Abstract

BACKGROUND: Due to widespread use of pesticides, an individual’s lifetime exposure to pesticide mixtures is unavoidable, resulting in potentiation of toxic effects such as changing metabolic signaling temporarily or permanently due to the formation of free radicals among exposed individuals. OBJECTIVE: This study then looked at the expression of leptin and insulin receptors in Wistar rats exposed to pyrethroid and its effects on adipokines and glycemic indices. METHODS: 84 Wistar rats were randomly selected and divided into two groups. 51 rats were exposed to 1.2 % w/v pyrethroid insecticides, while the remaining 33 rats were grouped as non-exposed. The groups were divided into three different groups, each with 7, 21, and 41 days. The animals were anesthetically sacrificed and samples of blood were collected after days of exposure. The levels of total antioxidant status (TAS), malondialdehyde (MDA), glutathione (GSH), hydrogen peroxide (H2O2), nitric oxide (NO), glucose and lipids were determined. Blood activities of superoxide dismutase (SOD), glutathione peroxidase (GPX), and catalase (CAT) were also determined. ELISA was used to assess leptin, adiponectin, insulin, CRP, IL-6, and TNFα. Glycaemic indices were calculated appropriately. Leptin and Insulin expression was determined using the reverse transcriptase-polymerase chain reaction (RT-PCR) method. Data obtained were statistically compared, and P≤0.05 was considered significant. RESULTS: The mean TChol, TAG, and HDL-C were significantly different (p < 0.05) among the exposed groups. The serum mean levels of SOD, GPx, CAT, GSH, TAS, QUICKI, TNFα, IL6, and CRP were significantly reduced (p < 0.05), while mean levels of MDA, H2O2, NO, insulin, HOMA-IR, FIRI, leptin, and adiponectin were significantly elevated (p < 0.05) in exposed groups. The relative expression of insulin and leptin genes in exposed and non-exposed groups was also shown by column. CONCLUSION: It is self-evident that pyrethroid chemicals exposure may disrupt carbohydrate and lipid metabolism by raising the risk of obesity among the exposed groups.

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