title: 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.
authors.affiliation: Laboratory of Secretion Cell Biology, Department of Cell Biology and Genetics, State University of Maringá, Maringá, Brazil.
authors.forename: Renato Chaves Souto
authors.initials: RC
authors.lastname: Branco
authors.forename: Júlio Cezar
authors.initials: JC
authors.lastname: de Oliveira
authors.forename: Sabrina
authors.initials: S
authors.lastname: Grassiolli
authors.forename: Rosiane Aparecida
authors.initials: RA
authors.lastname: Miranda
authors.forename: Luiz Felipe
authors.initials: LF
authors.lastname: Barella
authors.forename: Rodrigo Mello
authors.initials: RM
authors.lastname: Gomes
authors.forename: Luiz Augusto
authors.initials: LA
authors.lastname: Bataglini
authors.forename: Rosana
authors.initials: R
authors.lastname: Torrezan
authors.forename: Clarice
authors.initials: C
authors.lastname: Gravena
authors.forename: Paulo Cezar
authors.initials: PC
authors.lastname: de Freitas Mathias
mesh_terms: D000818:Animals; D001835:Body Weight; D003921:Diabetes Mellitus, Experimental / Q000378:metabolism* / Q000628:therapy; D018753:Diet, Protein-Restricted; D005260:Female; D005947:Glucose / Q000378:metabolism; D005951:Glucose Tolerance Test; D006706:Homeostasis; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D007515:Islets of Langerhans / Q000378:metabolism*; D016381:Islets of Langerhans Transplantation / Q000379:methods*; D018811:Maternal Exposure; D008954:Models, Biological; D011247:Pregnancy; D011270:Pregnancy, Animal; D051381:Rats; D017208:Rats, Wistar; D013311:Streptozocin / Q000494:pharmacology
chemical_list: D007328:Insulin; D013311:Streptozocin; D005947:Glucose