17β-Estradiol and testosterone in sarcopenia: Role of satellite cells

Colla, Anabela Belén la; Pronsato, Lucía; Milanesi, Lorena Magdalena; Vasconsuelo, Andrea Anahi

doi:10.1016/j.arr.2015.07.011

Cited by 56 publications

(33 citation statements)

References 186 publications

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“…Gender‐related differences in the population and behaviour of skeletal muscle satellite cells in normal and diseased states are inconsistently reported in the literature (La Colla et al. ; Williams et al. ).…”

Section: Does the Pc Form Part Of The Functional Skin Unit? Role In Dmentioning

confidence: 99%

The panniculus carnosus muscle: an evolutionary enigma at the intersection of distinct research fields

et al. 2018

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The panniculus carnosus is a thin striated muscular layer intimately attached to the skin and fascia of most mammals, where it provides skin twitching and contraction functions. In humans, the panniculus carnosus is conserved at sparse anatomical locations with high interindividual variability, and it is considered of no functional significance (most possibly being a remnant of evolution). Diverse research fields (such as anatomy, dermatology, myology, neuroscience, surgery, veterinary science) use this unique muscle as a model, but several unknowns and misconceptions remain in the literature. In this article, we review what is currently known about panniculus carnosus structure, development, anatomical location, response to environmental stimuli and potential function(s), with the aim of putting together the evidence arising from the different research communities and raising interest in this unique muscle, which we postulate as an ideal model for both vascular and muscular research.

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Section: Does the Pc Form Part Of The Functional Skin Unit? Role In Dmentioning

confidence: 99%

The panniculus carnosus muscle: an evolutionary enigma at the intersection of distinct research fields

et al. 2018

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“…The primary indication for the prescription of testosterone for women is loss of libido [153]Sarcopenia, namely the decline in muscle mass and strength which occurs with ageing, has been associated with a deficiency in both 17β-estradiol and testosterone, two sex hormones which act on satellite cells. These remain quiescent throughout life and are activated in response to stressful events, enabling them to guide repair and regeneration of the skeletal muscle [154]Obese men tend to be hypogonadic as a result of the functional suppression of the hypothalamic–pituitary–testicular axis [155]. However, weight loss obtained with either a low-calorie diet or bariatric surgery is associated with the normalization of sex hormone levels exhibiting a significant increase in bound and unbound testosterone and gonadotropin levels and a decrease in estradiol [156].…”

Section: Role Of Gender Reproductive Status and Age In The Heterogementioning

confidence: 99%

NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk

et al. 2017

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Nonalcoholic fatty liver disease (NAFLD) spans steatosis through nonalcoholic steatohepatis, cirrhosis, and hepatocellular carcinoma (HCC) associated with striking systemic features and excess cardiovascular and liver-related mortality. The pathogenesis of NAFLD is complex and multifactorial. Endocrine derangements are closely linked with dysmetabolic traits. For example, in animal and human studies, female sex is protected from dysmetabolism thanks to young individuals’ ability to partition fatty acids towards ketone body production rather than very low density lipoprotein (VLDL)-triacylglycerol, and to sex-specific browning of white adipose tissue. Ovarian senescence facilitates both the development of massive hepatic steatosis and the fibrotic progression of liver disease in an experimental overfed zebrafish model. Consistently, estrogen deficiency, by potentiating hepatic inflammatory changes, hastens the progression of disease in a dietary model of nonalcoholic steatohepatitis (NASH) developing in ovariectomized mice fed a high-fat diet. In humans, NAFLD more often affects men; and premenopausal women are equally protected from developing NAFLD as they are from cardiovascular disease. It would be expected that early menarche, definitely associated with estrogen activation, would produce protection against the risk of NAFLD. Nevertheless, it has been suggested that early menarche may confer an increased risk of NAFLD in adulthood, excess adiposity being the primary culprit of this association. Fertile age may be associated with more severe hepatocyte injury and inflammation, but also with a decreased risk of liver fibrosis compared to men and postmenopausal status. Later in life, ovarian senescence is strongly associated with severe steatosis and fibrosing NASH, which may occur in postmenopausal women. Estrogen deficiency is deemed to be responsible for these findings via the development of postmenopausal metabolic syndrome. Estrogen supplementation may at least theoretically protect from NAFLD development and progression, as suggested by some studies exploring the effect of hormonal replacement therapy on postmenopausal women, but the variable impact of different sex hormones in NAFLD (i.e., the pro-inflammatory effect of progesterone) should be carefully considered.

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“…In non-skeletal muscle tissues, estradiol is known to protect against apoptosis (e.g., Guo et al, 2013) and immortalized myoblasts were also found to undergo less apoptosis in vitro in the presence of estradiol (Boland et al, 2008;La Colla et al, 2016;Vasconsuelo et al, 2010). It has been suggested that apoptosis plays an important role in skeletal muscle health, ultimately affecting strength (La Colla et al, 2015;Pallafacchina et al, 2013;Sanchez et al, 2014). However, it is important to point out that in healthy unperturbed muscle, apoptotic cells are from other lineages and that rates of apoptosis of quiescent satellite cells during homeostatic conditions are nearly zero (Fry et al, 2016;Hirai et al, 2010;Shea et al, 2010).…”

Section: Apoptosis Of Satellite Cells With Estradiol Deficiencymentioning

confidence: 99%

Estrogen Regulates the Satellite Cell Compartment in Females

Collins

Arpke

Larson

et al. 2018

Preprint

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Skeletal muscle mass, strength, and regenerative capacity decline with age, with many measures showing greater deterioration in females about the time estrogen levels decrease at menopause. Here we show that maintenance of muscle stem cells, satellite cells, as well as selfrenewal and differentiation into muscle fibers, are severely compromised by estrogen deficiency.Mechanistically, by hormone replacement, use of a selective estrogen-receptor modulator (bazedoxifene), and conditional estrogen receptor knockout, we implicate 17β-estradiol and satellite cell expression of estrogen receptor a (ERa) and show that estrogen signaling through this receptor is necessary to prevent apoptosis of satellite cells. Early data from a biopsy study of women who transitioned from peri-to post-menopause are consistent with the loss of satellite cells coincident with the decline in estradiol in humans. Together, these results demonstrate an important role for estrogen in satellite cell maintenance and muscle regeneration in females.3

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17β-Estradiol and testosterone in sarcopenia: Role of satellite cells

Cited by 56 publications

References 186 publications

The panniculus carnosus muscle: an evolutionary enigma at the intersection of distinct research fields

The panniculus carnosus muscle: an evolutionary enigma at the intersection of distinct research fields

NAFLD as a Sexual Dimorphic Disease: Role of Gender and Reproductive Status in the Development and Progression of Nonalcoholic Fatty Liver Disease and Inherent Cardiovascular Risk

Estrogen Regulates the Satellite Cell Compartment in Females

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