Abstract
In the skeletal system glucose serves as an essential source of energy for the development, growth, and maintenance of bone and articular cartilage. It is particularly needed for skeletal morphogenesis during embryonic growth and fetal development. Glucose is vital for osteogenesis and chondrogenesis, and is used as a precursor for the synthesis of glycosaminoglycans, glycoproteins, and glycolipids. Glucose sensors are present in tissues and organs that carry out bulk glucose fluxes (i.e., intestine, kidney, and liver). The beta cells of the pancreatic islets of Langerhans respond to changes in blood glucose concentration by varying the rate of insulin synthesis and secretion. Neuronal cells in the hypothalamus are also capable of sensing extracellular glucose. Glucosensing neurons use glucose as a signaling molecule to alter their action potential frequency in response to variations in ambient glucose levels. Skeletal muscle and adipose tissue can respond to changes in circulating glucose but much less is known about glucosensing in bone and cartilage. Recent research suggests that bone cells can influence (and be influenced by) systemic glucose metabolism. This focused review article discusses what we know about glucose transport and metabolism in bone and cartilage and highlights recent studies that have linked glucose metabolism, insulin signaling, and osteocalcin activity in bone. These new findings in bone cells raise important questions about nutrient sensing, uptake, storage and processing mechanisms and how they might contribute to overall energy homeostasis in health and disease. The role of glucose in modulating anabolic and catabolic gene expression in normal and osteoarthritic chondrocytes is also discussed. In summary, cartilage and bone cells are sensitive to extracellular glucose and adjust their gene expression and metabolism in response to varying extracellular glucose concentrations.
Highlights
All living cells must be able to regulate their metabolic activity when faced with nutrient fluctuations in the extracellular environment (Mobasheri et al, 2008)
Osteocalcin deficiency in knockout mice leads to decreased insulin and adiponectin secretion, insulin resistance, higher serum glucose levels, and increased adiposity (Wolf, 2008). These links highlight the importance of glucose metabolism and insulin action in bone and how insulin signaling in osteoblasts contributes to whole-body glucose homeostasis by increasing the expression and activity of osteocalcin
Various regulatory and signaling systems are known to be involved in maintaining bone and cartilage health, our basic understanding of these processes is limited compared to other tissues and organs
Summary
All living cells must be able to regulate their metabolic activity when faced with nutrient fluctuations in the extracellular environment (Mobasheri et al, 2008). This focused review article discusses the importance of glucose as a universal energy currency and the molecular mechanisms involved in glucose sensing in the pancreas and the gut before focusing on glucose transport and metabolism in bone and cartilage and highlighting areas for future research. In many experimental models of diabetes, GLUT2 gene expression is decreased in pancreatic β cells, which could lead to a loss of glucose-induced insulin secretion.
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