ABSTRACT
In the present study we have investigated the effect of a high-protein feeding on glucose induced-insulin secretion patterns from high dose streptozotocin (SZ) injected rats and mice, and from mice given multiple low doses of SZ. For this purpose male rats and mice were fed either a high-protein, carbohydrate-free diet, or control diets, before and after i.p. injections of SZ, or citrate buffer only. Our results show that when SZ was given as a single diabetogenic dose, rats and mice kept on the high-protein diet presented lower serum glucose levels, normal basal insulin values, and higher first and second phases of stimulated insulin release, when compared with diabetic animals on control diets. Furthermore, when rats prolonged their high-protein feeding from 4 to 11 days after SZ injection, there was an additional increment in insulin secretory capacity with a further diminution in serum glucose levels. We also show that high-protein feeding in mice given multiple low doses of SZ (a model of autoimmune diabetes), produced a diminution in serum glucose values, and an improvement in both phases of stimulated insulin release. Thus, in the two models of experimental diabetes used here, high-protein feeding exerts beneficial effects in beta cell responsiveness to glucose.
ABSTRACT
We have used a model of experimental protein-energy malnutrition induced in weaned rats by administration of a protein free diet during 2 weeks. Some malnourished rats were then refed with a control diet for 4, 9 or 30 days. Control rats were fed for the same periods with the balanced control diet. Malnourished rats showed a loss in body weight of approximately 25
. After 30 days of refeeding, the animals gained weight reaching values higher than that of control rats. Insulin secreted by perifused pancreatic slices from malnourished rats, was impaired in first and second glucose-induced secretory phases. Basal secretion was also diminished in incubation of pancreatic slices. When malnourished rats were refed for 4 days, basal insulin secretion reached control values. Stimulated insulin secretion was normalized at 9 and 30 days of refeeding. Our result on somatostatin (SRIF) secretion in malnourished rats showed basal hypersecretion and diminished first and second glucose-induced secretory phases. During refeeding basal SRIF secretion was normalized from day 4. On the contrary stimulated secretion was significantly increased at 4 and 9 days of refeeding, and on day 30 values did not differ from controls. In protein energy malnutrition, the disturbed hormonal state can represent adaptative mechanisms to the protein depletion and hormonal changes have also an essential role in refeeding.
ABSTRACT
In the present study we have investigated the effect of a high-protein feeding on glucose induced-insulin secretion patterns from high dose streptozotocin (SZ) injected rats and mice, and from mice given multiple low doses of SZ. For this purpose male rats and mice were fed either a high-protein, carbohydrate-free diet, or control diets, before and after i.p. injections of SZ, or citrate buffer only. Our results show that when SZ was given as a single diabetogenic dose, rats and mice kept on the high-protein diet presented lower serum glucose levels, normal basal insulin values, and higher first and second phases of stimulated insulin release, when compared with diabetic animals on control diets. Furthermore, when rats prolonged their high-protein feeding from 4 to 11 days after SZ injection, there was an additional increment in insulin secretory capacity with a further diminution in serum glucose levels. We also show that high-protein feeding in mice given multiple low doses of SZ (a model of autoimmune diabetes), produced a diminution in serum glucose values, and an improvement in both phases of stimulated insulin release. Thus, in the two models of experimental diabetes used here, high-protein feeding exerts beneficial effects in beta cell responsiveness to glucose.
ABSTRACT
We have used a model of experimental protein-energy malnutrition induced in weaned rats by administration of a protein free diet during 2 weeks. Some malnourished rats were then refed with a control diet for 4, 9 or 30 days. Control rats were fed for the same periods with the balanced control diet. Malnourished rats showed a loss in body weight of approximately 25
. After 30 days of refeeding, the animals gained weight reaching values higher than that of control rats. Insulin secreted by perifused pancreatic slices from malnourished rats, was impaired in first and second glucose-induced secretory phases. Basal secretion was also diminished in incubation of pancreatic slices. When malnourished rats were refed for 4 days, basal insulin secretion reached control values. Stimulated insulin secretion was normalized at 9 and 30 days of refeeding. Our result on somatostatin (SRIF) secretion in malnourished rats showed basal hypersecretion and diminished first and second glucose-induced secretory phases. During refeeding basal SRIF secretion was normalized from day 4. On the contrary stimulated secretion was significantly increased at 4 and 9 days of refeeding, and on day 30 values did not differ from controls. In protein energy malnutrition, the disturbed hormonal state can represent adaptative mechanisms to the protein depletion and hormonal changes have also an essential role in refeeding.
ABSTRACT
Definimos como "remisión diabética" la suspensión del tratamiento insulínico por un período mayor de 15 días, luego de la normalización de as glucemias y desaparición de las glucosurias. Hemos estudiado 21 niños diabéticos insulino-dependientes en el período de remisión (10 niños y 11 niñas) y 29 niños normales como control. Dos clases de pruebas fueron realizadas: glucosa intravenosa (GEV) y glucosa post-tolbutamida (GPT). Se separaron dos grupos en los niños que efectuaron la prueba de GEV. En uno se dosó glucosa, insulina, somatotrofina y glucagon plasmáticos y en el otro se determinó glucosa y péptido-C. La glucemia fue menor en los normales que en los niños en remisión. La desaparicióon de la glucosa (constante "K") fue máas alta en los normales (p < 0,001) indicando claramente el hipoinsulinismo hallado. La secreción de insulina lluego de ;a glucosa EV fue muy baja en el grupo en remisión, no pasando del valor basal. Solo dos niñas mostraron un valor normal o alto luego de la sobrecarga de glucosa y una de ellas en uns egundo estudio mostró el hipoinsulinismo común del grupo diabético en remisión. La cinética de la secreción de glucagon y somatotrofina en elg rupo en remisión fue normal, pero los niveles de glucagon fueron bajos. Cuando el área integrada (0-120 min) fue determinada para la insulina, somatotrofina y glucagon, se observó que la insulina y el glucagon eran bajos en relación a los normales (p < 0,05) y la somatotrofina igual. Sin embargo , la relación insulina/glucagon fue similar en ambos grupos. El péptido-C en la prueba de GEV mostró en los niños en remisión un valor menor que en el grupo normal semejando el comportamiento del otro grupo en remisión en donde se dosó la insulina. Durante la prueba de glucosa psot-tolbutamida, el grupo normal respondió con un pico de secreción de insulina en cada estímulo, siendo mayor la respuesta a la glucosa post-tolbutamida. En el grupo en remisión, la glucemia fue más elevada que en el grupo normal y la secreción de insulina no sobrepasó el nivel basal luego de los estímulos. La secreción de la somatotrofina en la fase de glucosa fue mas baja que en los normales y el glucagon fue consistentemente menor en este grupo. Podemos concluir que los niños en remisión no presentan una velocidad de desaparición de glucosa normal, coincidente con un marcado hipoinsulinismo. El glucagon es proporcionalmente tan bajo como la secreción de insulina, lo que permite que el índice insulina/glucagon sea similar en lo