Chronic administration of beta-adrenergic agonists can mimic the stimulative effect of cold exposure on protein synthesis in rat brown adipose tissue

When mammals are exposed to a cold environment for a long time, the capacity of nonshivering thermogenesis by brown adipose tissue (BAT) increases in association with the stimulation of synthesis of some specific proteins and tissue hyperplasia, which are totally dependent on sympathetic innervation...

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Bibliographic Details
Published in:Journal of biochemistry (Tokyo) 1995, Vol.117 (1), p.96-100
Main Authors: Tsukazaki, K, Nikami, H, Shimizu, Y, Kawada, T, Yoshida, T, Saito, M
Format: Article
Language:English
Subjects:
adipose tissue
Adipose Tissue, Brown - drug effects
Adipose Tissue, Brown - metabolism
Adipose Tissue, Brown - pathology
adrenergic agonist
Adrenergic beta-Agonists - pharmacology
Animals
beta-adrenergic agonists
Body Temperature Regulation - physiology
brown adipose tissue
cold exposure
cold stress
Cold Temperature
Denervation
Female
glucose
glucose transporter
Glucose Transporter Type 4
Hyperplasia
Monosaccharide Transport Proteins - metabolism
Muscle Proteins
nutrient transport
Protein Biosynthesis
protein synthesis
Rats
Rats, Wistar
uncoupling protein
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Summary:When mammals are exposed to a cold environment for a long time, the capacity of nonshivering thermogenesis by brown adipose tissue (BAT) increases in association with the stimulation of synthesis of some specific proteins and tissue hyperplasia, which are totally dependent on sympathetic innervation to this tissue. To clarify the roles of the adrenergic mechanisms for the cold-induced protein synthesis and hyperplasia in BAT, in this study, the effects of chronic treatment with adrenergic agonists using an osmotic mini-pump were examined in rats. Continuous administration of noradrenaline or isoproterenol (beta-agonist) for 10 days resulted in increased synthesis of the mitochondrial uncoupling protein and an isoform of glucose transporter (GLUT4), and tissue hyperplasia, in the same way as after cold exposure of the same duration. Phenylephrine (alpha-agonist) administration did not have any significant effect. Surgical sympathetic denervation completely abolished the effects of cold exposure, whereas it did not influence those of adrenergic agonists at all. These results indicate that the stimulative effects of cold exposure on protein synthesis and hyperplasia of BAT are attributable solely to the beta-adrenergic of nonadrenaline secreted from the sympathetic nerves in this tissue.
ISSN:0021-924X
1756-2651
DOI:10.1093/oxfordjournals.jbchem.a124728