Fig. 8: Proposed mechanisms for the amelioration of L. reuteri on dyslipidemia in circadian dysrhythmia-induced PCOS-like rats. | npj Biofilms and Microbiomes

Fig. 8: Proposed mechanisms for the amelioration of L. reuteri on dyslipidemia in circadian dysrhythmia-induced PCOS-like rats.

From: Alleviation of Limosilactobacillus reuteri in polycystic ovary syndrome protects against circadian dysrhythmia-induced dyslipidemia via capric acid and GALR1 signaling

Fig. 8

Left, circadian dysrhythmia due to constant darkness resulted in dyslipidemia and reproductive hallmarks of PCOS in rats. Elevated galanin-GALR1 induced by darkness exposure functioned as an upstream factor of PI3K/AKT pathway and further suppressed NR1D1-induced SREBF1 transcription and translation, thus inducing hepatic lipid accumulation in PCOS-like rats. Right, L. reuteri supplementation ameliorated dyslipidemia and reproductive hallmarks in circadian dysrhythmia-induced PCOS-like rats. L. reuteri restructured microbiome-metabolome network in darkness rats ameliorating the abundance of Lactobacillus, Clostridium sensu stricto 1, Ruminococcaceae UCG-010, and Family XIII AD3011 group, followed by varied serum levels of cortisol, cis-9-palmitoleic acid, 13-methylmyristic acid, capric acid, and dUMP. Notably, capric acid mediated the inhibition of L. reuteri on hepatic GALR1-PI3K/AKT-NR1D1-SREBP1 pathway, which eventually alleviated dyslipidemia.

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