1. Young Wistar rats were used as an experimental model to determine the effects of protein-energy malnutrition on glucose tolerance and insulin release. 2. Malnourished rats presented some of the features commonly found in human protein-energy malnutrition, such as failure to gain weight, hypoalbuminaemia, fatty infiltration of the liver and intolerance of oral and intravenous glucose loads. 3. The rate of disappearance of glucose from the gut lumen was greater in the malnourished rats but there was no significant difference in portal blood glucose concentration between normal and malnourished rats 5 and 10 min after an oral glucose load. 4. Insulin resistance was not thought to be the cause of the glucose intolerance in the malnourished animals since these rats had a low fasting plasma insulin concentration with a normal fasting blood glucose concentration and no impairment in their hypoglycaemic response to exogenous insulin administration. Furthermore, fasting malnourished rats were unable to correct the insulin-induced hypoglycaemia despite high concentrations of hepatic glycogen. 5. Malnourished rats had lower peak plasma insulin concentrations than normal control animals after provocation with oral and intravenous glucose, intravenous tolbutamide and intravenous glucose plus aminophyllin. This was not due to a reduction in the insulin content of the pancreas or potassium deficiency. Healthy weanling rats, like the older malnourished rats, had a diminished insulin response to intravenous glucose and intravenous tolbutamide. However, their insulin response to stimulation with intravenous glucose plus aminophyllin far exceeded that of the malnourished rats. Thus the impairment of insulin release demonstrated in the malnourished rats cannot be ascribed to a ‘functional immaturity’ of the pancreas.
1. Bone and calcium metabolism in protein-deprived 5-week-old male rats who exhibited no biochemical or histological features of rickets were compared with age-and weight-matched control animals. 2. Intestinal calcium absorption was significantly lower in protein-deprived rats. This was associated with a smaller exchangeable calcium pool and lower bone formation as measured by calcium accretion and proline incorporation into hydroxyproline. However, calcium resorption from bone barely changed in this group and a disproportionately high fraction of the calcium pool continued to be excreted. 3. As a consequence, retarded bone growth occurred in the protein-deprived rat, leading to bones which were shorter and lighter than those of age-matched control animals, the epiphyseal regions appearing to bear the brunt of the growth retardation. This was not accompanied by a change in quality of bone, as the percentage ash content of extirpated bone remained normal. 4. Though alternative hypotheses are possible, the data are consistent with a primary disturbance of intestinal, and possibly renal tubular, calcium transport, perhaps associated with impaired synthesis of calcium-binding protein. An independent depression of collagen synthesis is likely.
1. A formula breakfast containing protein, carbohydrate and fat was given on two occasions to nine middle-aged male convalescent patients and to ten young men. The meals differed only in the type of carbohydrate given; sucrose or an isocalorific amount of glucose. 2. After the formula meal containing sucrose; (a) the alimentary lipaemia was cleared more slowly; (b) insulin response was smaller, and (c) there was a lower blood sugar curve than after the glucose meal. 3. The degree of lipaemia showed a significant positive correlation with insulin response which was, as expected, lower after sucrose than glucose. While attempting to confirm a report (Schilling, Hashim & Leonardy, 1964) that serum triglycerides are not significantly elevated after the ingestion of a small mixed meal, it was noticed that the triglyceride concentrations seemed to depend on the type of carbohydrate given (Mann & Truswell, 1971). Albrink, Fitzgerald & Mann (1958) and Sullivan (1960) have shown that the lipaemia which occurs after a fatty meal is diminished by the addition of glucose to the meal. Krut & Barsky (1964) found that postprandial lipaemia in patients with ischaemic heart disease is decreased by intravenous infusion of glucose and insulin. These considerations led us to examine the effects of glucose and sucrose and subsequent insulin release on alimentary lipaemia.