The isolation and metabolism of brown fat cells

JN Fain, N Reed, R Saperstein - Journal of Biological Chemistry, 1967 - Elsevier
JN Fain, N Reed, R Saperstein
Journal of Biological Chemistry, 1967Elsevier
A procedure is described by which free brown fat cells can be obtained from the dorsal
interscapular brown fat of rats. The brown fat cells accounted for less than 25% of the cells
present in the intact tissue. The ratio of triglyceride to nitrogen in brown fat cells was about
10% of that in white fat cells. Growth hormone and 9α-fluoro-11β, 17α, 21-trihydroxy-16α-
methyl-1, 4-pregnadien-3, 20-dione (dexamethasone) did not accelerate brown fat cell
lipolysis. The response of brown fat cells to adrenocorticotrophic hormone was less marked …
A procedure is described by which free brown fat cells can be obtained from the dorsal interscapular brown fat of rats. The brown fat cells accounted for less than 25% of the cells present in the intact tissue. The ratio of triglyceride to nitrogen in brown fat cells was about 10% of that in white fat cells.
Growth hormone and 9α-fluoro-11β, 17α,21-trihydroxy-16α-methyl-1,4-pregnadien-3,20-dione (dexamethasone) did not accelerate brown fat cell lipolysis. The response of brown fat cells to adrenocorticotrophic hormone was less marked than that of white fat cells. However, the dose-response curve for stimulation by epinephrine of glycerol or fatty acid release in brown fat cells was similar to that observed in white fat cells. Epinephrine markedly stimulated oxygen consumption by brown fat cells. The Qoo2 for brown fat cells (based on lipid-free dry weight) was greater than 100 in the presence of epinephrine.
Brown fat cells utilized considerably more free glycerol for re-esterification of fatty acids than did white fat cells. The conversion of labeled glycerol to carbon dioxide and fatty acid by brown fat cells was much greater than that by white fat cells and was unaffected by insulin.
The metabolism of glucose by brown fat cells increased progressively over an 8-hour incubation period and was not inhibited by dexamethasone. Insulin accelerated the metabolism of glucose by brown fat cells and also decreased the stimulation of both fatty acid and glycerol release by epinephrine in either the presence or absence of glucose. Epinephrine increased glucose conversion to glyceride glycerol only in the presence of insulin.
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