Pre- and postnatal low protein diet affect pancreatic islet blood flow and insulin release in adult rats

• Published in: Endocrinology (Philadelphia) Vol. 137; no. 9; p. 3797
• Main Authors: Iglésias-Barreira, V, Ahn, M T, Reusens, B, Dahri, S, Hoet, J J, Remacle, C
• Format: Journal Article
• Language: English
• Published: United States 01.09.1996
• Subjects: Aging - metabolism; Animals; Animals, Newborn - anatomy & histology; Body Weight; Dietary Proteins - administration & dosage; Dietary Proteins - pharmacology; Female; Glucose - metabolism; Homeostasis; Insulin - metabolism; Islets of Langerhans - blood supply; Islets of Langerhans - metabolism; Organ Size; Pregnancy; Rats; Rats, Wistar; Regional Blood Flow - drug effects
• ISSN: 0013-7227
• DOI: 10.1210/endo.137.9.8756549

The pancreatic islet blood flow and insulin secretion of adult rats submitted to an isocaloric low protein diet (8% vs. 20%) during pre- and postnatal life were investigated by the nonradioactive microsphere technique. In the basal state, female rats chronically exposed to a low protein diet (LP) displayed a specific marked decrease in islet blood flow (10 +/- 2 vs. 29 +/- 5 microliters/min.g pancreas; P < 0.01) and overall pancreatic blood flow (P < 0.01). The plasma insulin level, however, was not affected. During a glucose challenge, the control animals enhanced their islet blood flow 2.3-fold, whereas the LP group reached control values with a 6-fold increase. Plasma insulin levels rose similarly in the control and LP animals. A third group of animals designated the recuperation group, exposed to a low protein diet only in utero, displayed islet blood flow comparable to control values, but increased basal plasma insulin (2.0 +/- 0.3 vs. 1.2 +/- 0.1 ng/ml; P < 0.05). These data are consistent with the possibility of dissociation of islet blood flow and insulin release under basal conditions, which may not be the case after a glucose challenge. Furthermore, the low blood flow values in the LP group may reflect an adaptive physiological response, an impaired pancreatic vasculogenesis, or a dysfunction of endothelial cells.