Journal article
Progesterone increases skeletal muscle mitochondrial H2O2 emission in nonmenopausal women
American journal of physiology: endocrinology and metabolism, Vol.300(3), pp.E528-E535
03/2011
DOI: 10.1152/ajpendo.00389.2010
PMCID: PMC3064007
PMID: 21189359
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 H
2
O
2
emission (mE
H2O2
) and insulin resistance. To determine whether serum levels of P4 and/or E
2
are related to mitochondrial function, mE
H2O2
and respiratory O
2
flux (
J
o
2
) were measured in permeabilized myofibers from insulin-sensitive (IS,
n
= 24) and -resistant (IR,
n
= 8) nonmenopausal women (IR = HOMA-IR > 3.6). Succinate-supported mE
H2O2
was more than 50% greater in the IR vs. IS women (
P
< 0.05). Interestingly, serum P4 correlated positively with succinate-supported mE
H2O2
(
r
= 0. 53,
P
< 0.01). To determine whether P4 or E2 directly affect mitochondrial function, saponin-permeabilized vastus lateralis myofibers biopsied from five nonmenopausal women in the early follicular phase were incubated in P4 (60 nM), E2 (1.4 nM), or both. P4 alone inhibited state 3
J
o
2
, supported by multisubstrate combination (
P
< 0.01). However, E2 alone or in combination with P4 had no effect on
J
o
2
. In contrast, during state 4 respiration, supported by succinate and glycerophosphate, mE
H2O2
was increased with P4 alone or in combination with E2 (
P
< 0.01). The results suggest that
1
) P4 increases mE
H2O2
with or without E2;
2
) P4 alone inhibits
J
o
2
but not when E2 is present; and
3
) P4 is related to the mE
H2O2
previously linked to skeletal muscle insulin resistance.
Details
- Title: Subtitle
- Progesterone increases skeletal muscle mitochondrial H2O2 emission in nonmenopausal women
- Creators
- Daniel A Kane - The East Carolina Diabetes and Obesity InstituteChien-Te Lin - The East Carolina Diabetes and Obesity InstituteEthan J Anderson - The East Carolina Diabetes and Obesity InstituteHyo-Bum Kwak - The East Carolina Diabetes and Obesity InstituteJulie H Cox - The East Carolina Diabetes and Obesity InstitutePatricia M Brophy - The East Carolina Diabetes and Obesity InstituteRobert C Hickner - The East Carolina Diabetes and Obesity InstituteP. Darrell Neufer - The East Carolina Diabetes and Obesity InstituteRonald N Cortright - The East Carolina Diabetes and Obesity Institute
- Resource Type
- Journal article
- Publication Details
- American journal of physiology: endocrinology and metabolism, Vol.300(3), pp.E528-E535
- DOI
- 10.1152/ajpendo.00389.2010
- PMID
- 21189359
- PMCID
- PMC3064007
- NLM abbreviation
- Am J Physiol Endocrinol Metab
- ISSN
- 0193-1849
- eISSN
- 1522-1555
- Publisher
- American Physiological Society; Bethesda, MD
- Grant note
- R01 DK-075880; DK-074825; DK-073488 / National Institutes of Health
- Language
- English
- Date published
- 03/2011
- Academic Unit
- Pharmaceutical Sciences and Experimental Therapeutics; Fraternal Order of Eagles Diabetes Research Center; Health, Sport, and Human Physiology
- Record Identifier
- 9984065312902771
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