Elevated Plasma Free Fatty Acid Concentrations in Patients with Pheochromocytoma

1964 ◽  
Vol 270 (17) ◽  
pp. 865-870 ◽  
Author(s):  
Karl Engelman ◽  
Peter S. Mueller ◽  
Albert Sjoerdsma
1971 ◽  
Vol 49 (5) ◽  
pp. 394-398 ◽  
Author(s):  
W. D. Wagner ◽  
R. A. Peterson ◽  
R. J. Cenedella

Plasma free fatty acid (FFA) levels and the effects of prostaglandin E1 (PGE1) were studied in cold-acclimated and cold-exposed chickens and compared to controls. Chickens cold-acclimated at 4–7 or 8–11 °C for 4 weeks had significantly elevated plasma FFA when compared to the controls at 19–21 °C. Although PGE1 had no effect on the basal level of FFA of controls, a significantly lower plasma FFA was seen after injection of either 10 or 30 μg PGE1/kg in cold-acclimated chickens. Chickens cold-exposed to 2–3 °C for 4 h demonstrated significant elevations of plasma FFA when compared to controls. Only 30 μg PGE1/kg significantly depressed the plasma FFA in the cold-exposed birds. No inhibition of basal FFA release was seen in control animals. From these experiments, it is concluded that chickens mobilize FFA extensively under cold-exposure and that this stimulated lipolysis is inhibited by PGE1.


Diabetes ◽  
2005 ◽  
Vol 54 (6) ◽  
pp. 1640-1648 ◽  
Author(s):  
R. Belfort ◽  
L. Mandarino ◽  
S. Kashyap ◽  
K. Wirfel ◽  
T. Pratipanawatr ◽  
...  

1987 ◽  
Vol 253 (4) ◽  
pp. R535-R540
Author(s):  
H. T. Yang ◽  
K. I. Carlson ◽  
W. W. Winder

Previous reports have indicated that adrenodemedullated (ADM) rats exhibit an impairment in muscle glycogenolysis and elevated plasma insulin during exercise. This study was designed to determine whether the impaired muscle glycogenolysis in ADM rats is due to absence of epinephrine or to the inappropriately elevated plasma insulin. Fasted ADM rats were infused with saline, with epinephrine (0.045 micrograms . 100 g-1 . min-1), or with epinephrine + insulin (1.6, 3.3, 6.6, and 8.3 ng . 100 g-1 . min-1) during a 30-min run on the treadmill (21 m/min, 10% grade). Soleus muscle glycogen decreased from 5.1 +/- 0.2 mg/g in resting ADM rats to 4.0 +/- 0.2, 0.8 +/- 0.1, and 0.8 +/- 0.1 mg/g in the exercising saline-, epinephrine-, and epinephrine + insulin (8.3 ng . 100 g-1 . min-1)-infused rats, respectively. Glycogen utilization in gastrocnemius and red and white quadriceps muscles during exercise was likewise unaffected by insulin infusion. Blood glucose concentrations were 3.75 +/- 0.08, 2.65 +/- 0.14, 3.93 +/- 0.20, and 2.03 +/- 0.09 mM in the same groups at the end of exercise. Blood lactate was 50% lower and the blood 3-hydroxybutyrate and plasma free fatty acid concentrations were significantly higher in the ADM + saline rats than the other exercising rats. We conclude that inappropriately elevated plasma insulin does not impair epinephrine-stimulated muscle glycogenolysis in fasted ADM rats during exercise.


Diabetes ◽  
2009 ◽  
Vol 59 (1) ◽  
pp. 26-32 ◽  
Author(s):  
K. Kiilerich ◽  
M. Gudmundsson ◽  
J. B. Birk ◽  
C. Lundby ◽  
S. Taudorf ◽  
...  

2000 ◽  
Vol 278 (6) ◽  
pp. G967-G973 ◽  
Author(s):  
Robert E. Shangraw ◽  
Farook Jahoor

On the basis of the finding that plasma glycerol concentration is not controlled by clearance in healthy humans, it has been proposed that elevated plasma free fatty acid (FFA) and glycerol concentrations in cirrhotic subjects are caused by accelerated lipolysis. This proposal has not been validated. We infused 10 volunteers, 10 cirrhotic subjects, and 10 patients after orthotopic liver transplantation (OLT) with [1-13C]palmitate and [2H5]glycerol to compare fluxes (Ra) and FFA oxidation. Cirrhotic subjects had higher plasma palmitate (52%) and glycerol (33%) concentrations than controls. Palmitate Ra was faster (1.45 ± 0.18 vs. 0.85 ± 0.17 μmol ⋅ kg−1 ⋅ min−1) but glycerol Ra and clearance slower (1.20 ± 0.09 vs. 1.90 ± 0.24 μmol ⋅ kg−1 ⋅ min−1and 21.2 ± 1.2 vs. 44.7 ± 4.9 ml ⋅ kg− ⋅ h−1, respectively) than in controls. After OLT, plasma palmitate and glycerol concentrations and palmitate Ra did not differ, but glycerol Ra (1.16 ± 0.11 μmol ⋅ kg−1 ⋅ min−1) and clearance (26.7 ± 2.4 ml ⋅ kg− ⋅ h−1) were slower than in controls. We conclude that 1) impaired reesterification, not accelerated lipolysis, elevates FFA in cirrhotic subjects; 2) normalized FFA after OLT masks impaired reesterification; and 3) plasma glycerol concentration poorly reflects lipolytic rate in cirrhosis and after OLT.


1980 ◽  
Vol 49 (1) ◽  
pp. 102-106 ◽  
Author(s):  
K. M. Baldwin ◽  
A. M. Hooker ◽  
R. E. Herrick ◽  
L. F. Schrader

This study was undertaken to determine the effects of propylthiouracil-induced thyroid deficiency on a) the capacity of muscle homogenates to oxidize [2-14C]pyruvate and [U-14C]palmitate and b) glycogen depletion during exercise in liver and in fast-oxidative-glycogenolytic (FOG), fast-glycogenolytic (FG), and slow-oxidative (SO) muscle. Relative to the rates for normal rats, oxidation with pyruvate was reduced by 53, 68, and 58%, and palmitate by 40, 50, and 48% in FOG, FG, and SO muscle, respectively (P less than 0.05). Normal rats ran longer than thyroid-deficient rats at 26.7 m/min (87 ± 8 vs. 37 ± 5 min). After 40 min of running (22 m/min), the amount of glycogen consumed in normal FOG, FG, and SO muscle and in liver amounted to only 23, 12, 66, and 52%, respectively, of that for their thyroid-deficient counterparts. Also, normal rats maintained higher plasma free fatty acid levels than thyroid-deficient rats during both rest and exercise (P less than 0.05). These findings suggest that thyroid deficiency causes a reduced potential for FFA utilization in skeletal muscle that enhances its consumption of glycogen, thereby limiting endurance capacity.


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