Metabolic Activity of Diabetic Monocytes

Author:

Kitahara Mitsuo1,Eyre Harmon J1,Lynch Robert E1,Rallison Marvin L1,Hill Harry R1

Affiliation:

1. Howard Hughes Medical Institute Laboratories, the Division of Clinical Immunology and Allergy, and the Division of Hematology and Oncology; Departments of Medicine, Pediatrics, and Pathology, University of Utah Salt Lake City Utah. Dr. Lynch is an Associate Investigator, Dr. Hill is an Investigator of the Institute

Abstract

There have been several reported abnormalities in the cellular components of the acute inflammatory response in diabetes mellitus. These studies have dealt primarily with polymorphonuclear leukocytes. In the present investigations, we have examined monocyte metabolic activity in diabetic patients and controls. Following particle ingestion, the microbicidal mechanisms of the monocyte are activated and excited molecular oxygen and carboxyl groups are generated. Upon decay to the ground state, these molecules emit photons, which can be measured as chemiluminescence. Chemiluminescence production was significantly increased in 27 patients with poorly controlled diabetes (blood glucose levels from 208 to 712 mg/dl). The mean peak in the diabetics was 31.3 ± 8.2 (SD) × 103 cpm versus 25.8 ± 3.8 × 103 cpm in controls. Hexose monophosphate shunt activity as determined by 14 C-I-glucose utilization was also increased (667 ± 284 percent increase in diabetics versus 425 ± 154 in controls). Superoxide dismutase-inhibitable superoxide production was also significantly augmented in diabetic monocytes (9.77 ± 3.06 nmol/106 monocytes/20 min versus 6.36 ± 1.10 nmol). Addition of glucose to whole blood from a normal individual, or to normal or diabetic monocyte suspensions, resulted in marked enhancement of chemiluminescence production. Increasing blood sugar levels appear, therefore, to be associated with monocyte metabolic activation in diabetic patients. Such activation could conceivably be detrimental to the diabetic host by contributing to cell damage through the release of toxic oxygen products.

Publisher

American Diabetes Association

Subject

Endocrinology, Diabetes and Metabolism,Internal Medicine

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