A-ZIP/F-1 mice lacking white fat: a model for understanding lipoatrophic diabetes.
The A-ZIP/F-1 mouse is lacking virtually all white adipose tissue. Like humans with extensive deficiencies of adipose tissue, the A-ZIP/F-1 mice develop a severe form of insulin resistant diabetes. We have studied the physiology of the A-ZIP/F-1 mice. Their adaptation to fasting is notable for its rapidity and the use of torpor, a hibernation-like state, to minimize energy needs. Transplantation of adipose tissue reversed the metabolic manifestations in the mice, demonstrating that the lack of adipose tissue is the cause of the insulin resistance. Leptin replacement is not very effective in reversing the diabetes of the A-ZIP/F-1 mice, which contrasts with its efficacy in the aP2-SREBP-lc mouse.
Reitman
M L
ML
Diabetes Branch, National Institute of Diabetes and Digestive and Kidney Diseases, Bethesda, Maryland 20892-1770, USA. mlr@helix.nih.gov
Gavrilova
O
O
D000273:Adipose Tissue / Q000473:pathology / Q000637:transplantation; D000818:Animals; D001823:Body Composition; D003923:Diabetes Mellitus, Lipoatrophic / Q000209:etiology / Q000601:surgery; D004195:Disease Models, Animal; D005215:Fasting / Q000502:physiology; D006801:Humans; D007333:Insulin Resistance; D020738:Leptin / Q000502:physiology; D051379:Mice; D008822:Mice, Transgenic / Q000502:physiology*; D010641:Phenotype; D014157:Transcription Factors
D020738:Leptin; C406806:Tg(AZIP-F)1Vsn protein, mouse; D014157:Transcription Factors