Cold exposure suppresses serum adiponectin levels through sympathetic nerve activation in mice.
OBJECTIVE
Several lines of evidence suggest important roles for adiponectin in glucose and lipid metabolism and atherosclerosis. However, the mechanisms regulating serum adiponectin levels and adiponectin production are still not completely understood. Our aim was to determine whether adiponectin synthesis is physiologically regulated by the sympathetic nervous system (SNS).


METHODS
Mice were exposed to cold (4 degrees C) for 12 hours and for 24 hours with or without inhibition of noradrenaline synthesis or pan-beta adrenergic function, followed by measurement of serum adiponectin concentrations and levels of adiponectin and uncoupling protein (UCP) 1 expressions in various white adipose tissues (WATs).


RESULTS
Cold exposure significantly reduced serum adiponectin concentrations without changing body weights or WAT sizes in either subcutaneous or intra-abdominal fat tissues. The serum adiponectin reduction was associated with a decrease in adiponectin mRNA expression in subcutaneous, epididymal, and mesenteric fat tissues. In these adipose tissues, UCP1 expression was markedly enhanced, suggesting SNS activation in these tissues. Administration of alpha-methyl-p-tyrosine or a combination of SR59230A and propranolol reversed the cold-exposure-induced decreases in serum adiponectin concentrations and adiponectin mRNA expression in these tissues. In contrast, in retroperitoneal fat, the effects of cold exposure on adiponectin and UCP1 expressions were strikingly weak but were not reversed by SNS inhibitors.


CONCLUSIONS
SNS physiologically regulates serum adiponectin levels and adiponectin synthesis in WATs in vivo, although responsiveness to SNS stimulation differs markedly among WATs. Sympathetic activation might be involved in development of the metabolic syndrome by modulation of serum adiponectin concentrations.
Imai
Junta
J
Division of Molecular Metabolism and Diabetes, Center for Translational and Advanced Animal Research, Tohoku University Graduate School of Medicine, 2-1 Seiryo-machi, Aoba-ku, Sendai 980-8575, Japan.
Katagiri
Hideki
H
Yamada
Tetsuya
T
Ishigaki
Yasushi
Y
Ogihara
Takehide
T
Uno
Kenji
K
Hasegawa
Yutaka
Y
Gao
Junhong
J
Ishihara
Hisamitsu
H
Sasano
Hironobu
H
Oka
Yoshitomo
Y
D052242:Adiponectin / Q000096:biosynthesis / Q000097:blood*; D000273:Adipose Tissue / Q000378:metabolism*; D000818:Animals; D001835:Body Weight / Q000502:physiology; D003080:Cold Temperature; D005786:Gene Expression Regulation; D007473:Ion Channels / Q000378:metabolism*; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D024101:Mitochondrial Proteins / Q000378:metabolism*; D012333:RNA, Messenger / Q000032:analysis; D011897:Random Allocation; D013564:Sympathetic Nervous System / Q000502:physiology*; D013997:Time Factors; D000071256:Uncoupling Protein 1
D052242:Adiponectin; D007473:Ion Channels; D024101:Mitochondrial Proteins; D012333:RNA, Messenger; C000604372:Ucp1 protein, mouse; D000071256:Uncoupling Protein 1