The great roundleaf bat (Hipposideros armiger) as a good model for cold-induced browning of intra-abdominal white adipose tissue.
BACKGROUND
Inducing beige fat from white adipose tissue (WAT) is considered to be a shortcut to weight loss and increasingly becoming a key area in research into treatments for obesity and related diseases. However, currently, animal models of beige fat are restricted to rodents, where subcutaneous adipose tissue (sWAT, benign WAT) is more liable to develop into the beige fat under specific activators than the intra-abdominal adipose tissue (aWAT, malignant WAT) that is the major source of obesity related diseases in humans.


METHODS
Here we induced beige fat by cold exposure in two species of bats, the great roundleaf bat (Hipposideros armiger) and the rickett's big-footed bat (Myotis ricketti), and compared the molecular and morphological changes with those seen in the mouse. Expression of thermogenic genes (Ucp1 and Pgc1a) was measured by RT-qPCR and adipocyte morphology examined by HE staining at three adipose locations, sWAT, aWAT and iBAT (interscapular brown adipose tissue).


RESULTS
Expression of Ucp1 and Pgc1a was significantly upregulated, by 729 and 23 fold, respectively, in aWAT of the great roundleaf bat after exposure to 10°C for 7 days. Adipocyte diameters of WATs became significantly reduced and the white adipocytes became brown-like in morphology. In mice, similar changes were found in the sWAT, but much lower amounts of changes in aWAT were seen. Interestingly, the rickett's big-footed bat did not show such a tendency in beige fat.


CONCLUSIONS
The great roundleaf bat is potentially a good animal model for human aWAT browning research. Combined with rodent models, this model should be helpful for finding therapies for reducing harmful aWAT in humans.
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Yao
Y
Wang
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Tengteng
T
Zhu
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Shanshan
S
Ke
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Na
N
Fang
Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada.
David M
DM
Irwin
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Ming
M
Lei
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Junpeng
J
Zhang
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Huizhen
H
Shi
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Shuyi
S
Zhang
Institute of Molecular Ecology and Evolution, East China Normal University, Shanghai, China.
Zhe
Z
Wang
D000222:Adaptation, Physiological; D002001:Adipose Tissue, Brown / Q000502:physiology*; D052436:Adipose Tissue, White / Q000502:physiology*; D000818:Animals; D002685:Chiroptera / Q000502:physiology*; D003080:Cold Temperature; D005786:Gene Expression Regulation; D050152:Intra-Abdominal Fat / Q000502:physiology*; D007473:Ion Channels / Q000378:metabolism; D051379:Mice; D024101:Mitochondrial Proteins / Q000378:metabolism; D023421:Models, Animal; D050151:Subcutaneous Fat / Q000502:physiology; D022722:Thermogenesis / Q000235:genetics; D000071256:Uncoupling Protein 1; D015431:Weight Loss
D007473:Ion Channels; D024101:Mitochondrial Proteins; C000604371:UCP1 protein, human; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1