Oral ethinylestradiol-levonorgestrel normalizes fructose-induced hepatic lipid accumulation and glycogen depletion in female rats.

Oral ethinylestradiol-levonorgestrel normalizes fructose-induced hepatic lipid accumulation and glycogen depletion in female rats. Can J Physiol Pharmacol. 2019 Jul 23;: Authors: Olaniyi KS, Olatunji LA Abstract The present study investigated effects of oral ethinylestradiol-levonorgestrel (EEL) on hepatic lipid and glycogen contents during high fructose (HF) intake and determined whether pyruvate dehydrogenase kinase-4 (PDK-4) and Glucose-6-phosphate dehydrogenase (G6PD) activity were involved in HF and/or EEL-induced hepatic dysmetabolism. Female Wistar rats weighing between 140-160g were divided into groups. Control, EEL, HF and EEL+HF groups received water (vehicle, p.o), 1.0µg ethinylestradiol plus 5.0µg levonorgestrel (p.o), fructose (10%; w/v) and EEL plus HF respectively, daily for 8 weeks. Results revealed that EEL or HF led to insulin resistance, hyperinsulinemia, increased hepatic uric acid production, triglyceride (0.80 ± 0.06 or 1.21 ± 0.08 versus control; 0.41 ± 0.05mg/100mg tissue; p<0.05), reduced glycogen content (0.59 ± 0.11 or 0.61 ± 0.10 versus control; 1.15 ± 0.09ug/100mg tissue; p<0.05), plasma or hepatic glutathione- and G6PD-dependent antioxidants. HF but not EEL also increased fasting glucose and hepatic PDK-4. Nonetheless, these alterations were attenuated by EEL in HF-treated rats. Our results demonstrate that hepatic lipid accumulation and glycogen depletion induced by HF is accompanied by in...
Source: Canadian Journal of Physiology and Pharmacology - Category: Drugs & Pharmacology Authors: Tags: Can J Physiol Pharmacol Source Type: research