title: [Effects of liver hydrolysate on the blood glucose in metabolic syndrome model rats (SHR/NDmcr-cp)].
abstract: 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.
authors.affiliation: Interdisciplinary Graduate School of Agriculture and Engineering, University of Miyazaki, Japan.
authors.forename: Naonori
authors.initials: N
authors.lastname: Inoue
authors.forename: Shuji
authors.initials: S
authors.lastname: Hidaka
authors.forename: Naoyoshi
authors.initials: N
authors.lastname: Miura
authors.forename: Kotaro
authors.initials: K
authors.lastname: Yamada
authors.forename: Masahiro
authors.initials: M
authors.lastname: Fukahori
authors.forename: Masugi
authors.initials: M
authors.lastname: Maruyama
authors.forename: Satoshi
authors.initials: S
authors.lastname: Kawahara
authors.forename: Kazuyoshi
authors.initials: K
authors.lastname: Ohta
authors.forename: Michio
authors.initials: M
authors.lastname: Muguruma
mesh_terms: D000804:Angiotensin II / Q000097:blood; D000806:Angiotensin-Converting Enzyme Inhibitors; D000818:Animals; D000975:Antioxidants; D001786:Blood Glucose / Q000378:metabolism*; D003864:Depression, Chemical; D004195:Disease Models, Animal; D005951:Glucose Tolerance Test; D006442:Glycated Hemoglobin / Q000378:metabolism; D007333:Insulin Resistance; D008099:Liver / Q000378:metabolism*; D008297:Male; D024821:Metabolic Syndrome / Q000097:blood* / Q000209:etiology*; D018384:Oxidative Stress / Q000187:drug effects / Q000502:physiology; D011492:Protein Hydrolysates / Q000008:administration & dosage / Q000494:pharmacology*; D051381:Rats; D011918:Rats, Inbred SHR
chemical_list: D000804:Angiotensin II; D000806:Angiotensin-Converting Enzyme Inhibitors; D000975:Antioxidants; D001786:Blood Glucose; D006442:Glycated Hemoglobin; D011492:Protein Hydrolysates; C517652:hemoglobin A1c protein, human