Modifications in the abundance of solute-carrier (SLC) transcripts in tandem with adjustments in genes-associated with energy homeostasis during the postpartum transition of the mammary epithelial cells (MEC) from nonsecretory to secretory is pivotal for supporting milk synthesis. The goal of this study was to identify differentially expressed SLC genes across key metabolic tissues between late pregnancy and onset of lactation. Total RNA was isolated from the mammary, liver, and adipose tissues collected from rat dams on day 20 of pregnancy (P20) and day 1 of lactation (L1) and gene expression was measured with Rat 230 2.0 Affymetrix GeneChips. LIMMA was utilized to identify the differential gene expression patterns between P20 and L1 tissues. Transcripts engaged in conveying anions, cations, carboxylates, sugars, amino acids, metals, nucleosides, vitamins, and fatty acids were significantly increased (P < 0.05) in MEC during the P20 to L1 shift. Downregulated (P < 0.05) genes in the mammary during the physiological transition included GLUT8 and SLC45a3. In the liver, SLC genes encoding for anion, carbonyl, and nucleotide sugar transporters were upregulated (P < 0.05) at L1. while genes facilitating transportation of anions and hexose were increased (P < 0.05), from P20 to L1 in the adipose tissue. GLUT1 and GLUT4 in the liver, along with GLUT4 and SGLT2 in the adipose tissue, were repressed (P < 0.05) at L1. Our results illustrate that MEC exhibit dynamic molecular plasticity during the nonsecretory to secretory transition and increase biosynthetic capacity through a coordinated tissue specific SLC transcriptome modification to facilitate substrate transfer.

中文翻译：

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在乳腺上皮细胞从非分泌型到分泌型的产后进化过程中，分析关键代谢组织中的溶质-载体转运蛋白。

乳腺上皮细胞（MEC）从非分泌型向分泌型过渡后，溶质载体（SLC）转录本的大量修饰与能量稳态相关基因的调节是支持牛奶合成的关键。这项研究的目的是鉴定妊娠晚期和哺乳期之间关键代谢组织中差异表达的SLC基因。在怀孕第20天（P20）和哺乳第1天（L1）从大鼠大坝收集的乳腺，肝脏和脂肪组织中分离总RNA，并用Rat 230 2.0 Affymetrix GeneChips测量基因表达。LIMMA用于鉴定P20和L1组织之间的差异基因表达模式。参与传送阴离子，阳离子，羧酸盐，糖，氨基酸，金属，核苷的转录物，在P20向L1转变期间，MEC中的维生素和脂肪酸显着增加（P <0.05）。在生理转变过程中，乳腺中的下调基因（P <0.05）包括GLUT8和SLC45a3。在肝脏中，编码L1的阴离子，羰基和核苷酸糖转运蛋白的SLC基因上调（P <0.05）。而促进阴离子和己糖转运的基因从脂肪组织中的P20到L1增加（P <0.05）。肝脏中的GLUT1和GLUT4以及脂肪组织中的GLUT4和SGLT2在L1时被抑制（P <0.05）。我们的结果表明，MEC在非分泌到分泌的过渡过程中表现出动态的分子可塑性，并通过协调的组织特异性SLC转录组修饰来促进底物转移，从而提高了生物合成能力。在P20向L1转变期间，MEC中的脂肪酸显着增加（P <0.05）。在生理转变过程中，乳腺中的下调基因（P <0.05）包括GLUT8和SLC45a3。在肝脏中，编码L1的阴离子，羰基和核苷酸糖转运蛋白的SLC基因上调（P <0.05）。而促进阴离子和己糖转运的基因从脂肪组织中的P20到L1增加（P <0.05）。肝脏中的GLUT1和GLUT4以及脂肪组织中的GLUT4和SGLT2在L1时被抑制（P <0.05）。我们的结果表明，MEC在非分泌到分泌的过渡过程中表现出动态的分子可塑性，并通过协调的组织特异性SLC转录组修饰来促进底物转移，从而提高了生物合成能力。在P20向L1转变期间，MEC中的脂肪酸显着增加（P <0.05）。在生理转变过程中，乳腺中的下调基因（P <0.05）包括GLUT8和SLC45a3。在肝脏中，编码L1的阴离子，羰基和核苷酸糖转运蛋白的SLC基因上调（P <0.05）。而促进阴离子和己糖转运的基因从脂肪组织中的P20到L1增加（P <0.05）。肝脏中的GLUT1和GLUT4以及脂肪组织中的GLUT4和SGLT2在L1时被抑制（P <0.05）。我们的结果表明，MEC在非分泌到分泌的过渡过程中表现出动态的分子可塑性，并通过协调的组织特异性SLC转录组修饰来促进底物转移，从而提高了生物合成能力。