ISSN:
1432-0428
Keywords:
Isolated liver perfusion
;
insulin resistance
;
islet amyloid polypeptide
Source:
Springer Online Journal Archives 1860-2000
Topics:
Medicine
Notes:
Summary The impact of (pancreatic) islet amyloid polypeptide on glucose metabolism and insulin sensitivity was examined in isolated rat livers perfused in a non-recirculating system. Continuous infusion of 10−7mol/l islet amyloid polypeptide affected neither basal nor glucagon (10−9 mol/l)-stimulated glucose output by livers from fed rats, but it did increase the hepatic cyclic AMP release within 44 min (7.91±12.07 vs control: 0.07±0.03 pmol·100 g body weight−1). The effect of the peptide on the ability of insulin to inhibit glucagon-induced hepatic glycogenolysis was measured in three experimental groups (n = 6). As expected glucagon (7×10−11 mol/l) increased integral hepatic glucose release within 84 min (763.4±161.7 vs −25.7±73.2 μmol · 100 g body weight−1 in the control group, p〈0.001), while insulin (100 mU/l) decreased the glucagon-stimulated glucose production (395.2±180.0 μmol·100 g body weight−1, p〈0.01). Simultaneous infusion of 10−7 mol/l islet amyloid polypeptide however, was not able to reverse insulin-dependent inhibition of glucagon-stimulated hepatic glucose output (370.0±102.5 μmol·100 g body weight−1, NS) or to enhance lactate-induced gluconeogenesis of livers from 24 h fasted rats (n = 8). The glucose production stimulated by 10−9 mol/l glucagon was slightly greater in islet amyloid polypeptide-pre-treated livers than in a control group without addition of islet amyloid polypeptide (5 min: 3.60±3.36 vs 1.67±1.28 μmol·min−1·100 g body weight−1). These results suggest that islet amyloid polypeptide neither directly affects hepatic glycogenolysis nor causes insulin resistance to hormone-sensitive glucose production, but may increase the size of the hepatic glycogen pool by enhancing gluconeogenesis.
Type of Medium:
Electronic Resource
URL:
http://dx.doi.org/10.1007/BF00402542
Permalink
