Oxidation Model of Diabetes Validated – 20 Years Later

Majid Ali, M.D.

I published my oxidative model of diabetes in 1995. It was fully validated By Canadian Journal of Diabetes in 2015.


 

In my book RDA – Rats, Drugs, and Assumptions  (1995), on pages 277-280 I presented my oxidative theories of diabetes and Alzheimer’s disease. My purpose in presenting my oxidative theory of Type 2 diabetes (T2D) and Alzheimer’s disease (AD) together was to challenge the then-prevailing notions that T2D is caused by inappropriate secretion and functions of a pancreatic hormone amylin, as well as deposits of amyline protein in the pancreas and Alzheimer’s disease is caused by deposits of amyloid protein in the brain. My basic argument then was that both amylin and amyloid proteins are deposited as a result of oxidative damage to tissues and cannot be considered as root causes of T2D and AD.


Title and Abstract of the Article inCanadian Journal of Diabetes
Aouacheri  Q, Saka S, Krim M, et al. The Investigation of the Oxidative Stress-Related Parameters in Type 2 Diabetes Mellitus. 2015;39:44-49.
Abstract
Introduction
analysisResultsDiscussionConclusionAcknowledgementsAuthor DisclosuresReferences
Objective
Oxidative stress, defined as an imbalance between reactive oxygen species production and breakdown by endogenous antioxidants, is closely associated with diabetes mellitus. The diabetes is characterized by hyperglycemia together with biochemical alterations of glucose and lipid peroxidation. Oxidative stress has been implicated in the pathogenesis of type 2 diabetes and its complications.
Methods
This study was conducted to investigate the variation in oxidative stress-related parameters in type 2 diabetes. Blood serum samples were collected from diabetes patients and nondiabetes healthy controls. Glucose concentrations, levels of glycated hemoglobin (A1C) and serum oxidative stress markers (glucose-6-phosphate dehydrogenase [G6PDH], malondialdehyde [MDA], glutathione [GSH], glutathione reductase [GR], glutathione peroxidase [GPx] and superoxide dismutase [SOD]) were estimated.
Results
Fasting serum glucose concentration in type 2 diabetes patients of both sexes was increased significantly as compared with the healthy controls. Level of A1C was greater than standards. Significant elevation in MDA level and depletion in GSH content were observed in diabetes patients in comparison with controls. The diminution in G6PDH activity was accompanied in part by a decrease in the antioxidative enzymes activities (GPx and GR), and in part by an increase in SOD activity in all diabetes patients as compared with the control group. The regression analysis showed no correlation between diabetes duration and severity of oxidative stress; however, there was a significant association between A1C and severity of oxidative stress.
Conclusions
The present study shows that there is an oxidative stress state in type 2 diabetes patients compared with healthy subjects. Our data suggest that chronic hyperglycemia causes a significant change in oxidative stress markers.

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