Altered thyroid status in marihuana-exposed male rats

The effects of marihuana exposure, particularly of THC-free crude aqueous marihuana extract (CAME) on liver gycogen, total plasma cholesterol, BMR, Raw and growth rate were studied in male Wistar rats. Liver glycogen decreased following administration of CAME and T4 (P<0.01), and increased with methimazole (P<0.01). However, marihuana smoking did not affect liver glycogen. Both marihuana smoking and CAME administration decreased the levels of plasma cholesterol (P<0.01), and methimazole increased them (P,0.01). Airway resistance decreased in rats treated with CAME, T4 and marihuana smoking and decreased with methimazole. The growth rate with marihuana exposure improved slightly (AU)

Gross cardiac involvement in glycogen storage disease type 3

This report describes a patient with type 3 glycogenosis diagnosed during life but who died suddenly at home and was found at necropsy to have gross cardiac involvement. The immediate cause of death was not apparent but could possibly have been related to the very unusual degree of cardiac involvement (AU)

Some biochemical aspects of ackee poisoning (abstract only)

Administration of Hypoglycin (the toxic principle of the ackee) to rats causes a decrease in the total carbohydrate stores of the body. Liver glycogen is reduced almost to zero and blood glucose falls. Muscle glycogen is not greatly affected. Evidence is presented to show that the decrease in liver glycogen is a result of interference in the synthesis of glycogen by the liver, and the decrease in blood glucose is a result of the depletion of the liver glycogen. Experiments with radioactive glycogen indicate that the ackee poisoned rats converts very little of its glucose into muscle glycogen or fat, and most is excreted as carbon dioxide. This is in contrast to an insulin treated rat which converts an appreciable proportion of its glucose into muscle glycogen and fat.(AU)

Some effects of metabolic acidosis on carbohydrate metabolism in the rat

Metabolic acidosis was induced by feeding ammonium chloride to rats which were maintained on a carbohydrate diet for 48h. Fasting blood glucose was the same in acidotic and control animals, but there was an increase in liver glycogen in the former. Muscle glucogen was unchanged. In vitro glycogenesis was the same in liver slices from normal rats when incubated at a range of pH from 6.90 to 7.40. The peak blood glucose in response to intraperitoneal injections of glucagon was the same in control and acidotic rats. The rate of disappearence of glucose was slower in acidotic rats both after the glucagon induced hyperglycaemia and after intravenously injected glucose. Liver phosphorylase, total glycogen synthetase and the I form of this enzyme were unchanged in acidosis. The data are compatible with the hypothesis that in the acidotic rat there is a block in glycolysis-possibly at the phosphofructokinase step (Summary)

Alterations in carbohydrate metabolism in Jamaican children with severe malnutrition

Carbohydrate metabolism was studied in Jamaican children who had been admitted to hospital with protein-calorie malnutrition. Analysis of liver biopsies showed that levels of protein and glycogen were low in malnutrition and rose with recovery. Hepatic glucose-6-phosphatase was elevated in malnutrition but phosphorylase levels were normal. In the malnourished child there was normal hepatic glycogenolysis as shown by a normal blood glucose response to intravenous glucagon without any detectable rise in blood pyruvate and lactate. Fasting levels of blood lactate as well as lactate-pyruvate ratios rose with recovery from malnutrition. Galactose tolerance tests showed a delayed disappearance of injected galactose, but the maximum increase in blood glucose after galactose injection was the same in all clinical states. Glucose disappearance was delayed after both glucagon and galactose. Muscle glycogen was initially reduced, but there was a markeed "overshot" to supranormal levels during the recovery phase. (AU)

Some biological observations of hypoglycin A in presence of leucine - abstract

The present work was carried out to investigate the effect of leucine on the biological activity of hypoglycin A. Leucine-free hypoglycin A, prepared from the ackee (Blighia sapida) seeds, has been shown to cause inhibition of the growth of broad bean radicles. When supplied simultaneously, leucine had no effect on the degree of inhibition produced by hypoglycin A even when the leucine concentration was four times that of hypoglycin A. Although the acceped structure of hypoglycin A bears a relationship to that of leucine, yet leucine does not antagonise the inhibitory action of hypoglycin A. When injected intraperitoneally into rats, fasted for 48 hours to ensure complete depletion of their liver glycogen, hypoglycin A induced hypoglycemia. This hypoglycemia was potentiated by leucine when administered one hour before hypoglycin A. These findings indicate that the hypooglycemia induced by hypoglycin A is not a result of the exhaustion of the liver glycogen as was suggested by Patrick (1954). They also indicate that the liver is not the principal site of action as thought by Chen et al. (1957).(AU)

Halothane and carbohydrate metabolism

Halothane does not block the sympathetic response to surgery indicated by a rise in blood sugar and a fall in liver glycogen in Jamaican patients (Summary)

Acute toxic hypoglycaemia occurring in the vomiting sickness of Jamaica: morbid anatomical aspects

Seven autopsies and one clinical case of a syndrome known as the Vomiting Sickness of Jamaica are described. In these cases hypoglycaemia was associated with fatty metamorphosis of the liver and other organs, tissue oedema, and ailmentary lymphoid hyperplasia. During the acute phase biopsies and post mortem material show a depletion of liver glycogen. Evidence is presented that restoration can take place by intravenous glucose therapy. The mechanism of the change is discussed and it is suggested that the defect may be one of deficient gluconeogenesis. (AU)