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Insulin‐like growth factor‐I reverts testicular atrophy in rats with advanced cirrhosis
Author(s) -
CastillaCortazar Inma,
Garcia Maria,
Quiroga Jorge,
Diez Nieves,
DiezCaballero Fernando,
Calvo Alfonso,
Diaz Matias,
Prieto Jesus
Publication year - 2000
Publication title -
hepatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 5.488
H-Index - 361
eISSN - 1527-3350
pISSN - 0270-9139
DOI - 10.1002/hep.510310308
Subject(s) - medicine , endocrinology , cirrhosis , testicular atrophy , insulin like growth factor , anabolism , testosterone (patch) , growth factor , pathogenesis , atrophy , spermatogenesis , liver function , receptor
The pathogenesis of hypogonadism in cirrhosis is not completely understood. The levels of insulin‐like growth factor‐I (IGF‐I), an anabolic factor with trophic actions on testes, are reduced in cirrhosis. This study was undertaken to evaluate whether rats with advanced cirrhosis develop hypogonadism and whether the administration of IGF‐I exerts beneficial effects on testicular structure and function. Wistar rats with ascitic cirrhosis induced with CCl 4 were allocated into 2 groups (n = 10, each) to receive recombinant IGF‐I (20 μg · kg −1 · d −1 , subcutaneously) or vehicle for 3 weeks. Healthy rats receiving vehicle were used as the control group (n = 10). At baseline, both cirrhotic groups showed similar deterioration of liver function tests. Compared with controls, nontreated cirrhotic rats showed decreased serum levels of IGF‐I ( P < .05), reduced testicular size and weight ( P < .001), and intense histopathological testicular abnormalities, including reduced tubular diameters ( P < .001), loss of the germinal line ( P < .001), and diminutions in cellular proliferation, spermatogenesis ( P < .001), and testicular transferrin expression ( P < .001). In addition, low serum testosterone ( P < .01) and high serum LH ( P < .01) were present in untreated cirrhotic animals. Cirrhotic rats that received IGF‐I showed full recovery of testicular size and weight and of all histopathological abnormalities ( P < .001 to < .01 vs. nontreated cirrhotic rats; P = ns vs. controls). Serum levels of sex hormones tended to normalize. In conclusion, IGF‐I deficiency may play a pathogenetic role in hypogonadism of cirrhosis. Low doses of IGF‐I for a short period of time revert testicular atrophy and appear to improve hypogonadism in advanced experimental cirrhosis.