Fatty acid metabolism by the osteoblast

Abstract

The emergence of bone as an endocrine organ able to influence whole body metabolism, together with comorbid epidemics of obesity, diabetes, and osteoporosis, have prompted a renewed interest in the intermediary metabolism of the osteoblast. To date, most studies have focused on the utilization of glucose by this specialized cell, but the oxidation of fatty acids results in a larger energy yield. Osteoblasts express the requisite receptors and catabolic enzymes to take up and then metabolize fatty acids, which appears to be required during later stages of differentiation when the osteoblast is dedicated to matrix production and mineralization. In this article, we provide an overview of fatty acid β-oxidation and highlight studies demonstrating that the skeleton plays a significant role in the clearance of circulating lipoproteins and non-esterified fatty acids. Additionally, we review the requirement for long-chain fatty acid metabolism during post-natal bone development and the effects of anabolic stimuli on fatty acid utilization by osteoblasts. These recent findings may help to explain the skeletal manifestations of human diseases associated with impaired lipid metabolism while also providing additional insights into the metabolic requirements of skeletal homeostasis.

Exercise Degrades Bone in Caloric Restriction, Despite Suppression of Marrow Adipose Tissue (MAT)

“…MAT, derived from the differentiation of mesenchymal stem cells (MSC) into adipocytes, increases in bonefragility states; however, its potential role in promoting bone formation and/or resorption has not been elucidated, despite active investigation. Moreover, fatty acid β-oxidation markers rise in bone in the setting of exercise, concomitant with increased bone quantity; this along with research (9,20) demonstrating the reliance of the osteoblast on β-oxidation support MAT's role as an energy depot. (16)(17)(18) Recent work established MAT to be suppressed by exercise, in rodents (16,18) and humans, (19) suggesting that MAT may function similarly to white adipose tissue in a calorie-replete state as an energy depot.…”

“…(16)(17)(18) Recent work established MAT to be suppressed by exercise, in rodents (16,18) and humans, (19) suggesting that MAT may function similarly to white adipose tissue in a calorie-replete state as an energy depot. Moreover, fatty acid β-oxidation markers rise in bone in the setting of exercise, concomitant with increased bone quantity; this along with research (9,20) demonstrating the reliance of the osteoblast on β-oxidation support MAT's role as an energy depot.…”

“…MAT, derived from the differentiation of mesenchymal stem cells (MSC) into adipocytes, increases in bonefragility states; however, its potential role in promoting bone formation and/or resorption has not been elucidated, despite active investigation. (2)(3)(4)(5)(6)(7)(8)(9)(10)(11) Understanding of MAT has improved with quantification methods that permit exact investigations, including magnetic resonance spectroscopy (MRS) in humans (12)(13)(14)(15) as well as osmium-μCT and MRI with advanced image processing in rodents. (16)(17)(18) Recent work established MAT to be suppressed by exercise, in rodents (16,18) and humans, (19) suggesting that MAT may function similarly to white adipose tissue in a calorie-replete state as an energy depot.…”

Distinguish fatty acids impact survival, differentiation and cellular function of periodontal ligament fibroblasts

“…It already had been reported that HPdLF show a distinct osteogenic differentiation potential 31 , 32 , 56 , which can be stimulated by several external cues 35 , 57 – 59 . In addition, fatty acids can affect the differentiation of osteoblasts 60 . However, how they influence HPdLF was unknown so far.…”

Osteoglycin, a novel coordinator of bone and glucose homeostasis

“…Such a change presents multiple advantages for bone. Firstly, the reduction in insulin action would increase blood glucose, a fundamental substrate for bone formation [36] particularly in early osteoblasts [31] rather than later, when free fatty acids may be more important [37] . This bias in glucose utilisation toward early osteoblasts is consistent with the ability of NPY/Y1 receptors to regulate glucose homeostasis through osteoglycin release also being restricted to early, not late osteoblasts [7] , and suggests that osteoblast-mediated regulation of osteoglycin occurs in early osteoblasts, in line with its peak expression at this stage of differentiation [38] .…”