrial ROS as molecular actors implied in brain nutrient sensing. • Keywords: Hypertriglyceridemia, ROS production
• O2k-Network Lab: FR Toulouse Casteilla L, FR Dijon Leloup C
Labels:
Pathology: Diabetes
Stress:Oxidative stress;RONS
Organism: Rat
Tissue;cell: Nervous system
HRR: Oxygraph-2k
