CENEXA   05419
CENTRO DE ENDOCRINOLOGIA EXPERIMENTAL Y APLICADA
Unidad Ejecutora - UE
artículos
Título:
Sitagliptin prevents the development of metabolic and hormonal disturbances, increased B-cell apoptosis and liver steatosis induced by a fructose-rich diet in normal rats
Autor/es:
MAIZTEGUI B; BORELLI MI; MADRID VG; DEL ZOTTO H; RASCHIA MA; FRANCINI F; MASSA ML; FLORES LE; REBOLLEDO OR; GAGLIARDINO JJ
Revista:
CLINICAL SCIENCE (LONDON, ENGLAND : 1979)
Editorial:
PORTLAND PRESS LTD
Referencias:
Lugar: Londres; Año: 2010 vol. 120 p. 73 - 80
ISSN:
0143-5221
Resumen:
The aim of the present study was to test the effect of sitagliptin and exendin-4 upon metabolic alterations, B-cell mass decrease and hepatic steatosis induced by F (fructose) in rats. Normal adult male Wistar rats received a standard commercial diet without (C) or with 10% (w/v) F in the drinking water (F) for 3 weeks; animals from each group were randomly divided into three subgroups: untreated (C and F) and simultaneously receiving either sitagliptin (CS and FS; 115.2 mg/day per rat) or exendin-4 (CE and FE; 0.35 nmol/kg of body weight, intraperitoneally). Water and food intake, oral glucose tolerance, plasma glucose, triacylglycerol (triglyceride), insulin and fructosamine concentration, HOMA-IR [HOMA (homoeostasis model assessment) for insulin resistance], HOMA-B (HOMA for B-cell function) and liver triacylglycerol content were measured. Pancreas immunomorphometric analyses were also performed. IGT (impaired glucose tolerance), plasma triacylglycerol, fructosamine and insulin levels, HOMA-IR and HOMA-B indexes, and liver triacylglycerol content were significantly higher in F rats. Islet B-cell mass was significantly lower in these rats, due to an increase in the percentage of apoptosis. The administration of exendin-4 and sitagliptin to F animals prevented the development of all the metabolic disturbances and the changes in B-cell mass and fatty liver. Thus these compounds, useful in treating Type 2 diabetes, would also prevent/delay the progression of early metabolic and tissue markers of this disease.