scholarly journals Plasma ?-hydroxybutyric acid response to nicotinic acid-induced plasma free fatty acid decrease in man

Diabetologia ◽  
1966 ◽  
Vol 2 (2) ◽  
pp. 127-129 ◽  
Author(s):  
L. A. Carlson ◽  
J. �stman
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid ◽  
Hydroxybutyric Acid

Physical training reverses the increased activity of the hepatic ketone body synthesis pathway in chronically diabetic rats

2006 ◽  
Vol 290 (2) ◽  
pp. E207-E212 ◽  
Author(s):  
Adil El Midaoui ◽  
Jean Louis Chiasson ◽  
Gilles Tancrède ◽  
André Nadeau
Keyword(s):  
Diabetes Mellitus ◽  
Fatty Acid ◽  
Plasma Concentration ◽  
Free Fatty Acid ◽  
Physical Training ◽  
Ketone Body ◽  
Plasma Free Fatty Acid ◽  
Diabetic Rats ◽  
Hydroxybutyric Acid ◽  
Increased Activity

This study was designed to examine whether the training-induced improvement in the plasma concentration of ketone bodies in experimental diabetes mellitus could be explained by changes in the activity of the hepatic ketone body synthesis pathway and/or the plasma free fatty acid levels. Diabetes mellitus was induced by an intravenous injection of streptozotocin (50 mg/kg), and training was carried out on a treadmill. The plasma concentration of β-hydroxybutyric acid was increased ( P < 0.001) in sedentary diabetic rats, and this was partly reversed by training ( P < 0.001). The plasma concentration of free fatty acids was increased ( P < 0.001) in sedentary diabetic rats, and this was reversed to normal by training ( P < 0.001). Diabetes was also associated with an increased activity of the hepatic ketone body synthesis pathway. When the data are expressed as per total liver, physical training decreased the activity of the hepatic ketone body synthesis pathway by 18% in nondiabetic rats ( P < 0.05) and by 22% in diabetic rats ( P < 0.01), the activity present in trained diabetic rats being not statistically different from that of sedentary control rats. These data suggest that the beneficial effects of physical training on the plasma β-hydroxybutyric acid levels in the diabetic state are probably explained in part by a decrease in the activity of the hepatic ketone body synthesis pathway and in part by a decrease in plasma free fatty acid levels.

Mechanism of regulation of glucose production by lipolysis in humans

1992 ◽  
Vol 262 (3) ◽  
pp. E353-E358 ◽  
Author(s):  
F. Jahoor ◽  
S. Klein ◽  
R. Wolfe
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Plasma Insulin ◽  
Glucose Production ◽  
Plasma Free Fatty Acid ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Normal Humans ◽  
The Relationship

The relationship between the rate of lipolysis and rate of glucose production (Ra) was investigated in 14- and 86-h fasted humans. [6,6-2H]glucose and [2H]5glycerol were infused to measure glucose and glycerol Ra in response to infusions of nicotinic acid in 14- and 86-h fasted subjects (protocol 1). The response of glucose Ra to nicotinic acid alone and nicotinic acid plus unlabeled glycerol was also measured in 86-h fasted subjects (protocol 2). After a 14-h fast, nicotinic acid caused a 30% decrease in plasma insulin levels and a marked (66%) decrease in plasma free fatty acid levels but did not have any significant effect on glucose Ra and concentration. After 86 h of fasting, nicotinic acid decreased glycerol Ra and hence lipolytic rate by approximately 60%. This caused a significant decrease (P less than 0.05) of 16-20% in glucose Ra and uptake. This decrease in glucose Ra was abolished when unlabeled glycerol was also infused with nicotinic acid to maintain glycerol Ra. These findings suggest that, in normal humans, a decrease in the rate of lipolysis regulates glucose Ra via its effect on the availability of glycerol for gluconeogenesis.

Growth Hormone, Cortisol, and Glucagon Concentrations during Plasma Free Fatty Acid Depression: Different Effects of Nicotinic Acid and an Adenosine Derivative (BM 11.189)*

1983 ◽  
Vol 57 (2) ◽  
pp. 410-414 ◽  
Author(s):  
HANS-JÜRGEN QUABBE ◽  
ALFRED S. LUYCKX ◽  
MANFRED L’AGE ◽  
CORNELIUS SCHWARZ
Keyword(s):  
Growth Hormone ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid

Investigations on the Effect of Nicotinic Acid on Plasma Free Fatty Acid Levels

Pharmacology ◽  
1965 ◽  
Vol 12 (1) ◽  
pp. 8-14
Author(s):  
R. Bombelli ◽  
T. Farkas ◽  
R. Vertua
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid

scholarly journals Synergistic Effect of Propranolol and Nicotinic Acid on the Inhibition of Plasma Free Fatty Acid Release in the Dog

1971 ◽  
Vol 28 (2) ◽  
pp. 270-276 ◽  
Author(s):  
MANUEL J. LIPSON ◽  
SHAPUR NAIMI ◽  
SAMUEL PROGER
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Synergistic Effect ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid ◽  
Fatty Acid Release ◽  
Acid Release

scholarly journals The plasma free fatty acid rebound induced by nicotinic acid

1967 ◽  
Vol 8 (3) ◽  
pp. 239-244 ◽  
Author(s):  
Joseph N. Pereira
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Plasma Free Fatty Acid

Respiratory capacity and glycogen depletion in thyroid-deficient muscle

1980 ◽  
Vol 49 (1) ◽  
pp. 102-106 ◽  
Author(s):  
K. M. Baldwin ◽  
A. M. Hooker ◽  
R. E. Herrick ◽  
L. F. Schrader
Keyword(s):  
Skeletal Muscle ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Plasma Free Fatty Acid ◽  
Endurance Capacity ◽  
Glycogen Depletion ◽  
Respiratory Capacity ◽  
Rest And Exercise

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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