scholarly journals ON THE ACTION OF HORMONES WHICH ACCELERATE THE RATE OF OXYGEN CONSUMPTION AND FATTY ACID RELEASE IN RAT ADIPOSE TISSUE IN VITRO

1961 ◽  
Vol 47 (7) ◽  
pp. 932-941 ◽  
Author(s):  
E. G. Ball ◽  
R. L. Jungas
Keyword(s):  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Adipose Tissue In Vitro ◽  
Rate Of Oxygen Consumption ◽  
Fatty Acid Release ◽  
Acid Release ◽  
Rat Adipose Tissue

Glucose metabolism and mobilization of fatty acids by adipose tissue from obese mice

1961 ◽  
Vol 201 (1) ◽  
pp. 19-22 ◽  
Author(s):  
Bernard Leboeuf ◽  
Serene Lochaya ◽  
Nicole Leboeuf ◽  
Francis C. Wood ◽  
Jean Mayer ◽  
...  
Keyword(s):  
Fatty Acids ◽  
Adipose Tissue ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Glucose Metabolism ◽  
Swiss Mice ◽  
Adipose Tissue In Vitro ◽  
Fatty Acid Release ◽  
Acid Release

Free fatty acid mobilization and glucose metabolism to CO2, to glyceride-glycerol, to fatty acids and to glycogen by adipose tissue in vitro were studied in genetically obese hyperglycemic mice (O-H), in goldthioglucose-injected obese Swiss mice and in their respective nonobese littermates. Tissue from O-H mice metabolizes less glucose than tissue from their nonobese littermates in absence of added hormone or in the presence of insulin (0.1 unit/ml) or epinephrine (10–4 m). In addition, there is also a diminished ability for insulin to inhibit and for epinephrine to augment free fatty acid release. No such differences were observed between tissues from goldthioglucose-injected obese Swiss mice and tissues from their lean littermates. Possible significance of these in vitro results with regard to the pathogenesis of the obese hyperglycemic syndrome is discussed.

Some hormonal effects on the metabolism of acetate-i-C14 by rat adipose tissue

1960 ◽  
Vol 198 (3) ◽  
pp. 640-644 ◽  
Author(s):  
Rodney D. Orth ◽  
William D. Odell ◽  
Robert H. Williams
Keyword(s):  
Growth Hormone ◽  
Adipose Tissue ◽  
Oxygen Consumption ◽  
Basic Mechanism ◽  
Tissue Lipid ◽  
Hormonal Effects ◽  
Adipose Tissue In Vitro ◽  
Rat Adipose Tissue

The effects of various hormones on the metabolism of acetate-i-C14 by rat adipose tissue in vitro were investigated. Using an albumin-containing medium, it was found that ACTH, growth hormone, epinephrine and glucagon each caused increased oxygen consumption, a decreased incorporation of acetate into tissue lipid, and an increase in the amount of newly synthesized lipid attached to albumin. The basic mechanism involved in the production of such qualitatively similar effects by each of the hormones studied are unknown.

Catecholamine sensitivity in brown fat cells from cold-acclimated hamsters and rats

1982 ◽  
Vol 242 (3) ◽  
pp. C250-C257 ◽  
Author(s):  
J. Nedergaard
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Brown Fat ◽  
Fat Cells ◽  
Fatty Acid Level ◽  
Serum Fatty Acid ◽  
Bicarbonate Buffer ◽  
Rate Of Oxygen Consumption ◽  
Fatty Acid Release ◽  
Acid Release

Brown fat cells, freshly isolated from cold-acclimated hamsters and rats, did not respond to norepinephrine addition with the characteristic increase in oxygen consumption (heat production) seen in cells from control animals. However, incubation of these cells for 1 h in a Krebs-Ringer bicarbonate buffer, in the presence of 10 mM pyruvate, fully restored norepinephrine responsiveness. Cells treated in this way from cold-acclimated hamsters (a hibernator) increased the rate of oxygen consumption after maximal norepinephrine stimulation as much as cells from control hamsters; also norepinephrine-stimulated fatty acid release was unaltered, indicating that brown fat cells may partly be responsible for the increase in serum fatty acid level seen during arousal from hibernation. Similarly, preincubated cells from cold-acclimated rats (a nonhibernator) increased oxygen consumption and fatty acid release as much as cells from control rats; this suggests that also in cold-acclimated rats brown fat may supply the circulation with fatty acids during cold stress. Cells from cold-acclimated animals were, however, about 10 times less sensitive to norepinephrine than cells from control animals; this desensitization may be the result of a stimulated phosphodiesterase.

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