Impairment of trophic response of brown fat to cold in guanethidine-treated rats.
The aim of the present study was to investigate the role of the sympathetic nervous system in the trophic response of brown adipose tissue (BAT) to chronic cold exposure. The hyperplasia and the development of the mitochondria characterizing this response are usually considered as mainly controlled by the sympathetic activity in BAT, but this has never been clearly demonstrated. In the present work rats were sympathectomized by chronic administration of guanethidine and then exposed to cold during two weeks. The treatment induced a strong reduction of the noradrenaline content of BAT. The trophic response of the tissue to cold was largely impaired: no increase of the tissue weight, weak increase in the DNA, protein, and phospholipid content of the tissue. The development of the mitochondria was almost abolished. The increase in the proportion of the 32,000-dalton protein, a protein which regulates heat production by BAT, was suppressed and the GDP-binding to mitochondria, which is an index of BAT thermogenic capacity, was not increased as in normal cold-adapted rats. The ultrastructure of the tissue remained the same as in warm-adapted animals. It is concluded that the sympathetic nervous system plays an essential role in the control of the trophic response of BAT to the cold.
D000222:Adaptation, Physiological; D002001:Adipose Tissue, Brown / Q000378:metabolism / Q000502:physiology* / Q000648:ultrastructure; D000818:Animals; D003080:Cold Temperature; D004247:DNA / Q000378:metabolism; D006145:Guanethidine / Q000494:pharmacology*; D008854:Microscopy, Electron; D010743:Phospholipids / Q000378:metabolism; D011506:Proteins / Q000378:metabolism; D051381:Rats; D013564:Sympathetic Nervous System / Q000502:physiology*
D010743:Phospholipids; D011506:Proteins; D004247:DNA; D006145:Guanethidine