Abstract
Carbonic anhydrase is a pH regulatory enzyme, whose inhibition leads to metabolic acidosis. We investigated whether carbonic anhydrase inhibition may be associated with blood lactate accumulation in Streptozotocin (STZ) induced diabetic rats. The study aimed to provide a new marker to assist in identifying diabetic individuals at a high risk of developing lactic acidosis. Erythrocyte carbonic anhydrase activity with 4-nitrophenyl acetate as substrates was investigated in (STZ) induced diabetic rats. STZ induced diabetic rats showed significant increase in erythrocyte carbonic anhydrase (CA) activity of 9.7 ± 0.7 μMol/min/μL and blood lactate level of 6.2 ± 1.2 mMol/L when compared with Non Diabetic group CA enzyme activity of 5.5 ± 0.6 μMol/min/μL and blood lactate level of 3.9 ± 0.5 mMol/L. Inhibition of erythrocyte carbonic anhydrase activity with Acetazolamide results in 6.9 fold increase in blood lactate level when compared with Non diabetic group. Therefore inhibition of Carbonic anhydrase in STZ induced diabetic rats’ result in blood lactate accumulation and reduced blood glucose concentration.
Highlights
Compared with non-diabetics, diabetics produce increased amounts of lactic acid which is the end product of glycolysis in muscle cell and red blood cells
We investigated whether STZ induced diabetes exhibited an effect on erythrocyte carbonic anhydrase activity in vivo
We observe a decrease in glucose level and increase in lactate, cholesterol and triglyceride level in the non-diabetic fasted rats compared to non-diabetic random
Summary
Compared with non-diabetics, diabetics produce increased amounts of lactic acid which is the end product of glycolysis in muscle cell and red blood cells. Metabolic acidosis is the most common serious acid-base disorder complicating diabetes mellitus which poses considerable cellular stress, as alterations in pH affect the structure and activity of many enzymes, which affects cell signaling, transport and metabolic function. It has been reported that MCT dependent lactate-Hflux is facilitated by bicarbonate transporters and carbonic anhydrase (CA) activity in various cells and tissues [4,5,6,7]. Based on the association of carbonic anhydrase with metabolic acidosis, and the accumulating evidence linking carbonic anhydrase with lactate flux across MCT, the study aimed to discover the association of carbonic anhydrase with lactic acid accumulation in diabetes mellitus, we hypothesized that inhibition of carbonic anhydrase, may lead to blood lactate accumulation (BLA)
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