scholarly journals Relationships between Bone Turnover and Energy Metabolism

2017 ◽  
Vol 2017 ◽  
pp. 1-11 ◽  
Author(s):  
Tânia A. P. Fernandes ◽  
Luísa M. L. Gonçalves ◽  
José A. A. Brito
Keyword(s):  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Bone Turnover ◽  
Osteoporotic Fracture ◽  
Diabetic Complications ◽  
Bone Health ◽  
Conceptual Approach ◽  
Chronic Complications ◽  
Increased Risk

It is well established that diabetes can be detrimental to bone health, and its chronic complications have been associated with an increased risk of osteoporotic fracture. However, there is growing evidence that the skeleton plays a key role in a whole-organism approach to physiology. The hypothesis that bone may be involved in the regulation of physiological functions, such as insulin sensitivity and energy metabolism, has been suggested. Given the roles of insulin, adipokines, and osteocalcin in these pathways, the need for a more integrative conceptual approach to physiology is emphasized. Recent findings suggest that bone plays an important role in regulating intermediary metabolism, being possibly both a target of diabetic complications and a potential pathophysiologic factor in the disease itself. Understanding the relationships between bone turnover and glucose metabolism is important in order to develop treatments that might reestablish energy metabolism and bone health. This review describes new insights relating bone turnover and energy metabolism that have been reported in the literature.

scholarly journals Role of genetic factors in the pathogenesis of osteoporosis

2000 ◽  
Vol 166 (2) ◽  
pp. 235-245 ◽  
Author(s):  
TL Stewart ◽  
SH Ralston
Keyword(s):  
Bone Mass ◽  
Bone Turnover ◽  
Fracture Risk ◽  
Candidate Genes ◽  
Osteoporotic Fracture ◽  
Genetic Factors ◽  
Single Gene ◽  
Common Disease ◽  
Mineral Density ◽  
Increased Risk

Osteoporosis is a common disease with a strong genetic component characterised by low bone mass, microarchitectural deterioration of bone tissue and an increased risk of fracture. Twin and family studies have shown that genetic factors play an important role in regulating bone mineral density and other determinants of osteoporotic fracture risk, such as ultrasound properties of bone, skeletal geometry and bone turnover. Osteoporosis is a polygenic disorder, determined by the effects of several genes, each with relatively modest effects on bone mass and other determinants of fracture risk. It is only on rare occasions that osteoporosis occurs as the result of mutations in a single gene. Linkage studies in man and experimental animals have defined multiple loci which regulate bone mass but the genes responsible for these effects remain to be defined. Population-based studies and case-control studies have similarly identified polymorphisms in several candidate genes that have been associated with bone mass or osteoporotic fracture, including the vitamin D receptor, oestrogen receptor and collagen type IalphaI gene. The individual contribution of these genes to the pathogenesis of osteoporosis is small however, reflected by the fact that the relationship between individual candidate genes and osteoporosis has been inconsistent in different studies. An important aim of future work will be to define how the genes which regulate bone mass, bone turnover and other aspects of bone metabolism interact with each other and with environmental variables to cause osteoporosis in individual patients. If that aim can be achieved then there is every prospect that preventative therapy could be targeted to those at greatest risk of the osteoporosis, before fractures have occurred.

scholarly journals Bone health management in the continuum of prostate cancer disease: a review of the evidence with an expert panel opinion

ESMO Open ◽  
2020 ◽  
Vol 5 (2) ◽  
pp. e000652 ◽  
Author(s):  
Daniele Santini ◽  
Alfredo Berruti ◽  
Massimo Di Maio ◽  
Giuseppe Procopio ◽  
Sergio Bracarda ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Bone Turnover ◽  
Bone Health ◽  
Health Management ◽  
Unmet Need ◽  
Current Evidence ◽  
Current Standard ◽  
Cancer Disease ◽  
Risk Of Death ◽  
Increased Risk

Bone health impairment is a frequent detrimental consequence of the high bone tropism of prostate cancer (PCa) cells. It is further worsened by administration of androgen-deprivation therapy (ADT), the current standard of care in the management of advanced PCa, through a rapid and dramatic increase in bone turnover and body mass changes. As a result, patients may experience substantial pain and poor quality of life (QoL) and have an increased risk of death. Notwithstanding the importance of this issue, however, bone health preservation is not yet a widespread clinical goal in daily practice.To address this urgent unmet need, following a thorough discussion of available data and sharing of their clinical practice experience, a panel of Italian experts in the field of bone health and metabolism formulated a number of practical advices for optimising the monitoring and treatment of bone health in men undergoing ADT during all phases of the disease. The rationale behind the venture was to raise awareness on the importance of bone preservation in this complex setting, while providing an instrument to support physicians and facilitate the management of bone health.Current evidence regarding the effects on bone health of ADT, of novel hormone therapies (which improve progression delay, pain control and QoL while consistently carrying the risk of non-pathological fractures in both non-metastatic and metastatic PCa) and of bone turnover inhibitors (whose use is frequently suboptimal) is reviewed. Finally, the expert opinion to optimise bone health preservation is given.

scholarly journals Lower temperatures in the bedroom helps to reduce weight and improve insulin sensitivity

2014 ◽  
Vol 11 (3) ◽  
pp. 63
Author(s):  
Tat'yana Sergeevna Borodich
Keyword(s):  
Adipose Tissue ◽  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Brown Adipose Tissue ◽  
Improve Insulin Sensitivity ◽  
Thermal Plasticity ◽  
It Impacts ◽  
Brown Adipose ◽  
Diet Induced Thermogenesis

In rodents, brown adipose tissue (BAT) regulates cold- and diet-induced thermogenesis (CIT; DIT). Whether BAT recruitment is reversible and how it impacts on energy metabolism have not been investigated in humans. Regulatory links between BAT thermal plasticity and glucose metabolism in humans, opening avenues to harnessing BAT for metabolic benefits. 

scholarly journals Maternal protein restriction before pregnancy reduces offspring early body mass and affects glucose metabolism in C57BL/6JBom mice

2012 ◽  
Vol 3 (5) ◽  
pp. 364-374 ◽  
Author(s):  
A. Dudele ◽  
S. Lund ◽  
N. Jessen ◽  
G. Wegener ◽  
G. Winther ◽  
...  
Keyword(s):  
Birth Weight ◽  
Insulin Sensitivity ◽  
Glucose Metabolism ◽  
Body Mass ◽  
Crude Protein ◽  
Recovery Period ◽  
Protein Restriction ◽  
Maternal Protein Restriction ◽  
Increased Risk ◽  
Catch Up

Dietary protein restriction in pregnant females reduces offspring birth weight and increases the risk of developing obesity, type 2 diabetes and cardiovascular disease. Despite these grave consequences, few studies have addressed the effects of preconceptional maternal malnutrition. Here we investigate how a preconceptional low-protein (LP) diet affects offspring body mass and insulin-regulated glucose metabolism. Ten-week-old female mice (C57BL/6JBom) received either an LP or isocaloric control diet (8% and 22% crude protein, respectively) for 10 weeks before conception, but were thereafter fed standard laboratory chow (22.5% crude protein) during pregnancy, lactation and offspring growth. When the offspring were 10 weeks old, they were subjected to an intraperitoneal glucose tolerance test (GTT), and sacrificed after a 5-day recovery period to determine visceral organ mass. Body mass of LP male offspring was significantly lower at weaning compared with controls. A similar, nonsignificant, tendency was observed for LP female offspring. These differences in body mass disappeared within 1 week after weaning, a consequence of catch-up growth in LP offspring. GTTs of 10-week-old offspring revealed enhanced insulin sensitivity in LP offspring of both sexes. No differences were found in body mass, food intake or absolute size of visceral organs of adult offspring. Our results indicate that maternal protein restriction imposed before pregnancy produces effects similar to postconceptional malnutrition, namely, low birth weight, catch-up growth and enhanced insulin sensitivity at young adulthood. This could imply an increased risk of offspring developing lifestyle-acquired diseases during adulthood.

scholarly journals Interleukin-4 Promotes Myogenesis and Boosts Myocyte Insulin Efficacy

2019 ◽  
Vol 2019 ◽  
pp. 1-14 ◽  
Author(s):  
Yih-Hsin Chang ◽  
Jen-Ning Tsai ◽  
Tzu-Lin Chen ◽  
Kuo-Ting Ho ◽  
Hsin-Yi Cheng ◽  
...  
Keyword(s):  
Insulin Sensitivity ◽  
Energy Metabolism ◽  
Glucose Metabolism ◽  
Insulin Signaling ◽  
Energy Homeostasis ◽  
Interleukin 4 ◽  
Whole Body ◽  
Myocyte Differentiation ◽  
Anti Inflammatory Cytokine

Anti-inflammatory cytokine interleukin-4 (IL-4) promotes glucose tolerance and insulin sensitivity while reduces lipid deposits. However, the effects of IL-4 on energy metabolism in muscle, the largest insulin-targeting organ, remain obscure. The study aimed at addressing the roles of IL-4 in myocyte differentiation (myogenesis) and energy metabolism of muscle cells. Effects of IL-4 on myogenesis, and interaction between IL-4 and insulin on glucose metabolism of C2C12 myoblasts and the terminal differentiated myocytes were analyzed. IL-4 improved GLUT4 translocation and tended to elevate glucose uptake by boosting insulin signaling. In diabetic mice, transient and long-term IL-4 showed differential effects on insulin signaling and efficacy. The study provides evidence to address the roles of IL-4 in mediating whole-body muscle reservoir and glucose metabolism, as well as the interaction between immune responses and energy homeostasis. IL-4 has dual potential to act as an adjuvant therapeutic target for sarcopenia to preserve muscle mass and insulin resistance to improve insulin sensitivity, which implicates the regulation of immune system to the muscle differentiation and exercise performance.

scholarly journals Brain Glucose Metabolism in Health, Obesity, and Cognitive Decline—Does Insulin Have Anything to Do with It? A Narrative Review

2021 ◽  
Vol 10 (7) ◽  
pp. 1532
Author(s):  
Eleni Rebelos ◽  
Juha O. Rinne ◽  
Pirjo Nuutila ◽  
Laura L. Ekblad
Keyword(s):  
Insulin Resistance ◽  
Glucose Metabolism ◽  
Cognitive Decline ◽  
Fdg Pet ◽  
Metabolic Disorders ◽  
Brain Glucose ◽  
Brain Glucose Metabolism ◽  
Systemic Insulin Resistance ◽  
Increased Risk ◽  
18F Fdg

Imaging brain glucose metabolism with fluorine-labelled fluorodeoxyglucose ([18F]-FDG) positron emission tomography (PET) has long been utilized to aid the diagnosis of memory disorders, in particular in differentiating Alzheimer’s disease (AD) from other neurological conditions causing cognitive decline. The interest for studying brain glucose metabolism in the context of metabolic disorders has arisen more recently. Obesity and type 2 diabetes—two diseases characterized by systemic insulin resistance—are associated with an increased risk for AD. Along with the well-defined patterns of fasting [18F]-FDG-PET changes that occur in AD, recent evidence has shown alterations in fasting and insulin-stimulated brain glucose metabolism also in obesity and systemic insulin resistance. Thus, it is important to clarify whether changes in brain glucose metabolism are just an epiphenomenon of the pathophysiology of the metabolic and neurologic disorders, or a crucial determinant of their pathophysiologic cascade. In this review, we discuss the current knowledge regarding alterations in brain glucose metabolism, studied with [18F]-FDG-PET from metabolic disorders to AD, with a special focus on how manipulation of insulin levels affects brain glucose metabolism in health and in systemic insulin resistance. A better understanding of alterations in brain glucose metabolism in health, obesity, and neurodegeneration, and the relationships between insulin resistance and central nervous system glucose metabolism may be an important step for the battle against metabolic and cognitive disorders.

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