The effect of nitric oxide released from s-nitroso-glutathoine on glucagon and insulin in dogs

Nitric oxide (NO), a potent modulator of cellular function, and NO donors have been useful tools in both experimental and clinical setting. Low molecular weight thiols such as cysteine and glutathoine were proposed to act as NO-carriers. The study was undertaken to investigate the pharmacological activity of the NO donor, S-nitrosoglutathoine (GSNO), on the plasma glucose and on the gluco-regulatory hormones, insulin and glucagon in healthy normoglycaemic dogs. Plasma glucose levels were measured by the glucose oxidase method, while the insulin and glucagon levels were determined by radioimmunoassay. In healthy normoglycaemic dogs, administration of 50 mg/kg GSNO caused an increase in post-prandial plasma glucose levels. The plasma glucose levels were significantly (p<0.05) elevated at 1.5 hr, 2.0 hr and 2.5 hr of the oral glucose tolerance test. These values were significantly higher than those obtained for the controls. The increase in glucose level was associated with a significant decrease in insulin levels and increase in glucagon levels (p<0.05). The fasting insulin level was 8.0 ñ 0.3 IU/ml in the control. The insulin level increased to a maximum of 34.0 ñ 0.3 IU/ml 1.5 hr post-prandial, and then decreased to 12.4 ñ 0.4 IU/ml after 2.5 hr. On administration of 50 mg/kg GSNO, the insulin level increased to a maximum of 23.0 ñ 0.6 IU/,l after 1.5 hr post-prandial and then decreased to 17.0 ñ 0.4 IU/ml after 2.5 hr. The blood glucagon levels increased from 40.0 ñ 0.3 pg/ml to 53.0 ñ 0.3 pg/ml after 1 hr in controls. In dogs administered with GSNO, the blood glucagon level increases to a maximum level of 80.0 ñ 0.5 pg/ml 1.5hr post-prandial. These results suggest that in healthy normoglycaemic dogs, nitric oxide released from GSNO caused a transient increase in post-prandial plasma glucose levels, inhibited glucose stimulated insulin secretion and elevated glucagon levels.(AU)

Fasting pancreatic glucagon in Jamaican children during malnutrition and subsequent recovery

Fasting pancreatic glucagon was observed in Jamaican infants during malnutrition and subsequent recovery. Rehabilitation in two groups of children with isocaloric diets rich either in carbohydrate or fat produced no differences in the rate of weight gain. During malnutrition, plasma pancreatic glucagon concentration was 104ñ11 (n=20) pg/ml (meanñS.E.) significantly lower than during recovery when the maximum value was 180ñ24 (n=13) pg/ml during the later recovery phase. After clinical recovery glucagon levels declined to 127ñ13 (n=15) pg/ml. Plasma insulin followed a similar pattern, increasing significantly during catch-up growth and declining after recovery. Slower rates of growth were associated with the simultaneous decline in the concentrations of both hormones after clinical recovery. (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)

"J" type diabetes

The course of 24 "J" -type diabetics attending the University College Hospital of the West Indies was reviewed. The "J" type is not a separate subgroup. So-called "J" -type cases are type-II cases in which the diabetes has been badly treated.(AU)