Effects of Nicotinic Acid and Some of its Homologues on Lipolysis, Adenyl Cyclase, Phosphodiesterase and Cyclic AMP Accumulation in Isolated Fat Cells

Pharmacology ◽  
1971 ◽  
Vol 6 (6) ◽  
pp. 330-338 ◽  
Author(s):  
I.F. Skidmore ◽  
P.S. Schönhöfer ◽  
D. Kritchevsky
Keyword(s):  
Cyclic Amp ◽  
Nicotinic Acid ◽  
Adenyl Cyclase ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Cyclic Amp Accumulation

Effect of NAD, nicotinamide and nicotinic acid on cyclic AMP accumulation by fat cells

1979 ◽  
Vol 306 (2) ◽  
pp. 179-183 ◽  
Author(s):  
Francisco J. Moreno ◽  
Raymond E. Shepherd ◽  
John N. Fain
Keyword(s):  
Cyclic Amp ◽  
Nicotinic Acid ◽  
Fat Cells ◽  
Cyclic Amp Accumulation

Lipolysis and cyclic AMP accumulation in isolated fat cells from chicks

1975 ◽  
Vol 26 (2) ◽  
pp. 243-247 ◽  
Author(s):  
Thomas A. Boyd ◽  
Paul B. Wieser ◽  
John N. Fain
Keyword(s):  
Cyclic Amp ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Cyclic Amp Accumulation

Distribution of cyclic AMP phosphodiesterase in adipose tissue from trained rats

1986 ◽  
Vol 61 (4) ◽  
pp. 1546-1551 ◽  
Author(s):  
K. A. Kenno ◽  
J. L. Durstine ◽  
R. E. Shepherd
Keyword(s):  
Cyclic Amp ◽  
Specific Activity ◽  
Particulate Fraction ◽  
Fat Cells ◽  
Isolated Fat Cells ◽  
Sprague Dawley ◽  
Enzyme Form ◽  
Cyclic Amp Phosphodiesterase ◽  
Sprague Dawley Rats ◽  
Michaelis Constants

Fat cells were isolated from sedentary and exercise trained female Sprague-Dawley rats and cyclic AMP phosphodiesterase (cyclic AMP-PDE) activities were determined from crude homogenates of the fat cells in the whole homogenate, P5, P48, and S48 fractions. Exercise training resulted in a significant increase in the mean specific activity of cyclic AMP-PDE (pmol X min-1 X mg-1) from the whole homogenate and S48 fraction at cyclic AMP concentrations of 4, 8, and 16 microM and in the P48 fraction at 8 and 16 microM cyclic AMP. Cyclic AMP-PDE kinetic plots according to Lineweaver-Burk for the calculation of Michaelis constants (Km) and maximum enzyme velocities (Vmax) were nonlinear, indicating both a low and high enzyme form. The Michaelis constants were significantly lower in trained rats than those of its control for the high Km form of cyclic AMP-PDE in the whole and soluble fractions and for the low Km form of the P5 particulate fraction. The Vmax of the high Km form of the P48 particulate fraction from trained animals was also significantly higher than that found in its control. Phosphodiesterase inhibition by methylxanthines in the various fractions was similar in both trained and sedentary animals. These changes in specific activity, Michaelis constants, and Vmax of cyclic AMP-PDE from crude homogenates of isolated fat cells from exercise trained animals may account for the decreased intracellular levels of cyclic AMP following catecholamine stimulation of isolated fat cells from trained rats.

Effect of amitriptyline on lipolysis and cyclic AMP concentration in isolated fat cells

Metabolism ◽  
1972 ◽  
Vol 21 (3) ◽  
pp. 223-229 ◽  
Author(s):  
Fred C. Lovrien ◽  
Ann A. Steele ◽  
Joseph D. Brown ◽  
Daniel B. Stone
Keyword(s):  
Cyclic Amp ◽  
Fat Cells ◽  
Isolated Fat Cells

scholarly journals Attenuated adenosine-sensitivity and decreased adenosine-receptor number in adipocyte plasma membranes in human obesity

1991 ◽  
Vol 279 (1) ◽  
pp. 17-22 ◽  
Author(s):  
J M Kaartinen ◽  
S P Hreniuk ◽  
L F Martin ◽  
S Ranta ◽  
K F LaNoue ◽  
...  
Keyword(s):  
Adipose Tissue ◽  
Cyclic Amp ◽  
Adenylate Cyclase ◽  
Adenosine Receptors ◽  
Plasma Membranes ◽  
Normal Weight ◽  
Fat Cells ◽  
Cyclic Amp Accumulation ◽  
Obese Subjects ◽  
Receptor Number

Fat-cells were isolated from patients of body-mass indices (BMIs) ranging from 17.9 to 83.9 kg/m2. Isoprenaline-stimulated cyclic AMP accumulation in cells prepared from obese subjects as compared with normal-weight subjects, was less sensitive to inhibition by the adenosine agonist N6-(phenylisopropyl)adenosine (PIA) (P = 0.047). The inhibition of 7 beta-desacetyl-7 beta-[gamma-(N-methylpiperazino) butyryl]-forskolin-stimulated adenylate cyclase by PIA in the presence of adenosine deaminase was also much attenuated in crude plasma membranes of adipocytes prepared from massively obese patients as compared with lean controls (P = 0.0143). This difference was probably not due to different cell size, because adenylate cyclase of crude plasma membranes of large adipocytes was actually more sensitive to PIA than was adenylate cyclase of membranes of smaller fat-cells co-isolated from the same individual. The stimulatory effect of PIA on glucose uptake in the presence of adenosine deaminase was depressed in adipocytes prepared from obese subjects and correlated with BMI at r = -0.626 (P = 0.007) at 100 nM-PIA. The adenosine receptors were studied by using the adenosine antagonist 1,3-[3H]dipropyl-8-cyclopentylxanthine. The binding was rapid and proportional to protein concentration. There was no difference in the affinities of receptors in membranes of obese and normal-weight subjects; Kd values of all patients averaged 3.3 nM. Bmax values were 54 and 130 fmol/mg of protein in membranes prepared from seven obese and five control patients respectively. The Bmax values calculated per mg of protein correlated with BMI at r = -0.539 (P = 0.047). The adenosine content of adipose tissue was higher in obese than in control subjects. These results demonstrate an attenuated response of cyclic AMP accumulation, adenylate cyclase and glucose uptake to adenosine in fat-cells prepared from obese subjects, and suggest that this change is at least partly due to changes in the amount of adenosine receptors, but not their affinity. The decreased receptor number could be due to higher adenosine content. A higher adenosine concentration in adipose tissue could explain why lipolysis is inhibited in situ in obesity, and the desensitization could explain the diminished response to adenosine analogues in isolated fat-cells.

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