Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease

Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E.

Risultato della ricerca: Article

14 Citazioni (Scopus)

Abstract

Obesity is associated with aberrant sodium/potassium-ATPase (NaC/KC-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of NaC/KC-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in NaC/KC-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of NaC/KC-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on NaC/KC-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on NaC/KC-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate NaC/KC-ATPase activity.
Lingua originaleEnglish
pagine (da-a)R13-R23
Numero di pagine10
RivistaEndocrinology
Volume218
Stato di pubblicazionePublished - 2013

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Adenosine Triphosphatases
Estradiol
Cardiovascular Diseases
Obesity
Heart Failure
Physiological Phenomena
Sodium-Potassium-Exchanging ATPase
Cardiac Glycosides
Hyperinsulinism
Cardiovascular System
sodium-translocating ATPase
Cardiac Myocytes
Dilatation
Theoretical Models
Steroids

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Endocrinology

Cita questo

Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E. (2013). Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease. Endocrinology, 218, R13-R23.

Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease. / Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E.

In: Endocrinology, Vol. 218, 2013, pag. R13-R23.

Risultato della ricerca: Article

Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E. 2013, 'Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease', Endocrinology, vol. 218, pagg. R13-R23.
Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E. Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease. Endocrinology. 2013;218:R13-R23.
Obradovic, M.; Bjelogrlic, P.; Katsiki, N.; Haidara, M.; Stewart, A.; Jovanovic, A.; Isenovic, E. / Effects of obesity and estradiol on Na+/K+-ATPase and their relevance to cardiovascular disease. In: Endocrinology. 2013 ; Vol. 218. pagg. R13-R23.
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N2 - Obesity is associated with aberrant sodium/potassium-ATPase (NaC/KC-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of NaC/KC-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in NaC/KC-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of NaC/KC-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on NaC/KC-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on NaC/KC-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate NaC/KC-ATPase activity.

AB - Obesity is associated with aberrant sodium/potassium-ATPase (NaC/KC-ATPase) activity, apparently linked to hyperglycemic hyperinsulinemia, which may repress or inactivate the enzyme. The reduction of NaC/KC-ATPase activity in cardiac tissue induces myocyte death and cardiac dysfunction, leading to the development of myocardial dilation in animal models; this has also been documented in patients with heart failure (HF). During several pathological situations (cardiac insufficiency and HF) and in experimental models (obesity), the heart becomes more sensitive to the effect of cardiac glycosides, due to a decrease in NaC/KC-ATPase levels. The primary female sex steroid estradiol has long been recognized to be important in a wide variety of physiological processes. Numerous studies, including ours, have shown that estradiol is one of the major factors controlling the activity and expression of NaC/KC-ATPase in the cardiovascular (CV) system. However, the effects of estradiol on NaC/KC-ATPase in both normal and pathological conditions, such as obesity, remain unclear. Increasing our understanding of the molecular mechanisms by which estradiol mediates its effects on NaC/KC-ATPase function may help to develop new strategies for the treatment of CV diseases. Herein, we discuss the latest data from animal and clinical studies that have examined how pathophysiological conditions such as obesity and the action of estradiol regulate NaC/KC-ATPase activity.

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