Key result
Resveratrol reduces litter mortality and restores uterine mitochondrial function in obese mice.
Why the study?
This study was conducted to elucidate the mechanism of obesity-related adverse pregnancy outcomes and investigate the effect of resveratrol on reproductive performance in an obese mouse model.
Does resveratrol improve reproductive performance and uterine mitochondrial function in high-fat diet-induced obese mice?
Does resveratrol improve reproductive performance and uterine mitochondrial function in high-fat diet-induced obese mice?
Resveratrol protects against high-fat diet-induced adverse pregnancy outcomes by improving uterine mitochondrial function.
No immediate clinical implications from murine data; leaves open translation of resveratrol benefits to human obese pregnancy.
This study elucidates the mechanism of obesity-related adverse pregnancy outcomes and further investigates the effect of resveratrol on reproductive performance in a short- or long-term HFD-induced obese mouse model. Results show that maternal weight had a significant positive correlation with litter mortality in mice. A long-term HFD increased body weight and litter mortality with decreased expression of uterine cytochrome oxidase 4 (COX4), which was recovered by resveratrol in mice. Moreover, HFD decreased the expression of peroxisome proliferator-activated receptor γ coactivator-1α (PGC-1α), nuclear respiratory factors-1 (Nrf-1), and phosphorylated adenosine 5'-monophosphate (AMP)-activated protein kinase (p-AMPK) and increased the expression of phosphorylated extracellular regulated protein kinases (p-ERK) in the uterus. Resveratrol, a polyphenol that can directly bind to the ERK protein, suppressed the phosphorylation of ERK, increased the expression of p-AMPK, PGC-1α and Nrf-1, and decreased litter mortality in mice.
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Yang et al. (2024) studied Obesity-related adverse pregnancy outcomes. Resveratrol vs. High-fat diet without resveratrol was evaluated on Litter mortality and uterine protein expression. Resveratrol decreased litter mortality and recovered uterine mitochondrial function markers in a high-fat diet-induced obese mouse model.
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