Table 1 Overview of adipose tissue phenotypes in animals that lack autophagy-related genes.
MoleculeSystemAdipocyte phenotypeReferences
Atg5Total knockoutWAT development is impaired.(40)
Atg5MEFs in vitroMEFs from total knockout mice have defects in white adipocyte differentiation in culture.(40)
Atg5Ucp1-CreBeige adipocytes are maintained in the absence of browning stimuli and retain mitochondria and UCP1.(39)
Atg7aP2-CreWAT is reduced and adipocytes have increased mitochondrial content with small lipid droplets. WAT in knockout mice contains increased numbers of beige adipocytes. Mice are protected from diet-induced obesity and insulin resistance.(42, 43)
Atg7Myf5-CreDeletion in Myf5+ progenitors impairs BAT development and promotes beige fat development.(41)
Atg7Mlclf-CreDeletion in skeletal muscle induces browning of WAT.(47)
Atg7Pomc-CreDeletion in POMC neurons induces browning of WAT.(71)
Atg12Ucp1-CreBeige adipocytes are maintained in the absence of browning stimuli and retain mitochondria and UCP1. Mice are protected from diet-induced obesity and insulin resistance.(39)
p62Total knockoutEnlarged adipocytes due to lipid accumulation. Mice are obese, glucose intolerant, and have decreased insulin sensitivity.(106)
p62aP2-CreBrown adipocytes accumulate defective mitochondria and have more lipid droplets. Mice are obese, glucose intolerant, and have decreased insulin sensitivity.(44)
ParkinTotal knockoutMice are resistant to high-fat diet–induced obesity. EpiWAT and BAT of these mice accumulate less lipid in response to a high-fat diet.(107)
RaptorAdiponectin-CreBrowning of WAT is disrupted in response to chronic cold exposure.(56)