The expression of T1R2 and T1R3 in renal tissue was detected by immunohistochemistry (Figure 2(a)), immunofluorescence (Figure 2(b)), and Western blotting (Figure 2(c)).
To determine whether STRs are regulated by glucose in renal innate cells, we first detected T1R2 and T1R3 expression in GMCs (SV-40 MES 13) and human proximal tubular cells (HK-2).
As expected, high-glucose-inhibited T1R2 and T1R3 expression in SV-40 MES 13 cells (Figure 4(b)) and HK-2 cells (Figure 4(c)) was obviously reversed by lactisole in a dose-dependent manner (p < 0.05).
Previous research showed that the intestinal STRs, T1R2 and T1R3, were expressed in distinct epithelial cells in the human proximal intestine and that their transcript levels varied with glycemic status in patients with type 2 diabetes [11, 19].
Karimian Azari et al., "Disruption of the sugar-sensing receptor T1R2 attenuates metabolic derangements associated with diet-induced obesity," American Journal of Physiology-Endocrinology and Metabolism, vol.
Representative images of immunohistochemistry (a) and immunofluorescence (b) staining showed that T1R2 and T1R3 expression was downregulated in renal tissue of DM mouse models.