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Sex-Specific Effects of Maternal and Post-Weaning High-Fat Diet on Adipose Tissue Remodeling and Asprosin Expression
Zhao Yang1,2,3, Jianan Jiang2,3, Miao Chen1
1Department of Obstetrics and Gynecology, the First Affiliated Hospital of Xi'an Jiaotong University, Xi'an, 710061, China.
Insights
Maternal high-fat diet (HFD) significantly impacts male offspring
Area of Science:
- Endocrinology
- Metabolic Syndrome Research
- Developmental Biology
Background:
- Perinatal exposure to a high-fat diet (HFD) is a known risk factor for developing metabolic disorders in offspring.
- Adipose tissue remodeling and adipokine dysregulation are key components of metabolic syndrome.
- Understanding sex-specific responses to maternal HFD is crucial for targeted interventions.
Purpose of the Study:
- To investigate the effects of maternal HFD on adipose tissue remodeling and adipokine expression in mice offspring.
- To characterize sex-specific metabolic alterations induced by perinatal HFD exposure.
- To identify potential biomarkers for HFD-induced metabolic dysfunction.
Main Methods:
- Female C57BL/6 mice were fed either a control (CHOW) or HFD for two weeks prior to mating, throughout gestation, and lactation.
- Offspring were weaned onto either CHOW or HFD, creating eight experimental groups based on sex and diet history (maternal and post-weaning).
- Body weight, glucose tolerance, adipose tissue mass, adipocyte hypertrophy, and serum adipokine levels (including asprosin) were analyzed.
Main Results:
- Maternal HFD exposure led to increased body weight, impaired glucose tolerance, and greater adipose tissue mass and hypertrophy exclusively in male offspring.
- Circulating asprosin levels were decreased in male offspring exposed to maternal HFD and negatively correlated with fasting blood glucose, cholesterol, and HDL levels.
- Depot- and sex-specific changes in adipokines were observed in response to maternal and/or post-weaning HFD.
Conclusions:
- Maternal HFD significantly influences metabolic phenotype, with male offspring exhibiting greater susceptibility to HFD-induced metabolic disorders.
- Asprosin may serve as a potential biomarker for HFD-induced metabolic dysfunction in male offspring.
- Dietary interventions during critical developmental windows are essential for mitigating metabolic disease risk.
Scope:
Perinatal high-fat diet (HFD) increases risk of metabolic disorders in offspring. Adipose tissue remodeling is associated with metabolic syndrome. The current study characterizes the profile of maternal HFD-induced changes in adipose tissue remodeling and adipokines expression in mice offspring.
Methods And Results:
Female C57BL/6 mice are fed with CHOW or HFD for 2 weeks before mating, throughout gestation and lactation. At weaning, pups are randomly fed with CHOW or HFD, resulting in eight groups according to sex and maternal diet: Male CHOW-CHOW (MCC), Male CHOW-HFD (MCH), Male HFD-CHOW (MHC), Male HFD-HFD (MHH), Female CHOW-CHOW (FCC), Female CHOW-HFD (FCH), Female HFD-CHOW (FHC), and Female HFD-HFD (FHH). Increased body weight, impaired glucose tolerance, increased adipose tissue mass and hypertrophy, and decreased circulating asprosin level are only observed in male offspring exposure to maternal HFD. Serum asprosin level negatively correlates with fasting blood glucose, serum cholesterol (CHO), and high-density lipoprotein (HDL) levels, while positively correlates with serum low-density lipoprotein (LDL) and glutamate-oxaloacetate transaminase (GOT) levels in male offspring. A combination of genetic and biochemical analyses of adipokines shows the depot- and sex-specific changes in response to maternal and/or post-weaning HFD.
Conclusion:
This study's results reveal the differential metabolic changes in response to maternal and/or post-weaning HFD in male and female offspring. The effect of maternal HFD on metabolic phonotype is more obvious in male offspring, supporting the notion that males are more susceptible to HFD-induced metabolic disorders.
