Abstract
Stearoyl-CoA desaturase (SCD) is known to be an important rate-limiting enzyme in the production of monounsaturated fatty acids (MUFAs). However, the role of this enzyme in goose follicular development is poorly understood. To investigate the metabolic mechanism of SCD during goose follicular development, we observed its expression patterns in vivo and in vitro using quantitative reverse-transcription (qRT)-PCR. Liquid chromatography-tandem mass spectrometry (LC-MS/MS) was used to determine a cellular model of SCD function in granulosa cells (GCs) via SCD overexpression and knockdown. qRT-PCR analysis showed that SCD was abundantly expressed in the GC layer, and was upregulated in preovulatory follicles. Peak expression was found in F1 and prehierarchal follicles with diameters of 4–6 mm and 8–10 mm, respectively. We further found that mRNA expression and corresponding enzyme activity occur in a time-dependent oscillation pattern in vitro, beginning on the first day of GC culture. By LC-MS/MS, we identified numerous changes in metabolite activation and developed an overview of multiple metabolic pathways, 10 of which were associated with lipid metabolism and enriched in both the overexpressed and knockdown groups. Finally, we confirmed cholesterol and pantothenol or pantothenate as potential metabolite biomarkers to study SCD-related lipid metabolism in goose GCs.
Highlights
An important rate-limiting enzyme in lipogenesis is stearoyl-coenzyme A (CoA) desaturase (SCD), which synthesizes monounsaturated fatty acids (MUFAs) from saturated fatty acids (SFAs) by introducing a cis-double bond into fatty acyl-CoAs [1]
The results showed that Stearoyl-CoA desaturase (SCD) was primarily expressed in the granulosa layer and weakly expressed in the theca layer
We speculated that the function of SCD in goose granulosa cells (GCs) is closely related to follicular development
Summary
An important rate-limiting enzyme in lipogenesis is stearoyl-CoA desaturase (SCD), which synthesizes monounsaturated fatty acids (MUFAs) from saturated fatty acids (SFAs) by introducing a cis-double bond into fatty acyl-CoAs [1]. The ratio of SFAs to MUFAs can influence a broad spectrum of cellular functions; the content and distribution of SFAs and MUFAs within the cell must be tightly controlled by SCD [3]. Research has revealed the influence of SCD on lipid metabolism, membrane fluidity, and energy metabolism [6,7,8]. SCD has been identified as an important metabolic control point and is emerging as a promising therapeutic target for the treatment of obesity, diabetes, and other metabolic diseases [3,9]. Some studies point to SCD as a main factor in the control of cancer cell growth [10,11]
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