Concomitant modulation of transcripts related to fiber type determination and energy metabolism in skeletal muscle of female ovariectomized mice by estradiol injection

Riedl, Isabelle; Yoshioka, Mayumi; St‐Amand, Jonny

doi:10.1016/j.jsbmb.2009.12.004

Cited by 7 publications

(6 citation statements)

References 59 publications

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“…However, it is also important to highlight that potential treatment with diverse sex hormones may also improve both insulin resistance and mitochondria dysfunction in muscle cells of older adults. In particular, female sex hormones, estrogen and progesterone, have been recently shown to impact animal and human skeletal muscle with concomitant role on improving insulin resistance (50,51). In particular, it was shown that in women the ovarian steroid hormones, estradiol and progesterone, influence insulin sensitivity via alterations in the production of mitochondrial H2O2 in skeletal muscle (51) with a direct effect on mitochondrial function in skeletal muscle.…”

Section: Discovering Pathways Of Sarcopenia In Older Adultsmentioning

confidence: 99%

Discovering pathways of sarcopenia in older adults: A role for insulin resistance on mitochondria dysfunction

Abbatecola

Paolisso

Fattoretti

et al. 2011

The Journal of nutrition, health and aging

106

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The precise cause of sarcopenia, skeletal muscle loss and strength, in older persons is unknown. However, there is a strong evidence for muscle loss due to insulin resistance as well as mitochondrial dysfunction over aging. Considering that epidemiological studies have underlined that insulin resistance may have a specific role on skeletal muscle fibre atrophy and mitochondrial dysfunction has also been extensively shown to have a pivotal role on muscle loss in older persons, a combined pathway may not be ruled out. Considering that there is growing evidence for an insulin-related pathway on mitochondrial signaling, we hypothesize that a high degree of insulin resistance will be associated with the development of sarcopenia through specific alterations on mitochondrial functioning. This paper will highlight recent reviews regarding the link between skeletal muscle mitochondrial dysfunction and insulin resistance. We will specifically emphasize possible steps involved in sarcopenia over aging, including potential biomolecular mechanisms of insulin resistance on mitochondrial functioning.

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Section: Discovering Pathways Of Sarcopenia In Older Adultsmentioning

confidence: 99%

Discovering pathways of sarcopenia in older adults: A role for insulin resistance on mitochondria dysfunction

Abbatecola

Paolisso

Fattoretti

et al. 2011

The Journal of nutrition, health and aging

106

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“…Overall, hormonal factors, endurance training, and weight gain may induce morphological adaptation by inducing specific gene programs [1][2][3][4]. Human skeletal muscle commonly consists of more than one fiber type to sustain a wide range of workload and metabolic requirements.…”

mentioning

confidence: 99%

“…These fibers are also known as fast glycolytic fibers. Overall, hormonal factors, endurance training, and weight gain may induce morphological adaptation by inducing specific gene programs [1][2][3][4].…”

mentioning

confidence: 99%

Mitochondrial fatty acid biosynthesis and muscle fiber plasticity in very long‐chain acyl‐CoA dehydrogenase‐deficient mice

et al. 2018

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The white skeletal muscle of very long-chain acyl-CoA-dehydrogenase-deficient (VLCAD ) mice undergoes metabolic modification to compensate for defective β-oxidation in a progressive and time-dependent manner by upregulating glucose oxidation. This metabolic regulation seems to be accompanied by morphologic adaptation of muscle fibers toward the glycolytic fiber type II with the concomitant upregulation of mitochondrial fatty acid biosynthesis (mFASII) and lipoic acid biosynthesis. Dietary supplementation of VLCAD mice with different medium-chain triglycerides over 1 year revealed that odd-chain species has no effect on muscle fiber switch, whereas even-chain species inhibit progressive metabolic adaptation. Our study shows that muscle may undergo adaptive mechanisms that are modulated by dietary supplementation. We describe for the first time a concomitant change of mFASII in this muscular adaptation process.

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“…Skeletal muscle metabolism is the major determinant of total EE (60), and OVX causes a decrease in the expression of important muscle genes, such as major histocompatibility complex IIx (42), and the genes involved in energy metabolism (49), such as the evident decrease in AMP-activated protein kinase (AMPK) signaling, which regulates EE (14,25). Additionally, OVX induces a time-dependent decrease in muscle glucose uptake (46,51).…”

mentioning

confidence: 99%

Role of estrogen on skeletal muscle mitochondrial function in ovariectomized rats: a time course study in different fiber types

Cavalcanti-de-Albuquerque

Salvador

Martins

et al. 2014

Journal of Applied Physiology

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Postmenopausal women are prone to develop obesity and insulin resistance, which might be related to skeletal muscle mitochondrial dysfunction. In a rat model of ovariectomy (OVX), skeletal muscle mitochondrial function was examined at short- and long-term periods after castration. Mitochondrial parameters in the soleus and white gastrocnemius muscle fibers were analyzed. Three weeks after surgery, there were no differences in coupled mitochondrial respiration (ATP synthesis) with pyruvate, malate, and succinate; proton leak respiration; or mitochondrial reactive oxygen species production. However, after 3 wk of OVX, the soleus and white gastrocnemius muscles of the OVX animals showed a lower use of palmitoyl-carnitine and glycerol-phosphate substrates, respectively, and decreased peroxisome proliferator-activated receptor-γ coactivator-1α expression. Estrogen replacement reverted all of these phenotypes. Eight weeks after OVX, ATP synthesis was lower in the soleus and white gastrocnemius muscles of the OVX animals than in the sham-operated and estrogen-treated animals; however, when normalized by citrate synthase activity, these differences disappeared, indicating a lower muscle mitochondria content. No differences were observed in the proton leak parameter. Mitochondrial alterations did not impair the treadmill exercise capacity of the OVX animals. However, blood lactate levels in the OVX animals were higher after the physical test, indicating a compensatory extramitochondrial ATP synthesis system, but this phenotype was reverted by estrogen replacement. These results suggest early mitochondrial dysfunction related to lipid substrate use, which could be associated with the development of the overweight phenotype of ovariectomized animals.

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Concomitant modulation of transcripts related to fiber type determination and energy metabolism in skeletal muscle of female ovariectomized mice by estradiol injection

Cited by 7 publications

References 59 publications

Discovering pathways of sarcopenia in older adults: A role for insulin resistance on mitochondria dysfunction

Discovering pathways of sarcopenia in older adults: A role for insulin resistance on mitochondria dysfunction

Mitochondrial fatty acid biosynthesis and muscle fiber plasticity in very long‐chain acyl‐CoA dehydrogenase‐deficient mice

Role of estrogen on skeletal muscle mitochondrial function in ovariectomized rats: a time course study in different fiber types

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