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NRF2 deficiency increases obesity susceptibility in a mouse menopausal model
Xunwei Wu1,2, Jun Huang3, Cong Shen4
1Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Plos One
|February 12, 2020
Summary
Nrf2 deficiency combined with estrogen decline significantly increases body weight in menopausal models. This may link to altered glucose, LDL metabolism, and reduced serotonin, increasing metabolic risks for women with antioxidant deficiencies.
Area of Science:
- Metabolic research
- Endocrinology
- Neuroscience
Background:
- Menopause-associated estrogen decline elevates metabolic abnormality risk.
- Nuclear factor E2-related factor 2 (NRF2) regulates energy metabolism and oxidative stress.
Purpose of the Study:
- To investigate the impact of NRF2 deficiency on metabolic changes in a mouse model of surgical menopause.
- To assess the combined effects of NRF2 knockout and ovariectomy on body weight, serum lipids, glucose, and neurotransmitters.
Main Methods:
- Utilized an ovariectomized Nrf2-knockout (KO) mouse model compared to wild-type (WT) controls.
- Monitored body weight and serum metabolic markers (TG, T-CHO, LDL, HDL, GLU) over nine weeks.
- Analyzed brain neurotransmitters (dopamine, serotonin) post-sacrifice.
Main Results:
- KO ovariectomized mice exhibited greater body weight gain than WT counterparts.
- Ovariectomized KO mice showed increased blood glucose and decreased LDL compared to WT.
- NRF2 deficiency and ovariectomy led to reduced serotonin levels in brain tissue.
Conclusions:
- Combined NRF2 deletion and estrogen decline promote significant body weight increase.
- Altered glucose metabolism, LDL levels, and reduced serotonin may contribute to metabolic dysfunction post-menopause.
- Antioxidant defense deficiency may heighten metabolic risks in postmenopausal women.
