期刊
AUTOPHAGY
卷 12, 期 8, 页码 1404-1405出版社
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2016.1185578
关键词
adipose; autophagy; cold; lipophagy; POMC
类别
资金
- NCRR NIH HHS [M01 RR000645] Funding Source: Medline
- NIA NIH HHS [RF1 AG043517, P01 AG031782] Funding Source: Medline
- NIDDK NIH HHS [P30 DK020541, P30 DK026687] Funding Source: Medline
- NATIONAL INSTITUTE OF DIABETES AND DIGESTIVE AND KIDNEY DISEASES [P30DK020541, P30DK026687] Funding Source: NIH RePORTER
- NATIONAL INSTITUTE ON AGING [R01AG043517, P01AG031782] Funding Source: NIH RePORTER
Autophagy maintains cellular quality control by degrading organelles, and cytosolic proteins and their aggregates in lysosomes. Autophagy also degrades lipid droplets (LD) through a process termed lipophagy. During lipophagy, LD are sequestered within autophagosomes and degraded by lysosomal acid lipases to generate free fatty acids that are -oxidized for energy. Lipophagy was discovered in hepatocytes, and since then has been shown to function in diverse cell types. Whether lipophagy degrades LD in the major fat storing cellthe adipocyteremained unclear. We have found that blocking autophagy in brown adipose tissues (BAT) by deleting the autophagy gene Atg7 in BAT MYF5 (myogenic factor 5)-positive progenitors increases basal lipid content in BAT and decreases lipid utilization during cold exposureindicating that lipophagy contributes to lipohomeostasis in the adipose tissue. Surprisingly, knocking out Atg7 in hypothalamic proopiomelanocortin (POMC) neurons also blocks lipophagy in BAT and liver suggesting that specific neurons within the central nervous system (CNS) exert telemetric control over lipophagy in BAT and liver.
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