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. 2010 Mar 1;120(4):1069–1083. doi: 10.1172/JCI39191

Figure 5. SLC23A1 SNPs and ascorbate intake.

Figure 5

(A) Distribution of SLC23A1 in kidney nephron segments. Serial Analysis of Gene Expression (SAGE) libraries GSM10419 and GSM10423–GSM10429 (53) containing expression data from microdissected glomeruli and 6 different nephron segments were interrogated (54); values are expressed as tags per million. (B) Effect of SLC23A1 SNPs on ascorbate transport. X. laevis oocytes were microinjected with the following SLC23A1 cRNAs: common type; sham injected; human deletion construct; and SNPs A652G rs34521685, G790A rs33972313, A772G rs35817838, and C180T rs6886922. (C) Population prevalences of SLC23A1 polymorphisms. Shown are averaged minor allelic frequencies of SLC23A1 genotypes in African (n = 48), American-African (n = 438), and white (n = 1,874) individuals, using pooled genotype data (35, 55, 56). (D) Modeled effects of SLC23A1 polymorphisms on plasma ascorbate concentrations in humans. Values in healthy young women for common type SLC23A1 are measured (stars; ref. 11) and calculated fasting steady-state plasma ascorbate concentrations. For women with SNPs, values are calculated. (E) Percentiles of 19- to 30-year-old, pregnant, and lactating women in relation to range of ascorbate plasma concentrations and intake. Plasma concentrations as a function of intake were calculated based on dose concentration pharmacokinetics data (D and ref. 11). Percentiles of women with varying intakes used food intake data (8); the y axis is not continuous because of the sigmoid relationship between ascorbate intake and plasma concentration (D and ref. 11).