IGF-1→Glucose→Interleukin-1→poly-ADP-ribose

• 17303558(IGF-1): Beta-arrestin and Mdm2 mediate IGF-1 receptor-stimulated ERK activation and cell cycle progression.

  These data suggest that beta-arrestin-dependent ERK signaling by the IGF-1R regulates cell cycle progression and may thus be an important regulator of the growth of normal and malignant cells.

• 2086453(Glucose): Metabolism and beta-cell function of rat pancreatic islets exposed to human interleukin-1 beta in the presence of a high glucose concentration.

  However , the D - (6-14C) glucose oxidation rate , i.e. , the metabolism of glucose in the Krebs cycle , was reduced by about 65 % in rIL-1 beta exposed islets kept at 11.1 mM glucose and 46 % in islets cultured at 56 mM glucose.

• 7958397(Interleukin-1): Nuclear response of pancreatic islets to interleukin-1 beta.

  Exposure of the nuclear fraction to rIL-1 beta (10 IU/ml) provoked DNA strand breaks and increased nuclear poly (ADP-ribose) synthetase activity (148.4 % , P (0.01).

• 6299867(poly-ADP-ribose): Effect of poly(ADP-ribose) synthetase inhibitor administration to rats before and after injection of alloxan and streptozotocin on islet proinsulin synthesis.

  Pretreatment with poly (ADP-ribose) synthetase inhibitors was found to protect against alloxan - or streptozotocin-induced decrease in proinsulin synthesis.