Difference between revisions of "Kane 2011 Am J Physiol Endocrinol Metab"
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|abstract=The luteal phase of the female menstrual cycle is associated with both 1) elevated serum progesterone (P4) and estradiol (E2), and 2) reduced insulin sensitivity. Recently, we demonstrated a link between skeletal muscle mitochondrial H2O2 emission (mEH2O2) and insulin resistance. To determine whether serum levels of P4 and/or E2 are related to mitochondrial function, mEH2O2 and respiratory O2 flux (JO2) were measured in permeabilized myofibers from insulin sensitive (IS, n = 24) and resistant (IR, n = 7) non-menopausal women (IR = HOMA-IR > 3.6). Succinate-supported mEH2O2 was more than 50% greater in the IR vs. IS women (P < 0.05). Interestingly, serum P4 correlated positively with succinate-supported mEH2O2 (r = 0. 53; P < 0.01). To determine whether P4 or E2 directly affect mitochondrial function, saponin-permeabilized vastus lateralis myofibers biopsied from 5 non-menopausal women in the early follicular phase were incubated in P4 (60 nM), E2 (1.4 nM), or both. P4 alone inhibited state 3 JO2 supported by multisubstrate combination (P < 0.01). However, E2 alone or in combination with P4 had no effect on JO2. In contrast, during state 4 respiration supported by succinate and glycerophosphate, mEH2O2 was increased with P4 alone or in combination with E2 (P < 0.01). The results suggest that 1) P4 increases mEH2O2 with or without E2; 2) P4 alone inhibits JO2, but not when E2 is present; and 3) P4 is related to the mEH2O2 previously linked to skeletal muscle insulin resistance. | |abstract=The luteal phase of the female menstrual cycle is associated with both 1) elevated serum progesterone (P4) and estradiol (E2), and 2) reduced insulin sensitivity. Recently, we demonstrated a link between skeletal muscle mitochondrial H2O2 emission (mEH2O2) and insulin resistance. To determine whether serum levels of P4 and/or E2 are related to mitochondrial function, mEH2O2 and respiratory O2 flux (JO2) were measured in permeabilized myofibers from insulin sensitive (IS, n = 24) and resistant (IR, n = 7) non-menopausal women (IR = HOMA-IR > 3.6). Succinate-supported mEH2O2 was more than 50% greater in the IR vs. IS women (P < 0.05). Interestingly, serum P4 correlated positively with succinate-supported mEH2O2 (r = 0. 53; P < 0.01). To determine whether P4 or E2 directly affect mitochondrial function, saponin-permeabilized vastus lateralis myofibers biopsied from 5 non-menopausal women in the early follicular phase were incubated in P4 (60 nM), E2 (1.4 nM), or both. P4 alone inhibited state 3 JO2 supported by multisubstrate combination (P < 0.01). However, E2 alone or in combination with P4 had no effect on JO2. In contrast, during state 4 respiration supported by succinate and glycerophosphate, mEH2O2 was increased with P4 alone or in combination with E2 (P < 0.01). The results suggest that 1) P4 increases mEH2O2 with or without E2; 2) P4 alone inhibits JO2, but not when E2 is present; and 3) P4 is related to the mEH2O2 previously linked to skeletal muscle insulin resistance. | ||
|keywords=Sex Hormones, Estradiol, Insulin Resistance, Oxidative Stress | |keywords=Sex Hormones, Estradiol, Insulin Resistance, Oxidative Stress | ||
|mipnetlab=US NC Greenville Neufer PD, US_NC Greenville_Anderson EJ, CA_Antigonish_Kane DA | |mipnetlab=US NC Greenville Neufer PD, US_NC Greenville_Anderson EJ, CA_Antigonish_Kane DA | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
{{Labeling | {{Labeling | ||
|organism=Human | |organism=Human | ||
|tissues=Skeletal muscle | |tissues=Skeletal muscle | ||
|preparations=Intact Organism, Permeabilized tissue | |preparations=Intact Organism, Permeabilized tissue | ||
|injuries=RONS; Oxidative Stress | |||
|couplingstates=OXPHOS | |couplingstates=OXPHOS | ||
|instruments=Oxygraph-2k | |||
|additional=Spectrophotometry; Spectrofluorimetry | |additional=Spectrophotometry; Spectrofluorimetry | ||
|discipline=Mitochondrial Physiology, Biomedicine | |discipline=Mitochondrial Physiology, Biomedicine | ||
}} | }} | ||
Revision as of 14:58, 22 August 2014
| Kane DA, Lin CT, Anderson EJ, Kwak HB, Cox JH, Brophy PM, Hickner RC, Neufer PD, Cortright RN (2011) Progesterone increases skeletal muscle mitochondrial H2O2 emission in non-menopausal women. Am J Physiol Endocrinol Metab 300: E528-E535. |
Kane DA, Lin CT, Anderson EJ, Kwak HB, Cox JH, Brophy PM, Hickner RC, Neufer PD, Cortright RN (2011) Am J Physiol Endocrinol Metab
Abstract: The luteal phase of the female menstrual cycle is associated with both 1) elevated serum progesterone (P4) and estradiol (E2), and 2) reduced insulin sensitivity. Recently, we demonstrated a link between skeletal muscle mitochondrial H2O2 emission (mEH2O2) and insulin resistance. To determine whether serum levels of P4 and/or E2 are related to mitochondrial function, mEH2O2 and respiratory O2 flux (JO2) were measured in permeabilized myofibers from insulin sensitive (IS, n = 24) and resistant (IR, n = 7) non-menopausal women (IR = HOMA-IR > 3.6). Succinate-supported mEH2O2 was more than 50% greater in the IR vs. IS women (P < 0.05). Interestingly, serum P4 correlated positively with succinate-supported mEH2O2 (r = 0. 53; P < 0.01). To determine whether P4 or E2 directly affect mitochondrial function, saponin-permeabilized vastus lateralis myofibers biopsied from 5 non-menopausal women in the early follicular phase were incubated in P4 (60 nM), E2 (1.4 nM), or both. P4 alone inhibited state 3 JO2 supported by multisubstrate combination (P < 0.01). However, E2 alone or in combination with P4 had no effect on JO2. In contrast, during state 4 respiration supported by succinate and glycerophosphate, mEH2O2 was increased with P4 alone or in combination with E2 (P < 0.01). The results suggest that 1) P4 increases mEH2O2 with or without E2; 2) P4 alone inhibits JO2, but not when E2 is present; and 3) P4 is related to the mEH2O2 previously linked to skeletal muscle insulin resistance. • Keywords: Sex Hormones, Estradiol, Insulin Resistance, Oxidative Stress
• O2k-Network Lab: US NC Greenville Neufer PD, US_NC Greenville_Anderson EJ, CA_Antigonish_Kane DA
Labels:
Stress:RONS; Oxidative Stress"RONS; Oxidative Stress" is not in the list (Cell death, Cryopreservation, Ischemia-reperfusion, Permeability transition, Oxidative stress;RONS, Temperature, Hypoxia, Mitochondrial disease) of allowed values for the "Stress" property. Organism: Human Tissue;cell: Skeletal muscle Preparation: Intact Organism"Intact Organism" is not in the list (Intact organism, Intact organ, Permeabilized cells, Permeabilized tissue, Homogenate, Isolated mitochondria, SMP, Chloroplasts, Enzyme, Oxidase;biochemical oxidation, ...) of allowed values for the "Preparation" property., Permeabilized tissue
Coupling state: OXPHOS
HRR: Oxygraph-2k
Spectrophotometry; Spectrofluorimetry
