The negative and detrimental effects of high fructose on the liver, with special reference to metabolic disorders

Diabetes, Metabolic Syndrome and Obesity:
Targets and Therapy 2019:12 821–826

Brandon H. Mai and Liang-Jun Yan.

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Objective

• This
  review focuses the discussion on the hepatic manifestations of high
  fructose-implicated liver metabolic disorders such as insulin resistance, obesity
  due to enhanced lipogenesis, non-alcoholic fatty liver disease (NAFLD),
  nonalcoholic steatohepatitis (NASH), and type 2 diabetes.

Background

• The increased consumption of fructose in the
  average diet through sweeteners such as high-fructose corn syrup (HFCS)
  and sucrose has resulted in negative outcomes in society through producing
  a considerable economic and medical burden on our healthcare system.
• Ingestion of fructose chronically has
  contributed to multiple health consequences, such as insulin resistance,
  obesity, liver disorders, and diabetes.
• Fructose metabolism starts with fructose
  phosphorylation by fructose kinase in the liver, and this process is not
  feedback regulated. Therefore, ingestion of high fructose can deplete ATP,
  increase uric acid production, and increase nucleotide turnover.

Methods

• No methodology was reported in this review.

Findings

• Studies have shown that hyperuricemia is associated
  with both NAFLD and NASH. Among the potential causes found, impaired beta
  oxidation of fatty acids in the liver and enhanced de novo lipogenesis are
  thought to contribute most towards this outcome.
• Fructokinase C has been especially noted to
  facilitate this fat accumulation in the liver via uric acid generation, a
  decrease of ATP, and increased nucleotide turnover.
• Still, there are contradictory findings in some
  studies that suggest fructose consumed over shorter durations or in lower
  doses may not express these relationships. Additionally, it should be
  noted that there are likely many other factors that contribute towards the
  magnitude of the effects of fructose which should be taken into
  consideration, such as physical inactivity and other dietary components,
  as well as gestation and lactation periods which lead to deep metabolic
  changes in mothers and in their progeny via metabolic early programming.

Conclusions

• Further
  research with larger clinical trials that examine the effects of lowering
  HCFS and sugar consumption as well as uric acid levels is warranted to confirm
  the impact of fructose on health.
• Further
  investigation to gain a better understanding of inhibiting or disrupting
  fructose metabolism in the liver and its effects on specific metabolic
  regulators may potentially lead to innovative solutions towards chronic
  liver disorder prevention and treatment that can change the landscape of healthcare.

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