Modulation of PON-1 by acetate reverses hepatic dysmetabolism in experimentally induced PCOS

Olaniyi, Kehinde S.; Areloegbe, Stephanie E.

doi:10.1007/s00580-024-03553-x

Cited by 1 publication

(1 citation statement)

References 32 publications

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“…In women with PCOS, the lipid and glucose regulating enzyme paraoxonase 1 (PON1) has already been linked to the emergence of cardio-metabolic abnormalities [ 8 , 9 ]. PON1 may contribute to high density lipoprotein (HDL)'s antiatherogenic, anti-inflammatory, and antioxidant properties [ 10 , 11 ]. PON1 also affects the modulation of glucometabolism, including fasting blood glucose, insulin sensitivity, glucose tolerance, and an upsurge in the expression of muscular glucose receptor 4 [ 12 ].…”

Section: Introductionmentioning

confidence: 99%

Diacerein mitigates endocrine and cardio-metabolic disruptions in experimental PCOS mice model by modulating AdipoR1/ PON 1

Shah,

Shrivastava,

Muzamil

et al. 2024

BMC Endocr Disord

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Background This study aimed to explore the impact of Diacerein (DIC) on endocrine and cardio-metabolic changes in polycystic ovarian syndrome (PCOS) mouse model. Methods A total of 18 adult female mice (Parkes strain), aged 4–5 weeks, were randomly assigned to three groups, each comprising 6 animals, as follows: Group I (control), received normal diet and normal saline as vehicle for 51 days; Group II received Letrozole (LET; 6 mg/kg bw) for 21 days to induce PCOS; Group III received LET, followed by daily oral gavage administration of DIC (35 mg/kg bw) for 30 days. Results This study indicates that treatment with LET resulted in PCOS with characteristics such as polycystic ovaries, elevated testosterone, weight gain, visceral adiposity, high levels of insulin as well as fasting blood glucose in addition to insulin resistance, improper handling of ovarian lipids, atherogenic dyslipidemia, impaired Na + /K + -ATPase activity and serum, cardiac, and ovarian oxidative stress. Serum/ovarian adiponectin levels were lowered in LET-treated mice. In mice treated with LET, we also discovered a reduction in cardiac and serum paraoxonase 1 (PON1). Interestingly, DIC restored ovarian andcardio-metabolic abnormalities in LET-induced PCOS mice. DIC prevented the endocrine and cardio-metabolic changes brought on by letrozole-induced PCOS in mice. Conclusion The ameliorative effects of DIC on letrozole-induced PCOS with concurrent oxidative stress, abdominal fat deposition, cardiac and ovarian substrate mishandling, glucometabolic dysfunction, and adiponectin/PON1 activation support the idea that DIC perhaps, restore compromised endocrine and cardio-metabolic regulators in PCOS.

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