TY - JOUR
T1 - Vanillin exerts therapeutic effects against hyperglycemia-altered glucose metabolism and purinergic activities in testicular tissues of diabetic rats
AU - Salau, Veronica F.
AU - Erukainure, Ochuko L.
AU - Olofinsan, Kolawole A.
AU - Islam, Md Shahidul
N1 - Publisher Copyright:
© 2021
PY - 2021/6
Y1 - 2021/6
N2 - Testicular dysfunctions leading to male infertility has been reported in type 2 diabetes (T2D), with glucose dysmetabolism, cholinergic and purinergic dysfunction being major contributors. In the present study, the effect of vanillin on glucose metabolism, purinergic and cholinergic dysfunctions were investigated in testicular tissues of T2D rats. Male Sprague-Dawley rats were divided into 6 groups containing 5 rats each. T2D was induced in rats by administering 10 % fructose ad libitum for 14 days followed by a single intraperitoneal injection (40 mg/kg body weight) of streptozotocin. T2D rats were orally administered with vanillin at 150 and 300 mg/kg body weight (bw). Diabetic control (DC) consisted of untreated diabetic rats, while normal control (NC) consisted of normal rats and they were administered with distilled water only. Metformin was used as the standard antidiabetic drug. After 5 weeks treatment, the rats were sacrificed, and the testes were harvested. Induction of T2D led to significantly depleted testicular levels of glutathione, glycogen content, superoxide dismutase and catalase enzyme activities, with concomitantly elevated levels of nitric oxide, malondialdehyde, acetylcholinesterase, glucose-6-phosphatase, fructose-1,6-biphophastase, glycogen phosphorylase, amylase and lipase activities. These activities and levels were significantly reversed to near normal in rats treated with both doses of vanillin as compared with metformin. These results, when taken together, suggest the therapeutic effect of vanillin against hyperglycemia-mediated metabolic dysfunctions in testes of T2D rats. This is depicted by the ability of the phenolic to attenuate oxidative imbalance, purinergic and cholinergic dysfunctions, while suppressing glucose dysmetabolism.
AB - Testicular dysfunctions leading to male infertility has been reported in type 2 diabetes (T2D), with glucose dysmetabolism, cholinergic and purinergic dysfunction being major contributors. In the present study, the effect of vanillin on glucose metabolism, purinergic and cholinergic dysfunctions were investigated in testicular tissues of T2D rats. Male Sprague-Dawley rats were divided into 6 groups containing 5 rats each. T2D was induced in rats by administering 10 % fructose ad libitum for 14 days followed by a single intraperitoneal injection (40 mg/kg body weight) of streptozotocin. T2D rats were orally administered with vanillin at 150 and 300 mg/kg body weight (bw). Diabetic control (DC) consisted of untreated diabetic rats, while normal control (NC) consisted of normal rats and they were administered with distilled water only. Metformin was used as the standard antidiabetic drug. After 5 weeks treatment, the rats were sacrificed, and the testes were harvested. Induction of T2D led to significantly depleted testicular levels of glutathione, glycogen content, superoxide dismutase and catalase enzyme activities, with concomitantly elevated levels of nitric oxide, malondialdehyde, acetylcholinesterase, glucose-6-phosphatase, fructose-1,6-biphophastase, glycogen phosphorylase, amylase and lipase activities. These activities and levels were significantly reversed to near normal in rats treated with both doses of vanillin as compared with metformin. These results, when taken together, suggest the therapeutic effect of vanillin against hyperglycemia-mediated metabolic dysfunctions in testes of T2D rats. This is depicted by the ability of the phenolic to attenuate oxidative imbalance, purinergic and cholinergic dysfunctions, while suppressing glucose dysmetabolism.
KW - Glucose dysmetabolism
KW - Testicular dysfunction
KW - Type 2 diabetes
KW - Vanillin
UR - https://www.scopus.com/pages/publications/85103721208
U2 - 10.1016/j.reprotox.2021.03.007
DO - 10.1016/j.reprotox.2021.03.007
M3 - Article
C2 - 33823243
AN - SCOPUS:85103721208
SN - 0890-6238
VL - 102
SP - 24
EP - 34
JO - Reproductive Toxicology
JF - Reproductive Toxicology
ER -