scholarly journals The time course of the effect of thyroid hormones upon basal oxygen consumption and plasma concentration of free fatty acid in rats

1967 ◽  
Vol 190 (1) ◽  
pp. 221-228 ◽  
Author(s):  
N. B. Myant ◽  
Sarah Witney
Keyword(s):  
Oxygen Consumption ◽  
Fatty Acid ◽  
Plasma Concentration ◽  
Free Fatty Acid ◽  
Thyroid Hormones ◽  
Time Course

scholarly journals Effects of Hyperglycemia on the Time Course of Changes in Energy Metabolism and pH during Global Cerebral Ischemia and Reperfusion in Rats: Correlation of 1H and 31P NMR Spectroscopy with Fatty Acid and Excitatory Amino Acid Levels

1992 ◽  
Vol 12 (3) ◽  
pp. 456-468 ◽  
Author(s):  
Hans Widmer ◽  
Hisashi Abiko ◽  
Alan I. Faden ◽  
Thomas L. James ◽  
Philip R. Weinstein
Keyword(s):  
Fatty Acid ◽  
Amino Acid ◽  
Energy Metabolism ◽  
Free Fatty Acid ◽  
Time Course ◽  
Excitatory Amino Acid ◽  
Serum Glucose ◽  
Peak Ratio ◽  
Amino Acid Levels ◽  
Complete Brain Ischemia

The effects of hyperglycemia on the time course of changes in cerebral energy metabolite concentrations and intracellular pH were measured by nuclear magnetic resonance (NMR) spectroscopy in rats subjected to temporary complete brain ischemia. Interleaved 31P and 1H NMR spectra were obtained every 5 min before, during, and for 2 h after a 30-min bilateral carotid occlusion preceded by permanent occlusion of the basilar artery. The findings were compared with free fatty acid and excitatory amino acid levels as well as with cations and water content in funnel-frozen brain specimens. One hour before occlusion, nine rats received 50% glucose (12 ml/kg i.p.) and five received 7% saline (12 ml/kg i.p.). Before ischemia, there were no differences in cerebral metabolite levels or pH between hyperglycemic rats and controls. During the carotid occlusion, the lactate/ N-acetylaspartate (Lac/NAA) peak ratio was higher (0.73–1.48 vs. 0.56–0.82; p < 0.05) and pH was lower (<6.0 vs. 6.45 ± 0.05; p < 0.05) in the hyperglycemic rats than in the controls. Phosphocreatine and adenosine triphosphate were totally depleted in both groups. Within 5–15 min after the onset of reperfusion, the Lac/NAA peak ratio increased further in all rats; however, only in extremely hyperglycemic rats (serum glucose > 960 mg/dl) did the lactic acidosis progress rather than recover later during reperfusion. Total free fatty acid and excitatory amino acid levels, but not cation concentration or water content, in brain correlated with serum glucose levels during and after ischemia and with NMR findings after 2 h of reperfusion. Although profound hyperglycemia (serum glucose of 970–1,650 mg/dl) appears to be associated with progression of anaerobic glycolysis and failure of cerebral energy metabolism to recover after temporary complete brain ischemia and with postischemic excitotoxic and lipolytic reactions thought to participate in delayed cellular injury, severe hyperglycemia (490–720 mg/dl) was associated with recovery of energy metabolism.

Influence of hypothyroidism on the lipolytic activity of norepinephrine in the newborn lamb

1986 ◽  
Vol 108 (3) ◽  
pp. 451-454 ◽  
Author(s):  
C. Wrutniak ◽  
G. Cabello
Keyword(s):  
Fatty Acid ◽  
Free Fatty Acid ◽  
Thyroid Hormones ◽  
Lipolytic Activity ◽  
Plasma Free Fatty Acid ◽  
Newborn Lamb ◽  
Group A ◽  
Group B ◽  
Infusion Of Norepinephrine ◽  
Medium Group

ABSTRACT The effects of hypothyroidism on the lipolytic activity of norepinephrine were assessed in the newborn lamb. Lambs were separated into three groups: group A were controls; groups B and C were made hypothyroid by administration of benzylthiouracil from birth until 11 days of age. In control lambs, plasma free fatty acid concentrations, used as an index of lipolytic activity, increased significantly (plus 0·45 mmol/l) during the infusion of norepinephrine, whereas they did not change in hypothyroid lambs (group B). Adding thyroxine and tri-iodothyronine to the infusion medium (group C) immediately restored the free fatty acid response to norepinephrine in hypothyroid lambs (plus 0·41 mmol/l). These results suggest that thyroid hormones could modulate the lipolytic activity of catecholamines in the newborn lamb without a latent period. J. Endocr. (1986) 108, 451–454

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.

Effects of noradrenaline and nicotinic acid on plasma free fatty acids and oxygen consumption in cold-adapted rats

1979 ◽  
Vol 57 (7) ◽  
pp. 725-730 ◽  
Author(s):  
Louise Lafrance ◽  
Danièle Routhier ◽  
Bernard Têtu ◽  
Christian Têtu
Keyword(s):  
Fatty Acids ◽  
Oxygen Consumption ◽  
Fatty Acid ◽  
Free Fatty Acid ◽  
Nicotinic Acid ◽  
Free Fatty Acids ◽  
Simultaneous Increase ◽  
Elevated Plasma ◽  
Cold Adapted ◽  
Plasma Ffa

A 3-h noradrenaline (NA) infusion (1.5 μg kg−1 min−1) produced a sustained enhanced oxygen consumption (O2 cons.) in cold-adapted rats. Plama free fatty acid (FFA) levels were elevated by NA in control and in cold-adapted rats, but to a lesser extent in cold-adapted rats; the increase was maintained at a plateau in both groups during the entire period of NA infusion. A 1-h nicotinic acid (Nic A) infusion (1.5 mg kg−1 min−1) added to the NA infusion inhibited the calorigenic response to NA in cold-adapted rats and reduced the elevated plasma FFA concentration in control and in cold-adapted rats to values below basal levels. However, when the Nic A infusion was stopped, the O2 cons, was increased again in cold-adapted rats by the uninterrupted NA infusion, without the simultaneous increase of the plasma FFA concentration; the plasma FFA concentration was maintained in cold-adapted rats below basal values and merely brought back to basal levels in control rats. From these results, it is suggested that plasma FFA are not an essential substrate to the calorigenic response to NA observed in cold-adapted rats, as 85% of the response can occur when the plasma FFA concentration is very low.

Clinical and Metabolic Features of Overdosage with Amesec

1979 ◽  
Vol 24 (3) ◽  
pp. 246-249 ◽  
Author(s):  
R. D. Adam ◽  
C. Robertson ◽  
D. R. Jarvie ◽  
M. J. Stewart ◽  
A. T. Proudfoot
Keyword(s):  
Fatty Acid ◽  
Plasma Concentration ◽  
Free Fatty Acid ◽  
Peak Plasma ◽  
Peak Plasma Concentration ◽  
Ventricular Dysrhythmias

A 23-year-old woman ingested 2g. amylobarbitone, 10.4g. aminophylline and 2g. ephedrine. She was deeply unconscious, hypothermic, and went on to have supraventricular and ventricular dysrhythmias, convulsions and haematemesis. During the last convulsion she aspirated vomitus and died. The peak plasma concentration of amylobarbitone was 19mg. per l. and those of ephedrine and theophylline were 13 times higher than accepted therapeutic levels. During the course of the poisoning marked hypokalaemia (1.8mmol./l.) and hyperinsulinaemia (>240mU./l.) were found in conjunction with mild hyperglycaemia (9.6mmol./l.) and elevation of free fatty acid levels (1860μmol./l.). The mechanism of these changes is discussed.

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