In South-west Nigeria, water decoctions of
hunteria umbellata
seeds are highly valued by traditional healers in the local management of diabetes mellitus, obesity and hyperlipidemia. Previous studies hypothesized one of the antihyperglycemic mechanisms of the aqueous seed extract of
Hunteria umbellata (
HU) to be mediated probably via increased peripheral glucose utilization. The present study, therefore, was designed at evaluating the peripheral glucose utilization and anti-oxidative mechanisms of 50 mg/kg, 100 mg/kg and 200 mg/kg of
HU in alloxan-induced diabetic rats in Groups IV-VI rats as well as in the control groups (Groups I-III). Experimental type 1 DM was induced in male Wistar rats through intraperitoneal injection of 150 mg/kg of alloxan monohydrate in cold 0.9% normal saline after which the diabetic rats were orally treated with 50-200 mg/kg of
HU for 14 days. Effects of
HU on the rat body weight, percentage body weight changes and fasting blood glucose (FBG) were determined on days 1 and 15 of the experiment. Also, on day 15 of the experiment,
HU effect on serum insulin, liver enzyme markers, proteins, albumin, triglyceride, total cholesterol and lactate dehydrogenase as well as on hepatic tissue oxidative stress markers, liver glycogen and glucose-6-phosphatase were determined after sacrificing the rats under diethyl ether anesthesia. Results showed that oral treatments with 50-200 mg/kg of
HU caused significant (
p<0.0001) improvements in the weight loss caused by alloxan-induced diabetes, while causing significant (
p<0.05,
p<0.001 and
p<0.0001) dose-related reductions in the FBG levels despite causing non-significant (p>0.05) alterations in the serum INS levels in the treated rats. Also, repeated oral treatment with
HU caused significant (
p<0.0001) reversal in the decrease and increase in the hepatic glycogen levels and glucose-6-phosphatase activity, respectively, caused by alloxan-induced diabetes. Similar significant (
p<0.0001) and complete reversal effects were recorded in the serum hepatic enzyme markers, total protein, albumin, triglyceride, total cholesterol and lactate dehydrogenase as well as on hepatic tissue oxidative stress markers such as superoxidase dismutase (SOD), catalase (CAT), malonialdehyde (MDA) and reduced glutathione (GSH) of
HU -treated rats when compared to that of untreated alloxan-induced diabetic rats. In conclusion, results of this study showed
HU treatment to significantly ameliorate the hyperglycemia and oxidative stress in alloxan-induced diabetic rats which was mediated via increased hepatic glycogen deposit, decreased hepatic glucose-6-phosphatase activity and improvement in antioxidant/free radicals scavenging activities.
