scholarly journals Effects of prolonged incubation of isolated fat cells on their response to hormones stimulating lipolysis and glucose metabolism

1966 ◽  
Vol 98 (2) ◽  
pp. 557-561 ◽  
Author(s):  
DJ Galton ◽  
JN Fain
Keyword(s):  
Glucose Metabolism ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Prolonged Incubation

scholarly journals Effects of cytochalasin B, colchicine and vincristine on the metabolism of isolated fat-cells

1974 ◽  
Vol 140 (2) ◽  
pp. 185-192 ◽  
Author(s):  
Ernest G. Loten ◽  
Bernard Jeanrenaud
Keyword(s):  
Glucose Metabolism ◽  
Transport System ◽  
Cytochalasin B ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Prolonged Incubation ◽  
Glucose Transport System ◽  
End Products ◽  
Release Of Glycerol ◽  
Cytochalasin A

1. Colchicine and vincristine only slightly inhibit the metabolism of glucose to CO2 and lipids by isolated fat-cells. 2. Prolonged incubation with these agents causes no further inhibition. 3. Cytochalasin B, however, inhibits glucose metabolism to both CO2 and lipids in fat-cells. 4. However, at a concentration that causes a strong inhibition of glucose metabolism cytochalasin B is without effect on the metabolism of pyruvate, lactate or arginine to these end products. The uptake of labelled α-aminoisobutyrate is likewise not modified. Similarly it does not affect release of glycerol or free fatty acid, or the actions of adrenaline, insulin or caffeine on these parameters. At 10μg/ml it slightly lowers ATP concentrations, an effect that does not occur at 2μg/ml. 5. The transport of fructose into adipocytes by a specific fructose-transport system is also not affected by the agent, but the uptake of 2-deoxyglucose is strongly inhibited. It is concluded that cytochalasin B may specifically inhibit the glucose-transport system of isolated fat-cells. 6. Cytochalasin A has a much weaker action than cytochalasin B on glucose metabolism.

Glucose Metabolism by Isolated Fat Cells from Sloth

1979 ◽  
Vol 87 (1) ◽  
pp. 65-71 ◽  
Author(s):  
Gladys E. Chiappe de Cingolani ◽  
M. do Carmo de Araujo Fraga ◽  
Vera L. de Menezes Lima
Keyword(s):  
Glucose Metabolism ◽  
Fat Cells ◽  
Isolated Fat Cells

Effects of Streptozocin-Induced Diabetes on Glucose Metabolism and Lactate Release by Isolated Fat Cells From Young Lean and Older, Moderately Obese Rats

Diabetes ◽  
1989 ◽  
Vol 38 (2) ◽  
pp. 237-243 ◽  
Author(s):  
F. D. Newby ◽  
F. Bayo ◽  
S. V. Thacker ◽  
M. Sykes ◽  
M. Digirolamo
Keyword(s):  
Glucose Metabolism ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Lactate Release ◽  
Obese Rats

scholarly journals Interrelationship and control of glucose metabolism and lipogenesis in isolated fat-cells. Control of pentose phosphate-cycle activity by cellular requirement for reduced nicotinamide adenine dinucleotide phosphate

1972 ◽  
Vol 128 (5) ◽  
pp. 1097-1102 ◽  
Author(s):  
H. Kather ◽  
M. Rivera ◽  
K. Brand
Keyword(s):  
Fatty Acid ◽  
Glucose Metabolism ◽  
Fatty Acid Synthesis ◽  
Nicotinamide Adenine Dinucleotide Phosphate ◽  
Acid Synthesis ◽  
Pentose Phosphate ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Pentose Phosphate Cycle ◽  
Phenazine Methosulphate

By using inhibitors and stimulators of different metabolic pathways the interdependence of the pentose phosphate cycle and lipogenesis in isolated fat-cells was studied. Rotenone, which is known to inhibit electron transport in the respiratory chain, blocked glucose breakdown at the site of pyruvate dehydrogenase. Consequently, because of the lack of acetyl-CoA, fatty acid synthesis was almost abolished. A concomitant decrease in pentose phosphate-cycle activity was observed. Phenazine methosulphate stimulated pentose phosphate-cycle activity about five- to ten-fold without a considerable effect on fatty acid synthesis. The influence of rotenone on both the pentose phosphate cycle and lipogenesis could be overcome by addition of phenazine methosulphate, indicating that rotenone has no direct effect on these pathways. The decreased rate of the pentose phosphate cycle in the presence of rotenone therefore has to be considered as a consequence of decreased fatty acid synthesis. The rate of glucose catabolism via the pentose phosphate cycle in adipocytes appears to be determined by the requirement of NADPH for lipogenesis. Treatment of cells with 6-aminonicotinamide caused an accumulation of 6-phosphogluconate, indicating an inhibition of 6-phosphogluconate dehydrogenase. The rate of glucose metabolism via the pentose phosphate cycle as well as the rate of fatty acid synthesis, however, was not affected by 6-aminonicotinamide treatment and could still be stimulated by addition of insulin. Since even in cells from starved animals, in which the pentose phosphate-cycle activity is extremely low, no accumulation of 6-phosphogluconate was observed, it is concluded that the control of this pathway is achieved by the rate of regeneration of NADP at the site of glucose 6-phosphate dehydrogenase.

Sign in / Sign up

Export Citation Format

Share Document