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Long-Term Soft Drink & Aspartame
Intake Induces Liver Damage


From Dr. Betty Martini, D.Hum
6-6-17

 
More information on aspartame on www.mpwhi.comwww.holisticmed.com/aspartame, www.aspartamekills.com As I read study after study showing what aspartame causes I think of the FDA saying when science becomes available that shows harm they will do something.  Are they waiting for Armageddon? 

Dr. Betty Martini, D.Hum, Founder
Mission Possible World Health Intl


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Nutr Res. 2017 May;41:47-55. doi: 10.1016/j.nutres.2017.04.002. Epub 2017 Apr 19.

Long-term soft drink and aspartame intake induces hepatic damage via dysregulation of adipocytokines and alteration of the lipid profile and antioxidant status.

Lebda MA1Tohamy HG2El-Sayed YS3.

Author information


Abstract

Dietary intake of fructose corn syrup in sweetened beverages is associated with the development of metabolic syndrome and obesity. We hypothesized that inflammatory cytokines play a role in lipid storage and induction of liver injury. Therefore, this study intended to explore the expression of adipocytokines and its link to hepatic damage. Rats were assigned to drink water, cola soft drink (free access) and aspartame (240 mg/kg body weight/day orally) for 2 months. The lipid profiles, liver antioxidants and pathology, and mRNA expression of adipogenic cytokines were evaluated. Subchronic intake of soft drink or aspartame substantially induced hyperglycemia and hypertriacylglycerolemia, as represented by increased serum glucose, triacylglycerol, low-density lipoprotein and very low-density lipoprotein cholesterol, with obvious visceral fatty deposition. These metabolic syndromes were associated with the up-regulation of leptin and down-regulation of adiponectin and peroxisome proliferator activated receptor- (PPAR- ) expression. Moreover, alterations in serum transaminases accompanied by hepatic oxidative stress involving induction of malondialdehyde and reduction of superoxide dismutase, catalase, and glutathione peroxidase and glutathione levels are indicative of oxidative hepatic damage. Several cytoarchitecture alterations were detected in the liver, including degeneration, infiltration, necrosis, and fibrosis, predominantly with aspartame. These data suggest that long-term intake of soft drink or aspartame-induced hepatic damage may be mediated by the induction of hyperglycemia, lipid accumulation, and oxidative stress with the involvement of adipocytokines.

Copyright 2017 Elsevier Inc. All rights reserved.

KEYWORDS:

Adipocytokines; Aspartame; Gene expression; Metabolic syndrome; Oxidative stress; Sweetened beveragesPMID:
28465000
DOI:
10.1016/j.nutres.2017.04.002
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