Key result
Adipocyte LPL deficiency in mice impairs fatty acid flux, altering bone marrow fatty acid composition.
Why the study?
The metabolic role of adipocytes in bone marrow and their contribution to systemic nutrient handling remain largely unclear.
The skeleton is a major organ for systemic glucose and fatty acid clearance, and adipocyte LPL regulates fatty acid transport to skeletal compartments.
LPL regulates skeletal fatty acid transport in mice without phenotype; extends mechanistic insight but leaves open human relevance.
Adipocytes are master regulators of energy homeostasis. Although the contributions of classical brown and white adipose tissue (BAT and WAT, respectively) to glucose and fatty acid metabolism are well characterized, the metabolic role of adipocytes in bone marrow remains largely unclear. Here, we quantify bone fatty acid metabolism and its contribution to systemic nutrient handling in mice. Whereas in parts of the skeleton the specific amount of nutrients taken-up from the circulation was lower than in other metabolically active tissues such as BAT or liver, the overall contribution of the skeleton as a whole organ was remarkable, placing it among the top organs involved in systemic glucose as well as fatty acid clearance. We show that there are considerable site-specific variations in bone marrow fatty acid composition throughout the skeleton and that, especially in the tibia, marrow fatty acid profiles resemble classical BAT and WAT. Using a mouse model lacking lipoprotein lipase (LPL), a master regulator of plasma lipid turnover specifically in adipocytes, we show that impaired fatty acid flux leads to reduced amounts of dietary essential fatty acids while there was a profound increase in de novo produced fatty acids in both bone marrow and cortical bone. Notably, these changes in fatty acid profiles were not associated with any gross skeletal phenotype. These results identify LPL as an important regulator of fatty acid transport to skeletal compartments and demonstrate an intricate functional link between systemic and skeletal fatty acid and glucose metabolism.
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Bartelt et al. (2017) studied this question. Lipoprotein lipase (LPL) deficiency in adipocytes vs. Wild-type mice (implied) was evaluated on Bone fatty acid metabolism and systemic nutrient handling. Adipocyte-specific lipoprotein lipase deficiency in mice impaired fatty acid flux, reducing dietary essential fatty acids and increasing de novo produced fatty acids in bone marrow and cortical bone.
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