Glucose inhibits myo-inositol uptake and reduces myo-inositol content in cultured rat glomerular mesangial cells
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Cited by (74)
miR-125a-5p impairs the metastatic potential in breast cancer via IP<inf>6</inf>K1 targeting
2021, Cancer LettersCitation Excerpt :We next evaluated whether myo-Ins treatment was capable of impact cancer cell metabolism. Negative feedback exists between myo-Ins and glucose, where high glucose concentrations inhibit myo-Ins uptake [30,31]. The expression of GLUT1 in triple-negative breast cancer and MCF-10A cells highlighted the ability of myo-Ins to inhibit the transcription of the glucose transporter (Fig. 5G and Figs. S5A–D).
Potential role of myo-inositol to improve ischemic stroke outcome in diabetic mouse
2018, Brain ResearchCitation Excerpt :Previous reports showed that glucose competes with myo-inositol and can reduce myo-inositol uptake in rat glomerular mesangial cells. Lower levels of myo-inositol may prevent the cerebrovascular benefit of osmoltye protection, which could partially explain why diabetic patients have more edema post-ischemic stroke as compared to non-diabetics (Haneda et al., 1990). The overall aim of the present study was to investigate the role of myo-inositol in ischemic stroke and to assess if myo-inositol by exogenous administration aids in improving ischemic outcome in both non-diabetic and diabetic animal models.
Heparin prevents intracellular hyaluronan synthesis and autophagy responses in hyperglycemic dividing mesangial cells and activates synthesis of an extensive extracellular monocyte-adhesive hyaluronan matrix after completing cell division
2014, Journal of Biological ChemistryCitation Excerpt :In response to high glucose, both renal mesangial and proximal tubule cells accumulate sorbitol (42). Furthermore, increased expression of the AR gene has been observed in response to hyperglycemic glucose in mesangial cell cultures and in experimental animal models (42–44), which could be regulated by an osmotic response element involving PKC activity. Particularly pertinent to our study, the AR promoter also contains a CCAAT-box (45), suggesting that AR can be regulated by C/EBPα, and the product of this pathway, fructose, can enter the hexosamine pathway and provide increases in the substrates for hyaluronan synthesis (46).
Uric Acid as a Mediator of Diabetic Nephropathy
2011, Seminars in Nephrology