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The polymorphonuclear leukocyte in diabetes mellitus
Journal of Clinical Chemistry and Clinical Biochemistry. Zeitschrift Fur Klinische Chemie Und Klinische Biochemie
|September 1, 1983
Summary
Diabetic patients show impaired glycolysis and glycogen synthesis in leukocytes due to reduced enzyme activity. Insulin treatment may restore the key synthase-phosphatase activity crucial for glucose metabolism.
Area of Science:
- Biochemistry
- Cell Biology
- Metabolic Disorders
Background:
- Polymorphonuclear leukocytes (PMNs) play a role in immune response and glucose metabolism.
- Diabetes mellitus is associated with altered cellular metabolic pathways.
- Glycogen synthesis and glycolysis are key energy-producing pathways in leukocytes.
Purpose of the Study:
- To investigate the defects in glycolysis and glycogen synthesis in leukocytes of diabetic patients.
- To elucidate the role of glycogen synthase activity and its regulation.
- To explore the potential impact of insulin treatment on these metabolic abnormalities.
Main Methods:
- Assessed phosphofructokinase activity and glycogen content in leukocytes.
- Measured glycogen synthesis rates and glycogen synthase activity.
- Investigated enzyme phosphorylation/dephosphorylation using microsomal fractions and calcium ion dependency.
Main Results:
- Severely diabetic patients exhibited decreased glycolysis and glycogen synthesis rates in leukocytes.
- Reduced phosphofructokinase activity and impaired glycogen synthase activation were observed.
- A specific synthase-phosphatase activity, dependent on Ca2+, was hypothesized to be deficient and restored by insulin.
Conclusions:
- Leukocyte dysfunction in diabetes involves impaired glucose metabolism due to reduced enzyme activities.
- Defective synthase-phosphatase activity is a key factor contributing to impaired glycogen synthesis in diabetic leukocytes.
- Insulin treatment shows potential to restore this critical phosphatase activity and improve leukocyte glucose metabolism.