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Alcohol Clin Exp Res. 2016 Apr;40(4):686-97. doi: 10.1111/acer.13008. Epub 2016 Mar 25.

Alcohol Toxicity in Diabetes and Its Complications: A Double Trouble?

Author information

1
Division of Hypertension and Vascular Research, Department of Internal Medicine, Henry Ford Health System, Detroit, Michigan.
2
Department of Cardiovascular Sciences, Center for Cardiovascular Regeneration, Houston Methodist Research Institute, Houston, Texas.
3
Department of Physiology, Wayne State University, Detroit, Michigan.

Abstract

BACKGROUND:

Eight percent of the U.S. population has been diagnosed with diabetes mellitus (DM), while another large percentage has gone undiagnosed. As the epidemiology of this disease constitutes a larger percentage of the American population, another factor presents a dangerous dilemma that can exacerbate the hazardous effects imposed by DM. Excessive alcohol consumption concerns the health of more than 50% of all adults. When this heavy-alcohol-drinking population overlaps with DM and its complications, the effects can be dangerous. In this review, we term it as "double trouble."

METHODS:

We provide evidence of alcohol-induced exacerbation of organ damage in diabetic conditions. In certain cases, we have explained how diabetes and alcohol induce similar pathological effects.

RESULTS:

Known exacerbated complications include those related to heart diseases, liver damage, kidney dysfunction, as well as retinal and neurological impairment. Often, pathophysiological damage concludes with end-stage disorders and even mortality. The metabolic, cell signaling, and pathophysiological changes associated with "double trouble" would lead to the identification of novel therapeutic targets.

CONCLUSIONS:

This review summarizes the epidemiology, diagnosis, pathophysiology, metabolic, and cell signaling alterations and finally brushes upon issues and strategies to manage the "double trouble."

KEYWORDS:

Alcohol Toxicity; Aldehyde Dehydrogenase; Cell Signaling; Diabetes Mellitus; Epidemiology; Mitochondrial Dysfunction; Pathophysiology

PMID:
27013182
DOI:
10.1111/acer.13008
[Indexed for MEDLINE]

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