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Difference between revisions of "Jorgensen 2009 Am J Physiol Endocrinol Metab"

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{{Publication
{{Publication
|title=Jørgensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B (2009) Changed mitochondrial function by pre- and/or postpartum diet alterations in sheep. Am. J. Physiol. Endocrinol. Metab. 297: E1349-E1357.
|title=Jørgensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B (2009) Changed mitochondrial function by pre- and/or postpartum diet alterations in sheep. Am. J. Physiol. Endocrinol. Metab. 297: E1349-E1357.
|authors=Joergensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B  
|authors=Joergensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B
|year=2009
|year=2009
|journal=American Journal of Physiology - Endocrinology and Metabolism
|journal=American Journal of Physiology - Endocrinology and Metabolism
|abstract=The mechanistic basis for the correlation between mitochondrial dysfunction and neurodegenerative disease is unclear, but evidence supports involvement of cytochrome ''C'' oxidase (CCO) deficits with age. Neurons isolated from the brains of 24 month and 9 month rats and cultured in common conditions provide a model of intrinsic neuronal aging. In situ CCO activity was decreased in 24 month neurons relative to 9 month neurons. Possible CCO-related deficits include holoenzyme activity, cofactor, and substrate. No difference was found between neurons from 24 month and 9 month rats in mitochondrial counts per neuron, CCO activity in submitochondrial particles, or basal respiration. Immunostaining for cytochrome ''C'' in individual mitochondria revealed an age-related deficit of this electron donor. 24 month neurons did not have adequate respiratory capacity to upregulate respiration after a glutamate stimulus, in spite of a two-fold upregulation of respiration seen in 9 month neurons. Respiration in 24 month neurons was inhibited by lower concentrations of potassium cyanide, suggesting a 50% deficit in functional enzyme in 24 month compared to 9 month neurons. In addition to cytochrome ''C'', CCO requires cardiolipin to function. Staining with nonylacridine orange revealed an age-related deficit in cardiolipin. Treatment of 24 month neurons with 17-beta-estradiol restored cardiolipin levels (10 ng/mL) and upregulated respiration under glutamate stress (1 pg/mL). Attempts to induce mitochondrial turnover by neuronal multiplication also rejuvenated CCO activity in 24 month neurons. These data suggest cytochrome C and cardiolipin levels are deficient in 24 month neurons, preventing normal upregulation of respiration needed for oxidative phosphorylation in response to stress. Furthermore, the data suggest this deficit can be corrected with estrogen treatment.
|abstract=In a sheep model, we investigated diet effects on skeletal muscle mitochondria to look for fetal programming. During pregnancy, ewes were fed normally (N) or were 50% food restricted (L) during the last trimester, and lambs born to these ewes received a normal (N) or a high-fat diet (H) for the first 6 mo of life. We examined mitochondrial function in permeabilized muscle fibers from the lambs at 6 mo of age (adolescence) and after 24 mo of age (adulthood). The postpartum H diet for the lambs induced an ~30% increase (P < 0.05) of mitochondrial VO2max and an ~50% increase (P < 0.05) of the respiratory coupling ratio (RCR) combined with lower levels of UCP3 and PGC-1{alpha} mRNA levels (P < 0.05). These effects proved to be reversible by a normal diet from 6 to 24 mo of age. However, at 24 mo, a long-term effect of the maternal gestational diet restriction (fetal programming) became evident as a lower VO2max (~40%, P < 0.05), a lower state 4 respiration (~40%, P < 0.05), and lower RCR (~15%, P < 0.05). Both PGC-1{alpha} and UCP3 mRNA levels were increased (P < 0.05). Two analyzed muscles were affected differently, and muscle rich in type I fibers was more susceptible to fetal programming. We conclude that fetal programming, seen as a reduced VO2max in adulthood, results from gestational undernutrition. Postnatal high-fat diet results in a pronounced RCR and VO2max increase in adolescence. However, these effects are reversible by diet correction and are not maintained in adulthood.
|keywords=Aging, Neuron culture, Cytochrome ''C'' oxidase, Mitochondria, Estrogen, Brain
|keywords=Metabolic syndrome, High-fat diet; nutrient restriction, Maternal diet, Respiratory coupling ratio
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19826104 PMID: 19826104 ]
|info=[http://www.ncbi.nlm.nih.gov/pubmed/19826104 PMID: 19826104 ]
}}
}}

Revision as of 16:31, 17 September 2010

Publications in the MiPMap
Jørgensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B (2009) Changed mitochondrial function by pre- and/or postpartum diet alterations in sheep. Am. J. Physiol. Endocrinol. Metab. 297: E1349-E1357.

» PMID: 19826104

Joergensen W, Gam C, Andersen JL, Schjerling P, Scheibye-Knudsen M, Mortensen OH, Grunnet N, Nielsen MO, Quistorff B (2009) American Journal of Physiology - Endocrinology and Metabolism

Abstract: In a sheep model, we investigated diet effects on skeletal muscle mitochondria to look for fetal programming. During pregnancy, ewes were fed normally (N) or were 50% food restricted (L) during the last trimester, and lambs born to these ewes received a normal (N) or a high-fat diet (H) for the first 6 mo of life. We examined mitochondrial function in permeabilized muscle fibers from the lambs at 6 mo of age (adolescence) and after 24 mo of age (adulthood). The postpartum H diet for the lambs induced an ~30% increase (P < 0.05) of mitochondrial VO2max and an ~50% increase (P < 0.05) of the respiratory coupling ratio (RCR) combined with lower levels of UCP3 and PGC-1{alpha} mRNA levels (P < 0.05). These effects proved to be reversible by a normal diet from 6 to 24 mo of age. However, at 24 mo, a long-term effect of the maternal gestational diet restriction (fetal programming) became evident as a lower VO2max (~40%, P < 0.05), a lower state 4 respiration (~40%, P < 0.05), and lower RCR (~15%, P < 0.05). Both PGC-1{alpha} and UCP3 mRNA levels were increased (P < 0.05). Two analyzed muscles were affected differently, and muscle rich in type I fibers was more susceptible to fetal programming. We conclude that fetal programming, seen as a reduced VO2max in adulthood, results from gestational undernutrition. Postnatal high-fat diet results in a pronounced RCR and VO2max increase in adolescence. However, these effects are reversible by diet correction and are not maintained in adulthood. Keywords: Metabolic syndrome, High-fat diet; nutrient restriction, Maternal diet, Respiratory coupling ratio


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Regulation: Respiration; OXPHOS; ETS Capacity"Respiration; OXPHOS; ETS Capacity" is not in the list (Aerobic glycolysis, ADP, ATP, ATP production, AMP, Calcium, Coupling efficiency;uncoupling, Cyt c, Flux control, Inhibitor, ...) of allowed values for the "Respiration and regulation" property. 


HRR: Oxygraph-2k