scholarly journals The Regulation of Glyceride Synthesis from Pyruvate in Isolated Fat Cells. The Effects of Palmitate and Alteration of Dietary Status

1971 ◽  
Vol 23 (1) ◽  
pp. 109-117 ◽  
Author(s):  
E. David Saggerson ◽  
G. Tomassi
Keyword(s):  
Fat Cells ◽  
Isolated Fat Cells ◽  
Glyceride Synthesis

scholarly journals Insulin-Receptor Interaction in Isolated Fat Cells

1969 ◽  
Vol 244 (19) ◽  
pp. 5181-5188
Author(s):  
T. Minemura ◽  
Oscar B. Crofford
Keyword(s):  
Insulin Receptor ◽  
Receptor Interaction ◽  
Fat Cells ◽  
Isolated Fat Cells

A procedure for measurement of distribution spaces in isolated fat cells

1972 ◽  
Vol 286 (1) ◽  
pp. 1-9 ◽  
Author(s):  
J. Gliemann ◽  
K. Østerlind ◽  
J. Vinten ◽  
S. Gammeltoft
Keyword(s):  
Fat Cells ◽  
Isolated Fat Cells ◽  
Distribution Spaces

scholarly journals The regulation of glyceride synthesis in isolated white-fat cells. The effects of palmitate and lipolytic agents

1972 ◽  
Vol 128 (5) ◽  
pp. 1057-1067 ◽  
Author(s):  
E. D Saggerson
Keyword(s):  
Fatty Acids ◽  
Fatty Acid ◽  
Free Fatty Acids ◽  
Fatty Acid Synthesis ◽  
Acid Synthesis ◽  
Fat Cells ◽  
Glyceride Synthesis ◽  
Glucose Incorporation ◽  
High Concentrations ◽  
Stimulation Of

1. 0.5mm-Palmitate stimulated incorporation of [U-14C]glucose into glyceride glycerol and fatty acids in normal fat cells in a manner dependent upon the glucose concentration. 2. In the presence of insulin the incorporation of 5mm-glucose into glyceride fatty acids was increased by concentrations of palmitate, adrenaline and 6-N-2′-O-dibutyryladenosine 3′:5′-cyclic monophosphate up to 0.5mm, 0.5μm and 0.5mm respectively. Higher concentrations of these agents produced progressive decreases in the rate of glucose incorporation into fatty acids. 3. The effects of palmitate and lipolytic agents upon the measured parameters of glucose utilization were similar, suggesting that the effects of lipolytic agents are mediated through increased concentrations of free fatty acids. 4. In fat cells from 24h-starved rats, maximal stimulation of glucose incorporation into fatty acids was achieved with 0.25mm-palmitate. Higher concentrations of palmitate were inhibitory. In fat cells from 72h-starved rats, palmitate only stimulated glucose incorporation into fatty acids at high concentrations of palmitate (1mm and above). 5. The ability of fat cells to incorporate glucose into glyceride glycerol in the presence of palmitate decreased with increasing periods of starvation. 6. It is suggested that low concentrations of free fatty acids stimulate fatty acid synthesis from glucose by increasing the utilization of ATP and cytoplasmic NADH for esterification of these free fatty acids. When esterification of free fatty acids does not keep pace with their provision, inhibition of fatty acid synthesis occurs. Provision of free fatty acids far in excess of the esterification capacity of the cells leads to uncoupling of oxidative phosphorylation and a secondary stimulation of fatty acid synthesis from glucose.

scholarly journals Factors affecting the permeability of isolated fat-cells from the rat to [42K]potassium and [36Cl]chloride ions

1970 ◽  
Vol 117 (3) ◽  
pp. 615-621 ◽  
Author(s):  
M. C. Perry ◽  
C. N. Hales
Keyword(s):  
Initial Phase ◽  
Chloride Ions ◽  
Fat Cells ◽  
Adrenocorticotrophic Hormone ◽  
Isolated Fat Cells ◽  
Free Medium ◽  
Fat Cell ◽  
Factors Affecting ◽  
Exchange Diffusion ◽  
High K

1. The effluxes of 42K+ and 36Cl− from isolated fat-cells from the rat were studied under a variety of conditions known to affect the metabolism of the cells. 2. 42K+ efflux from isolated fat cells was increased in a Na+-free–high-K+ medium and decreased in a K+-free medium. The existence of K+ exchange diffusion across the fat-cell membrane is suggested. 3. 36Cl− efflux from isolated fat-cells was decreased when the Cl− component of the wash medium was replaced by acetate. The basal 36Cl− efflux is suggested to be partly by Cl− exchange diffusion and partly in company with a univalent cation. 4. A variety of lipolytic stimuli, adrenaline, adrenocorticotrophic hormone, N-6,O-2′-dibutyryladenosine cyclic 3′:5′-monophosphate and theophylline, increased 42K+ efflux from isolated fat-cells. The adrenaline stimulation was biphasic; an initial, rapid and transient increase in 42K+ loss from the fat-cells was followed by a slower, more prolonged, increase in 42K+ efflux. The initial phase was inhibited by phentolamine but not by propranolol. 5. Insulin increased 42K+ efflux only after preincubation with the cells.

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