Key result
Depletion of adipocyte sphingosine kinase 1 in mice on a high-fat diet leads to cell hypertrophy, impaired lipolysis, and nonalcoholic fatty liver disease.
Adipocyte SPHK1 plays an essential homeostatic role in protecting against obesity-associated pathology, including insulin resistance and NAFLD.
Adipocyte SPHK1 depletion worsens diet-induced NAFLD in mice; hypothesis-generating for its role in human metabolic disease.
mice on a HFD, implicating a specific role for adipocyte SPHK1 in adipocyte function and inter-organ cross-talk that maintains overall metabolic homeostasis in obesity. Thus, SPHK1 serves a previously unidentified essential homeostatic role in adipocytes that protects from obesity-associated pathology. These findings may have implications for pharmacological targeting of the SPHK1/S1P signaling axis.
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Anderson et al. (2020) studied Obesity and nonalcoholic fatty liver disease. Depletion of adipocyte sphingosine kinase 1 (SPHK1) was evaluated on Cell hypertrophy, impaired lipolysis, and nonalcoholic fatty liver disease. Depletion of adipocyte sphingosine kinase 1 in mice on a high-fat diet leads to cell hypertrophy, impaired lipolysis, and nonalcoholic fatty liver disease.
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