Hidden chronic metabolic acidosis of diabetes type 2 (CMAD): Clues, causes and consequences

Interpretation of existing data revealed that chronic metabolic acidosis is a pathognomic feature for type 2 diabetes (T2D), which is described here as “chronic metabolic acidosis of T2D (CMAD)” for the first time. The biochemical clues for the CMAD are summarised in the following; low blood bicarbo...

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Bibliographic Details
Published in:Reviews in endocrine & metabolic disorders 2023-08, Vol.24 (4), p.735-750
Main Author: Giha, Hayder A.
Format: Article
Language:English
Subjects:
Acidosis
Acidosis - etiology
Acidosis - therapy
Amino acids
Bicarbonates
Carbonates
Chronic Disease
Diabetes
Diabetes mellitus (non-insulin dependent)
Diabetes Mellitus, Type 2 - complications
Diabetes Mellitus, Type 2 - metabolism
Diabetes Mellitus, Type 2 - physiopathology
Diabetes Mellitus, Type 2 - therapy
Endocrinology
Extracellular Space - chemistry
Extracellular Space - metabolism
Gastrointestinal Microbiome
Humans
Hydrogen-Ion Concentration
Insulin resistance
Internal Medicine
Intestinal microflora
Ion Transport
Medicine
Medicine & Public Health
Metabolic acidosis
Metabolism
Oxidative stress
Pantoprazole
Protons
Type 2 diabetes
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Summary:Interpretation of existing data revealed that chronic metabolic acidosis is a pathognomic feature for type 2 diabetes (T2D), which is described here as “chronic metabolic acidosis of T2D (CMAD)” for the first time. The biochemical clues for the CMAD are summarised in the following; low blood bicarbonate (high anionic gap), low pH of interstitial fluid and urine, and response to acid neutralization, while the causes of extra protons are worked out to be; mitochondrial dysfunction, systemic inflammation, gut microbiota (GM), and diabetic lung. Although, the intracellular pH is largely preserved by the buffer system and ion transporters, a persistent systemic mild acidosis leaves molecular signature in cellular metabolism in diabetics. Reciprocally, there are evidences that CMAD contributes to the initiation and progression of T2D by; reducing insulin production, triggering insulin resistance directly or via altered GM, and inclined oxidative stress. The details about the above clues, causes and consequences of CMAD are obtained by searching literature spanning between 1955 and 2022. Finally, the molecular bases of CMAD are discussed in details by interpretation of an up-to-date data and aid of well constructed diagrams, with a conclusion unravelling that CMAD is a major player in T2D pathophysiology. To this end, the CMAD disclosure offers several therapeutic potentials for prevention, delay or attenuation of T2D and its complications.
ISSN:1389-9155
1573-2606
DOI:10.1007/s11154-023-09816-2