The role of uterus mitochondrial function in high-fat diet-related adverse pregnancy outcomes and protection by resveratrol.
Xizi YangRuizhi HuLiping YaoWentao ZhangMingkun ShiJiatai GongXupeng YuanYanli LiJiahao YanYing WangQianjin ZhangZiyu HeDe-Xing HouZhiyong FanHongfu ZhangLiang ChenXi HeJian-Hua HeShusong WuPublished in: Food & function (2024)
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.
Keyphrases
- high fat diet
- pregnancy outcomes
- protein kinase
- poor prognosis
- insulin resistance
- high fat diet induced
- adipose tissue
- skeletal muscle
- binding protein
- body weight
- signaling pathway
- pregnant women
- weight loss
- metabolic syndrome
- mouse model
- type diabetes
- cardiovascular events
- oxidative stress
- cell proliferation
- pi k akt
- risk factors
- cardiovascular disease
- amino acid
- emergency department
- transcription factor
- coronary artery disease
- diabetic rats
- high glucose
- adverse drug
- electronic health record