Maternal Protein Malnutrition Does Not Impair Insulin Secretion from Pancreatic Islets of Offspring after Transplantation into Diabetic Rats

Abstract

Pancreatic islets from adult rats whose mothers were protein restricted during lactation undersecrete insulin. The current work analyzes whether this secretory dysfunction can be improved when the pancreatic islets are grafted into hyperglycemic diabetic rats. Two groups of rats were used: the adult offspring from dams that received a low protein diet (4%) during the initial 2/3 of lactation (LP) and, as a control, the adult offspring from dams that consumed a normal protein diet (23%) during the entire period of lactation (NP). Islets from NP- and LP-rats were transplanted into diabetic recipient rats, which were generated by streptozotocin treatment. The islets were transplanted via the portal vein under anesthesia. The fed blood glucose levels were monitored during the 4 days post-transplantation. Transplanted islets from LP-rats (T LP) decreased the fed glucose levels of diabetic rats 34% (21.37±0.24 mM, p<0.05); however, the levels still remained 2-fold higher than those of the sham-operated controls (6.88±0.39 mM, p<0.05). Grafts with NP-islets (T NP) produced the same effect as the LP-islets in diabetic rats. The high fasting blood glucose levels of diabetic rats were improved by the transplantations. Islet grafts from both rat groups recovered 50% of the retroperitoneal fat mass of the diabetic rats (0.55±0.08 g/100 g of body weight for T NP and 0.56±0.07 g/100 g of body weight for T LP, p<0.05). Because pancreatic islets from both the NP- and LP-rats were able to regulate fasting blood glucose concentrations in hyperglycemic rats, we propose that the altered function of pancreatic islets from LP-rats is not permanent.

Short- and long-term effects of maternal perinatal undernutrition are lowered by cross-fostering during lactation in the male rat

“…38 Recently, elegant studies reported that transplantation of pancreatic islets, from offspring whose mothers were protein restricted during lactation, was able to regulate fasting blood glucose concentrations in diabetic rats. 39 These results reinforce the idea that pancreatic islets from perinatally undernourished animals are not altered per se but presumably show a reduced number that may explain why β-cells are less sensitive to glucose stimulation. This decreased β-cell mass would explain the intolerance to glucose frequently observed in offspring from malnourished mothers.…”

“…It seems plausible that insulin production might not be sufficient to regulate glycemia in response to glucose challenge, as it has been reported that adult male rats from perinatally undernourished mothers present decreased β-cell mass associated with insulinopenia and marked glucose intolerance 38 . Recently, elegant studies reported that transplantation of pancreatic islets, from offspring whose mothers were protein restricted during lactation, was able to regulate fasting blood glucose concentrations in diabetic rats 39 . These results reinforce the idea that pancreatic islets from perinatally undernourished animals are not altered per se but presumably show a reduced number that may explain why β-cells are less sensitive to glucose stimulation.…”

Early postnatal low-protein nutrition, metabolic programming and the autonomic nervous system in adult life

“…Although the results showed no change in either β-cell metabolism or calcium buffering, an impairment of cholinergic transduction was reported [ 73 ]. Surprisingly, diabetic rats transplanted with pancreatic islets from adult rats that were protein-restricted during lactation showed improvement of their fasting glycemic, which may indicate that changes in β-cell activity provoked by poor perinatal protein nutrition are not permanent and could open possibilities to new therapeutics to treat metabolic diseases [ 74 ].…”