Insulin resistance associated with visceral fat
obesity has been suggested to be the pathological basis of
metabolic syndrome. Many studies have demonstrated increased
oxidant stress in diabetic patients and animal models of
diabetes mellitus. In this study, the effect of liver hydrolysate administration on the
blood glucose was examined in SHR/NDmcr-cp (SHR-cp) rats that show spontaneously occurring
metabolic syndrome-like abnormalities. The SHR-cp rats were fed diets containing 5% liver hydrolysate for 12 weeks, and the fasting
blood glucose and HbA1c were determined every 3 weeks. After administration of the liver hydrolysate-containing feed for 12 weeks, an oral
glucose tolerance test was conducted and the plasma
angiotensin II (AngII) concentrations were determined. The liver hydrolysate administration had no effect on the blood
insulin levels in the oral
glucose tolerance test, but significantly inhibited the
d-glucose-induced increases of the
blood glucose levels. Furthermore, the liver hydrolysate had almost no effect on the fasting
blood glucose level, but tended to inhibit the increase of HbA1c. The plasma AngII concentration after the 12-week administration of liver hydrolysate remained significantly lower than that in the control group. These results indicate that a component of liver hydrolysate inhibits
d-glucose-induced increase of the
blood glucose level, and may improve
insulin resistance. The
angiotensin converting enzyme (ACE)-inhibiting effect and
antioxidant effect of liver hydrolysate may be involved in this effect.