Rat Fetal Islets as a Useful Model for the Study of Insulin Release Failure

Effect of thawing rate and post-thaw culture on the cryopreserved fetal rat islets: Functional and morphological correlation

“…The late response of the fetal islets to 30 mmol/l glucose and the improper response to the final challenge with theophylline could be attributed to the immaturity of the fetal islets, as it was noticed in the control islets as well as in the slow and fast thawed islets. Similar findings were also reported in the literature and were attributed to the immaturity of the B-cells (Dudek et al, 1984;Hegre et al, 1984;Mourmeaux et al, 1985;Masaki et al, 1987;Tuch and Zheng, 1993;Bergsten et al, 1998;Mendonca et al, 1998). However, the underlying mechanism is not exactly known.…”

Upregulation of the expression of tight and adherens junction-associated proteins during maturation of neonatal pancreatic islets in vitro

“…*P < 0.05 in comparison with the N1d. accordance with our work, numerous studies have shown that fetal and neonatal islets, when cultured for a certain period of time, display an increased insulin response to suprastimulatory concentrations of glucose as well as to other secretagogues (Shimizu et al 1983, Dudek et al 1984, Freinkel et al 1984, Masaki et al 1987, Boschero et al 1993, Yderstraede & Flindt-Egebak 1995, Collares-Buzato et al 2001. Such process of in vitro maturation is even enhanced by exposure to prolactin (Boschero et al 1993, Crepaldi-Alves et al 1997, CollaresBuzato et al 2001.…”

“…In support of this idea, the culture-induced increase in the expression of junctional proteins occurred in parallel with an improvement in the insulin secretory response of cultured neonatal islets. It is well documented that fetal and neonatal rat islets exhibit a reduced secretory response to glucose when compared with adult islets (Masaki et al 1987, Boschero et al 1988. In Figure 2.…”

Autophagy plays a protective role in endoplasmic reticulum stress-mediated pancreatic β cell death

“…To explore the role of autophagy under insulin secretion deficiency, we generated a β cell line from islets isolated on 17-d mouse fetuses. Fetal islets are insulin secretion-deficient due to immaturity of the complex metabolic machinery required for secretion in β cells, [24][25][26] although we and others have previously shown that β cells isolated from fetal islets, and being unable to secrete insulin, still express insulin and other specific β cell markers ( Fig. S1A and S1B).…”

“…Transient expression of FLAG-tagged Rheb-Q64L impaired LC3B lipidation and machinery of these cells, as described previously. [24][25][26] We found increased autophagy in fetal β cells as a response to the accumulation of protein aggregates. Protein aggregates and their autophagic clearance have been previously observed in β cells from Zucker-diabetic fatty rats, 11 β cells from these animals have also been described as insulin secretion-deficient.…”