Effects of Subacute Exposure of Dibutyl Phthalate on the Homeostatic Model Assessment, Thyroid Function, and Redox Status in Rats

Abstract

Dibutyl phthalate is an endocrine disruptor used in a wide range of industrial and agriculture applications. The present study focuses on elucidating the effect of subacute exposure (4-weeks) of DBP on insulin and its sensitivity indexes, oxidative status, thyroid function, energy metabolites, serum biochemistry, and anthropometry in rats. A total of 64 rats were divided into 4 treatment groups as mg DBP/Kg body weight per day: (a) 0 mg/Kg (control), (b) 10 mg/Kg (DBP-10), (c) 50 mg/Kg (DBP-50), and (d) 100 mg/Kg (DBP-100). The rats in each treatment ( n = 16 ) were further divided into male ( n = 8 ) and female ( n = 8 ) rats for studying treatment and gender interactions. Intraperitoneal glucose tolerance test (IPGTT) was performed on the 21st day. Anthropometry, nutritional determinants, fasting plasma glucose, fasting plasma insulin, homeostatic model assessment (HOMA), thyroid hormones, energy metabolites, and oxidative status were studied during the experimental period. Two-way ANOVA was used to analyze the data ( p < 0.05 ). Tukey’s posthoc test was used for pair-wise comparisons. DBP increased body weight gain and feed efficiency in an inverted nonmonotonic U -shaped fashion. Hyperglycemia and increased blood glucose area under the curve were observed in DBP-100 at 120 minutes in IPGTT. The HOMA also showed a linear monotonic contrast. Thyroxin decreased significantly in the DBP-100 rats, whereas malondialdehyde, nonesterified fatty acids, and beta hydroxyl butyrate were increased with the DBP treatments. In conclusion, DBP could be attributed to the development of hyperglycemia and insulin resistance in rats. Further investigations into the lipid peroxidation pathways can improve our understanding of the mechanisms involved in metabolic disruption.

Apoptotic susceptibility of pancreatic alpha cells to environmentally relevant dose levels of bisphenol‐A versus dibutyl phthalate is mediated by HSP60/caspase‐3 expression in male albino rats

“…On the other hand, (Baralić, Živančević, et al, 2021) conducted a toxicogenomic analysis study and reported several genes linked to diabetes type 2 and mutual for BPA and DBP. Also, (Majeed et al, 2021) reported that hyperglycemia and insulin resistance, in rats could be attributed to DBP exposure. Such conflicting results might be explained by different doses, duration, mode of exposure, gender, and the experimental model used.…”

“…Also, (Majeed et al, 2021) reported that hyperglycemia and insulin resistance, in rats could be attributed to DBP exposure. Such supported by who reported an additive effect of both BPA and DBP combined in the induction of type 2 diabetes via apoptosis and oxidative stress-mediated mechanisms.…”