{"type": "root", "children": [{"type": "p", "children": [{"type": "t", "text": "\nRecent studies have revealed that the glucose transporter in question is expressed in multiple tissues. In adipose tissue, it is found in both mature adipocytes and stromal vascular cells, indicating a potential role in energy metabolism, while in the cochlea it localizes to the cuticular plate of hair cells—suggesting it may facilitate glucose transport across specialized cellular barriers."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "1"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn vascular and mitochondrial contexts, this transporter has been shown to localize predominantly within mitochondria, where it mediates the uptake of dehydroascorbic acid (the oxidized form of ascorbic acid). Through this mechanism, the transporter helps maintain intracellular vitamin C levels, thereby safeguarding cells—especially vascular smooth muscle cells—from oxidative stress. In models of arterial tortuosity syndrome, compromised function of the transporter has been linked to impaired ascorbate compartmentalization, defective extracellular matrix formation, and aberrant mitochondrial redox balance."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "3", "end_ref": "5"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nFurthermore, the transporter plays a pivotal role in metabolic regulation. By ensuring sufficient intracellular ascorbic acid, it supports ascorbate‐dependent DNA demethylation and activates the expression of key adipogenic genes—thereby promoting adipogenesis and proper white adipose tissue development, which in turn contributes to systemic glucose homeostasis. In vascular smooth muscle cells, its activity is linked to the maintenance of the contractile phenotype via a TET2/3‐mediated pathway that preserves mitochondrial function. Complementary observations in skeletal muscle suggest that perturbations in other regulatory factors can lead to compensatory alterations in its expression during critical developmental windows."}, {"type": "fg", "children": [{"type": "fg_fs", "start_ref": "6", "end_ref": "8"}]}, {"type": "t", "text": "\n"}]}, {"type": "t", "text": "\n\n"}, {"type": "p", "children": [{"type": "t", "text": "\nIn addition to its role in metabolic tissues and vascular cells, a novel testis‐specific gene—C17ORF64—has been identified that displays a restricted expression pattern in the testes. This gene appears to act as a negative regulator of cell viability by promoting apoptosis and enforcing G1/S cell cycle arrest, as evidenced by the modulation of apoptosis‐associated proteins. Although distinct from the aforementioned transporter functions, this discovery underscores the broader complexity of nutrient transporter and regulatory gene networks in maintaining tissue homeostasis."}, {"type": "fg", "children": [{"type": "fg_f", "ref": "9"}]}, {"type": "t", "text": "\n"}]}, {"type": "rg", "children": [{"type": "r", "ref": 1, "children": [{"type": "t", "text": "I Stuart Wood, Leif Hunter, Paul Trayhurn "}, {"type": "b", "children": [{"type": "t", "text": "Expression of Class III facilitative glucose transporter genes (GLUT-10 and GLUT-12) in mouse and human adipose tissues."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biochem Biophys Res Commun (2003)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1016/s0006-291x(03)01322-6"}], "href": "https://doi.org/10.1016/s0006-291x(03"}, {"type": "t", "text": "01322-6) PMID: "}, {"type": "a", "children": [{"type": "t", "text": "12890477"}], "href": "https://pubmed.ncbi.nlm.nih.gov/12890477"}]}, {"type": "r", "ref": 2, "children": [{"type": "t", "text": "Bei Chen, Yunfeng Wang, Manying Geng, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Localization of Glucose Transporter 10 to Hair Cells' Cuticular Plate in the Mouse Inner Ear."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Biomed Res Int (2018)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1155/2018/7817453"}], "href": "https://doi.org/10.1155/2018/7817453"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "30013986"}], "href": "https://pubmed.ncbi.nlm.nih.gov/30013986"}]}, {"type": "r", "ref": 3, "children": [{"type": "t", "text": "B L Callewaert, B L Loeys, C Casteleyn, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Absence of arterial phenotype in mice with homozygous slc2A10 missense substitutions."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Genesis (2008)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1002/dvg.20409"}], "href": "https://doi.org/10.1002/dvg.20409"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "18693279"}], "href": "https://pubmed.ncbi.nlm.nih.gov/18693279"}]}, {"type": "r", "ref": 4, "children": [{"type": "t", "text": "Yi-Ching Lee, Hsun-Yi Huang, Chia-Jung Chang, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Mitochondrial GLUT10 facilitates dehydroascorbic acid import and protects cells against oxidative stress: mechanistic insight into arterial tortuosity syndrome."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2010)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddq286"}], "href": "https://doi.org/10.1093/hmg/ddq286"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "20639396"}], "href": "https://pubmed.ncbi.nlm.nih.gov/20639396"}]}, {"type": "r", "ref": 5, "children": [{"type": "t", "text": "Annekatrien Boel, Joyce Burger, Marine Vanhomwegen, et al. "}, {"type": "b", "children": [{"type": "t", "text": "Slc2a10 knock-out mice deficient in ascorbic acid synthesis recapitulate aspects of arterial tortuosity syndrome and display mitochondrial respiration defects."}]}, {"type": "t", "text": " "}, {"type": "i", "children": [{"type": "t", "text": "Hum Mol Genet (2020)"}]}, {"type": "t", "text": " DOI: "}, {"type": "a", "children": [{"type": "t", "text": "10.1093/hmg/ddaa071"}], "href": "https://doi.org/10.1093/hmg/ddaa071"}, {"type": "t", "text": " PMID: "}, {"type": "a", "children": [{"type": "t", "text": "32307537"}], "href": "https://pubmed.ncbi.nlm.nih.gov/32307537"}]}, {"type": "r", "ref": 6, "children": [{"type": "t", "text": "Chung-Lin Jiang, Wei-Ping Jen, Chang-Yu Tsao, et al. 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