Hypoglycemia increases expression of several genes upregulated by hyperglycemia
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| Year of publication | 2014 |
| Type | Conference abstract |
| MU Faculty or unit | |
| Citation | |
| Description | Hyperglycemia-induced overproduction of mitochondrial reactive oxygen species (ROS) is the key event in the development and progression of diabetic microvascular complications. ROS activates several harmful pathways including increased production of advanced glycation end products (AGEs), increased expression of receptor for AGEs or polyol pathway flux. The effect of hypoglycemia on pathways activated by hyperglycemia is much less explored. Therefore we aimed to test the effect of low glucose on the expression of proteins/enzymes with established role in the hyperglycemia-driven cell damage in vitro. Specifically, we evaluated mRNA expression of superoxide dismutase (SOD1), heme oxygenase (HMOX), p65 subunit of nuclear factor kappa B, glyoxalase 1 (GLO1), receptor for advanced glycation end products and DJ-1 (an enzyme with established glyoxalase activity). Primary human umbilical vein endothelial cells were grown in EBM2 medium for 48 hours and then cultured for 24 hours in medium with different content of glucose: (i) normoglycemic (5.5 mmol/l), (ii) hyperglycemic (25.5 mmol/l) and (iii) hypoglycemic (2.75 mmol/l). Total RNA was extracted and reverse transcribed using commercial kits (Roche). Gene expression was determined using predesigned TaqMan probes (Life Technologies). Results were normalized to 18-S RNA. mRNA expression of all studied genes was increased in response to hyperglycemia compared to normoglycemia as expected although statistical significance was reached only in case of SOD1 and p65 (P < 0.05). Similar trends were observed in low glucose conditions compared to normoglycemia with exception of HMOX expression which was slightly but not significantly lower (P > 0.05). Our results suggest that hypoglycemia may have similar effect on primary endothelial cells with respect to established damaging pathways. |
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