The effects of maternal protein deprivation on the fetal rat pancreas: major structural changes and their recuperation

Abstract

There is evidence that low birth weight and poor growth in early life cause a long‐term predisposition to non‐insulin‐dependent diabetes. Morphological changes were assessed in fetal rat pancreas subjected to both pre‐ and post‐natal maternal protein deprivation (LP). Further groups were subjected to purely prenatal maternal protein deprivation (preLP) and purely postnatal maternal protein deprivation (postLP), as well as a control group. The results show that the LP and postLP groups had fewer but larger islets than the control group, while the preLP group had more numerous, smaller islets. All three low protein groups had more irregularly shaped islets than the control group. There was a reduction in the amount of beta cells within each islet in all three protein‐deprived groups. The LP and postLP groups showed a reduction in the percentage of islet tissue and beta cells per pancreas, but the percentage of islet tissue expressed per unit body weight was similar in all four groups. These results show that in maternal protein deprivation, homeostatic mechanisms ensure a constant amount of pancreatic endocrine tissue per unit of body weight. However, there remain major structural changes in the size, shape, and composition of the islets. These results support the theory that early development profoundly affects the structure of the pancreas and may play a role in the later development of adult diseases, such as non‐insulin‐dependent diabetes mellitus. © 1997 by John Wiley & Sons, Ltd.

Developmental origins of diabetes: The role of oxidative stress

“…In the rat, maternal dietary protein restriction (approximately 40-50% of normal intake) throughout gestation and lactation has been reported to alter glucose homeostasis and hypertension in the adult offspring (34)(35)(36)(37)(38)(39). Offspring are significantly growth retarded, remain growth retarded throughout life, and in some cases develop mild ß-cell secretory abnormalities (34)(35)(36)(37)(38) and in others insulin resistance (36,39). Aged rats develop hyperglycemia characterized by defects in insulin signaling in muscle, adipocytes, and liver (39)(40)(41)(42)(43).…”

Prenatal Programming of Hypertension

“…Hyperglycemia, impaired insulin secretion, insulin resistance, and even frank diabetes in the offspring have been induced by some prenatal maneuvers with or without IUGR (55,60 -66). Underlying mechanisms may include decreased number of pancreatic ␤ cells (67)(68)(69), upregulation of hepatic enzymes that may convey insulin resistance (55,60), and upregulation of the glucocorticoid receptor (60,70,71). In contrast, Gatford et al (72) reported that 5-yr-old sheep made that were hypertensive by prenatal administration of dexamethasone exhibited unchanged insulin sensitivity.…”

Maternal preconceptional nutrition leads to variable fat deposition and gut dimensions of adult offspring mice (C57BL/6JBom)

“…4,8 For example, the offspring of rodents fed a low protein (LP) diet have fewer but larger pancreatic islets and increased sensitivity to insulin in the muscles compared with rodents fed standard diet. 9,10 Moreover, increased preference for high-fat foods was developed in utero as an effect of protein-poor fetal diet in rodents. 11,12 One of the first epidemiological studies on humans during the Dutch Hunger Winter showed that adult men whose mothers had received poor nutrition during pregnancy had increased prevalence of obesity.…”