Liver damage due to aspartame linked to adipocytokines
03/20/2019 // Michelle Simmons // Views

A study shows that consumption of soft drinks and aspartame induces liver damage through dysregulation of adipocytokines and induction of hyperglycemia, lipid accumulation, and oxidative stress. The findings of the study were published in the journal Nutrition Research.

  • Consumption of fructose corn syrup in sweetened beverages is linked to the development of metabolic syndrome and obesity.
  • Researchers at Alexandria University and Damanhour University in Egypt hypothesized that inflammatory cytokines play a role in lipid storage and induction of liver injury.
  • For the study, the researchers examined the expression of adipocytokines and its link to liver damage.
  • To test their hypothesis, rats in the study received water, cola soft drink, and aspartame every day for two months.
  • Then, the researchers measured the rats' lipid profiles, liver antioxidants and pathology, and mRNA expression of adipogenic cytokines.
  • The results revealed that the consumption of soft drink and aspartame significantly induced metabolic syndromes hyperglycemia and hypertriacylglycerolemia.
  • Soft drink and aspartame intake also elevated transaminases and caused changes in the antioxidant status of the rats' liver, increasing oxidative stress and reducing antioxidant levels – all of which are indicative of oxidative liver damage.
  • Liver degeneration, infiltration, necrosis, and fibrosis were also detected, especially in rats given aspartame.

These findings, in sum, indicate that long-term consumption of soft drink or aspartame causes liver damage.

To read more studies on the harmful effects of soft drink and aspartame consumption, visit Aspartame.news.

Journal Reference:

Lebda MA, Tohamy HG, El-Sayed YS. LONG-TERM SOFT DRINK AND ASPARTAME INTAKE INDUCES HEPATIC DAMAGE VIA DYSREGULATION OF ADIPOCYTOKINES AND ALTERATION OF THE LIPID PROFILE AND ANTIOXIDANT STATUS. Nutrition Research. May 2017;47-55. DOI: 10.1016/j.nutres.2017.04.002



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