Convergence between bone and energy homeostases: Leptin regulation of bone mass

Karsenty, Gérard

doi:10.1016/j.cmet.2006.10.008

Cited by 369 publications

(287 citation statements)

References 51 publications

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“…RANK-L in turn regulates osteoclast function and results in increased bone resorption. 31 Leptin levels decrease significantly after bariatric surgery in proportion to loss of total body fat. 68 Furthermore, a decrease in leptin after bariatric surgery was inversely correlated with increased levels of markers of bone formation and resorption.…”

Section: Impact Of Bariatric Surgery On Bone Metabolismmentioning

confidence: 99%

“…However, recent insights into the convergence of bone and energy metabolism have demonstrated that a third mechanism involving neuro-hormonal regulation of bone turnover may also have a significant role. 31 Specifically, changes in adipose and gut hormones associated with bariatric surgery appear likely to significantly affect bone metabolism in the postoperative period. 32 Figure 1 present a schema of mechanisms by which bariatric surgery may impact bone metabolism.…”

Section: Impact Of Bariatric Surgery On Bone Metabolismmentioning

confidence: 99%

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Bariatric surgery and bone disease: from clinical perspective to molecular insights

et al. 2012

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Section: Impact Of Bariatric Surgery On Bone Metabolismmentioning

confidence: 99%

Section: Impact Of Bariatric Surgery On Bone Metabolismmentioning

confidence: 99%

Bariatric surgery and bone disease: from clinical perspective to molecular insights

et al. 2012

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“…Activation of this receptor suppresses the key transcription factor, ATF4, while it enhances RANKL production. (43)(44)(45) In contrast, genetically manipulated mice with adipocytespecific expression of FoxC2 transcription factor, which increases sensitivity to the beta-adrenergic-cAMP-protein kinase (PKA) signaling pathway, (46) are characterized by high bone mass and conversion of epididymal WAT to beige fat, and beiging of marrow adipocytes. A secretome of beige adipocytes overexpressing FoxC2 includes bone anabolic Wnt10b, IGFBP2, and IGF-1 proteins.…”

Section: Preclinical Insightsmentioning

confidence: 99%

“…Activation of this receptor suppresses the key transcription factor, ATF4, while it enhances RANKL production. (43)(44)(45) …”

mentioning

confidence: 99%

Energy Excess, Glucose Utilization, and Skeletal Remodeling: New Insights

Lecka‐Czernik

Rosen

2015

Journal of Bone and Mineral Research

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Skeletal complications have recently been recognized as another of the several comorbidities associated with diabetes. Clinical studies suggest that disordered glucose and lipid metabolism have a profound effect on bone. Diabetes-related changes in skeletal homeostasis result in a significant increased risk of fractures, although the pathophysiology may differ from postmenopausal osteoporosis. Efforts to understand the underlying mechanisms of diabetic bone disease have focused on the direct interaction of adipose tissue with skeletal remodeling and the potential influence of glucose utilization and energy uptake on these processes. One aspect that has emerged recently is the major role of the central nervous system in whole-body metabolism, bone turnover, adipose tissue remodeling, and beta cell secretion of insulin. Importantly, the skeleton contributes to the metabolic balance inherent in physiologic states. New animal models have provided the insights necessary to begin to dissect the effects of obesity and insulin resistance on the acquisition and maintenance of bone mass. In this Perspective, we focus on potential mechanisms that underlie the complex interactions between adipose tissue and skeletal turnover by focusing on the clinical evidence and on preclinical studies indicating that glucose intolerance may have a significant impact on the skeleton. In addition, we raise fundamental questions that need to be addressed in future studies to resolve the conundrum associated with glucose intolerance, obesity, and osteoporosis. © 2015 American Society for Bone and Mineral Research. KEY WORDS: BONE-FAT INTERACTIONS; SYSTEMS BIOLOGY; BONE INTERACTORS; CELL/TISSUE SIGNALING; TRANSCRIPTION FACTORS; DISEASES AND DISORDERS OF/RELATED TO BONE Clinical Insight Into the Effect of Disordered Glucose and Lipids Homeostasis on BoneD iabetes mellitus (DM) can be considered a disease of intracellular glucose starvation in muscle and fat, due to either lack of insulin (Type 1 [T1D]) or impaired insulin action (Type 2 [T2D]). Both types of DM are associated with an increase in fractures; however, the skeletal phenotype is very different. T1D patients have reduced bone mineral density (BMD), due to insulin and amylin deficiency, whereas T2D patients have either normal or high BMD. T2D is a disease of disordered energy storage as well as glucose intolerance and altered bone strength. Its prevalence is high and not abating. In the United States, 29.1 million people-9.3% of the population-have diabetes; among them, nearly 60% are characterized as obese (http://www.cdc.gov). Insulin resistance is a characteristic feature of T2D in liver, muscle, and fat, leading to glucose intolerance, elevated cardiometabolic risk factors (eg, low-density lipoprotein [LDL] cholesterol), and excess hepatic glucose output. Visceral adipocytes, in particular, are large and surrounded by fibrous and inflammatory elements.In clinical medicine a major paradox is the relationship of obesity to the skeleton. Obese individuals tend to have higher...

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“…The hypothalamus was one of the first regions of the brain that was identified as a leptin-sensitive target. Indeed, it is now well documented that leptin plays a key role in a number of hypothalamic functions including the regulation of energy homeostasis [3], bone formation [4], reproduction [5] and the hypothalamic-pituitary-adrenal axis [6]. However, recent studies have demonstrated that leptin is a pleitropic cytokine that evokes wide-spread biological actions on numerous extra-hypothalamic brain regions, including hippocampus.…”

Section: Introductionmentioning

confidence: 99%

A Tale of Two Hormones: Role of Leptin and Insulin in Hippocampal Synaptic Function

Harvey¹

2007

TONEURJ

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Abstract:It is well documented that the endocrine hormones, leptin and insulin provide signals to specific hypothalamic brain regions to regulate energy balance. However, the past decade of research has not only revealed the widespread expression of insulin and leptin receptors in the CNS, but has also identified numerous additional functions of these hormones in the brain. In particular, there is growing evidence that these hormones markedly influence hippocampal excitatory synaptic transmission as well as hippocampal synaptic plasticity. More recent studies have also identified links between dysregulation of leptin and insulin systems and the development of neurodegenerative disorders such as Alzheimer's disease. Here we review the recent evidence supporting a role for these hormones in modulating hippocampal synaptic function in health and disease.

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Convergence between bone and energy homeostases: Leptin regulation of bone mass

Cited by 369 publications

References 51 publications

Bariatric surgery and bone disease: from clinical perspective to molecular insights

Bariatric surgery and bone disease: from clinical perspective to molecular insights

Energy Excess, Glucose Utilization, and Skeletal Remodeling: New Insights

A Tale of Two Hormones: Role of Leptin and Insulin in Hippocampal Synaptic Function

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