High-sucrose-induced maternal obesity disrupts ovarian function and decreases fertility in Drosophila melanogaster

BIOCHIMICA ET BIOPHYSICA ACTA-MOLECULAR BASIS OF DISEASE

卷:1863

Article

Brookheart, Rita T.^1,2  Swearingen, Alison R.¹  Collins, Christina A.¹  Cline, Laura M.¹  Duncan, Jennifer G.¹ 

[1] Washington Univ, Sch Med, Dept Pediat, 660 South Euclid Ave,Campus Box 8208, St Louis, MO 63110 USA

[2] Washington Univ, Sch Med, Dept Med, 660 South Euclid Ave,Campus Box 8031, St Louis, MO 63110 USA

关键词: Obesity;    Drosophila;    Ovary;    Mitochondria;    Pregnancy;    Nutritional programming;   

DOI  :  10.1016/j.bbadis.2017.03.014

来源: Elsevier

【 摘 要 】

As the obesity epidemic worsens, the prevalence of maternal obesity is expected to rise. Both high-fat and high sucrose diets are known to promote maternal obesity and several studies have elucidated the molecular influence of high-fat feeding on female reproduction. However, to date, the molecular impact of a high-sucrose diet on maternal obesity remains to be investigated. Using our previously reported Drosophila high-sucrose maternal obesity model, we sought to determine how excess dietary sucrose impacted the ovary. High-sucrose diet (HSD) fed adult females developed systemic insulin resistance and exhibited an ovarian phenotype characterized by excess accumulation of lipids and cholesterol in the ovary, decreased ovary size, and impaired egg maturation. We also observed decreased expression of antioxidant genes and increased protein carbonylation in the ovaries of HSD females. HSD females laid fewer eggs; however, the overall survival of offspring was unchanged relative to lean control females. Ovaries of HSD females had increased mitochondrial DNA copy number and decreased expression of key mitochondrial regulators, suggestive of an ineffective compensatory response to mitochondrial dysfunction. Mitochondrial alterations were also observed in male offspring of obese females. This study demonstrates that high-sucrose-induced maternal obesity promotes insulin resistance, while disrupting ovarian metabolism and function.

【 授权许可】

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