Abrogation of GH action in Kupffer cells results in increased hepatic CD36 expression and exaggerated nonalcoholic fatty liver disease.
作者信息
Zhang Sherry, Lu Chunxia, Das Arun K, Pasupulati Anil K, Menon Ram K
机构信息
Departments of Pediatrics & Communicable Diseases, University of Michigan, United States.
Department of Internal Medicine, University of Michigan, United States.
出版信息
Growth Horm IGF Res. 2018 Oct-Dec;42-43:74-79. doi: 10.1016/j.ghir.2018.10.001. Epub 2018 Oct 4.
OBJECTIVE
To investigate the effects of GH signaling on Kupffer cells and the resulting changes in lipid homeostasis and their underlying mechanism(s) in the livers of diet-induced obese (DIO) mice.
DESIGN
Male macrophage specific-growth hormone receptor knockout mice (MacGHR KO) and their litter mate controls were fed a high fat diet containing 60% calories from fat for 26 weeks. Lipid content and lipid profiles in the liver and circulation were analyzed. Expression levels of CD36 in the liver were quantified by RT-PCR and Western Blot.
RESULTS
Increased hepatic lipid content and abundance of long-chain unsaturated fatty acids were observed in the liver of MacGHR KO mice. These findings were associated with increased steady state levels of CD36 mRNA and protein in MacGHR KO mice when compared with their litter mate controls.
CONCLUSION
GH action in Kupffer cells is required for maintaining hepatic lipid homeostasis, in part via regulation of hepatic CD36 expression.
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