Impaired activity of rat pancreatic islet mitochondrial glycerophosphate dehydrogenase in protein malnutrition.

Abstract

In rats that received a low protein isocaloric diet (protein content of the diet: 8 instead of 20%) during fetal life and thereafter up to the time of sacrifice at 12-13 weeks of age, a low plasma insulin concentration, a decreased insulin content of isolated pancreatic islets, and an impaired secretory response of the islets to either D-glucose or the association of L-leucine and L-glutamine coincided, in islet homogenates, with a low activity of the mitochondrial glycerophosphate dehydrogenase and an abnormally high ratio between glutamate-alanine and glutamate-aspartate transaminase activities. Opposite enzymatic changes were found in liver extracts of the same rats. No obvious change in these hormonal, secretory, and enzymatic variables were observed when the period of protein deficiency was restricted to fetal life. These findings support the view that, in protein malnutrition, an impaired activity of pancreatic B-cell mitochondrial glycerophosphate dehydrogenase contributes, possibly in association with other enzymatic anomalies, to the perturbation of islet function.

Increased L-CPT-1 activity and altered gene expression in pancreatic islets of malnourished adult rats: a possible relationship between elevated free fatty acid levels and impaired insulin secretion

“…It is possible that different steps in the mechanism of insulin gene expression, biosynthesis or secretion may be altered in islets from malnourished rats [4,5,7,8,[24][25][26].…”

Developmental Origins of the Metabolic Syndrome: Prediction, Plasticity, and Programming

“…At 4 mo of age, pancreatic and islet blood flow are not reduced in those offspring exposed to a low-protein diet only during pregnancy (228). There appears to be conflicting evidence as to whether the insulin secretory responses to either amino acids or glucose of islets from postnatal animals exposed to low-protein diets only in utero are or are not impaired in postnatal life (211,441). In vivo, basal plasma glucose and insulin levels are normal in offspring that were exposed to a low-protein diet during pregnancy, but the insulin response to an oral glucose challenge was abnormally low in adult female offspring and remained lower in these animals when they became pregnant (211).…”

Protein restriction during lactation alters the autonomic nervous system control on glucose-induced insulin secretion in adult rats

“…Protein restriction during gestation and lactation in rodents induce underweight, growth and development impairment in the offspring, and it is associated with irreversible metabolic disturbances when the pups turn into adult life (Dollet et al 1988;Rasschaert et al 1995;LangleyEvans 1997;Garofano et al 1999). It has been recognized that central nervous system (CNS) is pivotal for metabolism and body weight control, and the hypothalamus has been identified as the major area concentrating many neurons implicated in the reception of signals from the periphery, which induce efferent signals to correct excessive or insufficient food intake and energy storage (Steffens et al 1990).…”