Bone and energy metabolism

Abstract

There is an intimate relationship between fat and bone metabolism that has only recently been appreciated. Adipose depots regulate energy utilization in coordination with the liver and skeletal muscle through an intricate series of local, systemic, and neuronal mediators. Although adipose tissue is one of the largest organs in the body, its functions vary by location and origin. Adipocytes can act in an autocrine manner to regulate energy balance by sequestering triglycerides and subsequently, depending on demand, releasing fatty acids through lipolysis for energy utilization, and in some cases through uncoupling protein 1 for generating heat. Adipose tissue can also act in an endocrine or paracrine manner by releasing adipokines that modulate the function of other organs. Bone is one of those target tissues, although the skeleton can also reciprocate by releasing its own factors that modulate adipose tissue function and pancreatic islet cells production of insulin in the pancreas. The central nervous system is the final common pathway modulating these signals, both in the skeleton and in adipose tissue. Disruption in this complex regulatory circuit and its downstream tissues is manifested in a wide range of metabolic disorders, including type 2 diabetes mellitus (T2D). The aim of this chapter is to summarize our knowledge of common determinants in bone and adipose function.