Donepezil regulates energy metabolism and favors bone mass accrual

Bone ◽  
2016 ◽  
Vol 84 ◽  
pp. 131-138 ◽  
Author(s):  
Hazem Eimar ◽  
Sharifa Alebrahim ◽  
Garthiga Manickam ◽  
Ahmed Al-Subaie ◽  
Lina Abu-Nada ◽  
...  
Keyword(s):  
Energy Metabolism ◽  
Bone Mass ◽  
Bone Mass Accrual

scholarly journals The Central Regulation of Bone Mass, the First Link between Bone Remodeling and Energy Metabolism

2010 ◽  
Vol 31 (4) ◽  
pp. 607-607
Author(s):  
Gerard Karsenty ◽  
Franck Oury
Keyword(s):  
Energy Metabolism ◽  
Energy Expenditure ◽  
Bone Mass ◽  
Bone Remodeling ◽  
Molecular Pathways ◽  
Central Regulation ◽  
Clinical Observations ◽  
Bone Mass Accrual ◽  
Coordinated Regulation ◽  
The Brain

Abstract Evolutionary consideration and clinical observations led us to hypothesize 10 yr ago that there may be a coordinated regulation, endocrine in nature, of bone remodeling and energy metabolism. The existence of this coordinated regulation is motivated by the energetic needs of the skeleton; therefore, this regulation relies on hormones that appear during evolution with the skeleton, not with energy metabolism. Leptin is such a hormone, and it is a critical regulator of bone mass as well as of appetite and energy expenditure. This review goes over the anatomical route and molecular pathways used by leptin to inhibit both bone mass accrual and appetite through its signaling in the brain.

Foxp1 in osteoblasts regulates bone mass accrual and adipose tissue energy metabolism

2021 ◽  
Author(s):  
Wei Zhang ◽  
Pei Liu ◽  
Shifeng Ling ◽  
Fuhua Wang ◽  
Shaojiao Wang ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Bone Mass ◽  
Bone Mass Accrual

scholarly journals MECHANISMS IN ENDOCRINOLOGY: The endocrine role of the skeleton: background and clinical evidence

2012 ◽  
Vol 166 (6) ◽  
pp. 959-967 ◽  
Author(s):  
Verena Schwetz ◽  
Thomas Pieber ◽  
Barbara Obermayer-Pietsch
Keyword(s):  
Adipose Tissue ◽  
Energy Metabolism ◽  
Bone Resorption ◽  
Bone Mass ◽  
Feedback Loop ◽  
Clinical Evidence ◽  
Positive Effects ◽  
Bone Mass Accrual ◽  
Regulatory Feedback Loop

Based on the observation that diabetes, obesity, and hypogonadism influence bone metabolism, the existence of a feedback loop and a common regulation was postulated and an endocrine role ascribed to the skeleton. In the first part of this review, two pathways are described whereby adipose tissue acts on bone mass. In the first, leptin activates the sympathetic nervous system via serotonin and diminishes bone mass accrual. The second pathway functions via the activation ofCART(CARTPT) and inhibits bone resorption. The first pathway leads to a decrease in bioactivity of the osteoblast-produced hormone osteocalcin (OC) (part 2). In its undercarboxylated form, OC acts on the three targets pancreas, adipose tissue, and gonads (part 3) and thereby causes an increase in insulin secretion and sensitivity, β-cell proliferation, and male fertility. Insulin (part 4) is part of a recently discovered regulatory feedback loop between pancreas and osteoblasts. It is a strong counterplayer of leptin as it causes a decrease in OPG expression and enhances bone resorption and OC decarboxylation. Numerous clinical studies (part 5) have shown associations of total and undercarboxylated OC and markers of energy metabolism. Interventional studies, to date only performed in murine models, have shown positive effects of OC administration on energy metabolism. Whether bone tissue has an even further-reaching endocrine role remains to be elucidated.

The Effect of Hormonal Oral Contraception on Acquisition of Peak Bone Mineral Density of Adolescents and Young Women

2012 ◽  
Vol 25 (3) ◽  
pp. 331-340 ◽  
Author(s):  
Susan Ziglar ◽  
Tracy S. Hunter
Keyword(s):  
Bone Mineral Density ◽  
Bone Mass ◽  
Bone Mineral ◽  
Young Women ◽  
Bone Mineralization ◽  
Critical Time ◽  
Health Concern ◽  
Mineral Density ◽  
Peak Bone Mineral Density ◽  
Bone Mass Accrual

Maximizing bone mass in youth is touted as the best strategy to offset the natural losses of aging and the menopausal transition. Not achieving maximum peak bone mineral density (BMD) is an independent risk factor for osteoporosis and thus a public health concern. Adolescence is a critical time of bone mineralization mediated by endogenous estradiol. Research has shown that the highest velocity of bone mass accrual occurs 1 year before menarche and after the first 3 years. Low-peak attainment of BMD in young women is associated with contributing factors such as diets low in calcium, eating disorders, lack of exercise, smoking, and low estrogen states. Oral contraceptives (OCs) suppress endogenous estradiol production by suppressing the hypothalamic–pituitary–ovarian axis. Thus, OCs, by replacing endogenous estradiol with ethinyl estradiol (EE), establish and maintain new hormone levels. The early initiation and the use of very low dose of EE raises the possibility that bone mass accrual at a critical time of bone mineralization in young women or adolescents may be jeopardized. This review examines the studies of BMD in adolescents and young women that use combination hormonal contraception. Some studies had inherent limitations, such as small trial, poor control of confounders, failure to exclude women with prior use of hormonal contraceptives, or prior pregnancy from control groups. The vast majority of reviewed studies showed OCs containing 20 to 30 µg of EE interfere with acquisition of peak BMD. Limited numbers of studies examine the effects of OCs containing 35 µg on adolescents and young adults. Additionally, studies are needed evaluating the progestin component of OCs as their differing androgenic properties may affect bone mineralization as well.

scholarly journals Relatively higher bone formation markers during puberty are correlated with more bone mass accrual independent of longitudinal growth in boys

Bone Reports ◽  
2020 ◽  
Vol 13 ◽  
pp. 100671
Author(s):  
Thiberiu Banica ◽  
Sara Vandewalle ◽  
Hans-Georg Zmierczak ◽  
Stefan Goemaere ◽  
Jean De Schepper ◽  
...  
Keyword(s):  
Bone Formation ◽  
Bone Mass ◽  
Longitudinal Growth ◽  
Bone Formation Markers ◽  
Bone Mass Accrual

scholarly journals Impact of the Autonomic Nervous System on the Skeleton

2018 ◽  
Vol 98 (3) ◽  
pp. 1083-1112 ◽  
Author(s):  
Florent Elefteriou
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Bone Mass ◽  
Bone Remodeling ◽  
Cancer Metastasis ◽  
Bone Development ◽  
Autonomic Nerves ◽  
Bone Homeostasis ◽  
Bone Mass Accrual ◽  
The Central Nervous System

It is from the discovery of leptin and the central nervous system as a regulator of bone remodeling that the presence of autonomic nerves within the skeleton transitioned from a mere histological observation to the mechanism whereby neurons of the central nervous system communicate with cells of the bone microenvironment and regulate bone homeostasis. This shift in paradigm sparked new preclinical and clinical investigations aimed at defining the contribution of sympathetic, parasympathetic, and sensory nerves to the process of bone development, bone mass accrual, bone remodeling, and cancer metastasis. The aim of this article is to review the data that led to the current understanding of the interactions between the autonomic and skeletal systems and to present a critical appraisal of the literature, bringing forth a schema that can put into physiological and clinical context the main genetic and pharmacological observations pointing to the existence of an autonomic control of skeletal homeostasis. The different types of nerves found in the skeleton, their functional interactions with bone cells, their impact on bone development, bone mass accrual and remodeling, and the possible clinical or pathophysiological relevance of these findings are discussed.

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