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Related Experiment Videos

Enzymatic changes in polymorphonuclear cells isolated from type II diabetics.

E Ryder, G Campos, L M Morales-Villalobos

    Biochemical Medicine and Metabolic Biology
    |April 1, 1987
    PubMed
    Summary

    Type II diabetes patients show decreased key glycolytic enzymes in polymorphonuclear cells, suggesting impaired glucose metabolism beyond phosphofructokinase. This metabolic alteration is linked to insulin resistance, not just insulin deficiency.

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    Area of Science:

    • Biochemistry
    • Metabolic Disorders
    • Cellular Biology

    Background:

    • Type II diabetes is characterized by hyperglycemia and insulin resistance.
    • Polymorphonuclear (PMN) cells play a role in inflammatory responses and metabolic processes.
    • Understanding enzyme activity in PMN cells can provide insights into diabetic complications.

    Purpose of the Study:

    • To investigate the activity of specific enzymes involved in glycolysis within PMN cells of Type II diabetic patients.
    • To correlate enzyme levels with glycemic control and insulin resistance markers.

    Main Methods:

    • Isolation of PMN cells from fasting Type II diabetic patients (without insulin treatment) and a control group using the dextran flotation technique.
    • Assay of enzyme activity (phosphofructokinase, lactate dehydrogenase, malate dehydrogenase, hexokinase, glucose-6-phosphate dehydrogenase) in whole cell homogenates.

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  • Measurement of serum glucose and immunoreactive insulin (IRI) levels.

    • Main Results:

    • Significant decreases (40%) in phosphofructokinase and lactate dehydrogenase activities were observed in diabetic PMN cells compared to controls.
    • A 25% decrease in malate dehydrogenase activity was noted in diabetic PMN cells.
    • No significant differences in hexokinase and glucose-6-phosphate dehydrogenase activities were found.
    • Diabetic patients exhibited hyperglycemia and normal to elevated IRI levels, indicating insulin resistance.

    Conclusions:

    • Glycolysis appears to be affected in PMN cells of Type II diabetics, particularly at steps beyond phosphofructokinase.
    • The observed metabolic alterations are more likely attributable to defective insulin action (insulin resistance) rather than a simple lack of insulin.
    • These findings highlight potential cellular mechanisms contributing to metabolic dysfunction in Type II diabetes.