Fructose as a key player in the development of fatty liver disease
Open accessAbstract
We aimed to investigate whether increased consumption of fructose is linked to the increased prevalence of fatty liver. The prevalence of nonalcoholic steatohepatitis (NASH) is 3% and 20% in nonobese and obese subjects, respectively. Obesity is a low-grade chronic inflammatory condition and obesity-related cytokines such as interleukin-6, adiponectin, leptin, and tumor necrosis factor-α may play important roles in the development of nonalcoholic fatty liver disease (NAFLD). Additionally, the prevalence of NASH associated with both cirrhosis and hepatocellular carcinoma was reported to be high among patients with type 2 diabetes with or without obesity. Our research group previously showed that consumption of fructose is associated with adverse alterations of plasma lipid profiles and metabolic changes in mice, the American Lifestyle-Induced Obesity Syndrome model, which included consumption of a high-fructose corn syrup in amounts relevant to that consumed by some Americans. The observation reinforces the concerns about the role of fructose in the obesity epidemic. Increased availability of fructose (e.g., high-fructose corn syrup) increases not only abnormal glucose flux but also fructose metabolism in the hepatocyte. Thus, the anatomic position of the liver places it in a strategic buffering position for absorbed carbohydrates and amino acids. Fructose was previously accepted as a beneficial dietary component because it does not stimulate insulin secretion. However, since insulin signaling plays an important role in central mechanisms of NAFLD, this property of fructose may be undesirable. Fructose has a selective hepatic metabolism, and provokes a hepatic stress response involving activation of c-Jun N-terminal kinases and subsequent reduced hepatic insulin signaling. As high fat diet alone produces obesity, insulin resistance, and some degree of fatty liver with minimal inflammation and no fibrosis, the fast food diet which includes fructose and fats produces a gene expression signature of increased hepatic fibrosis, inflammation, endoplasmic reticulum stress and lipoapoptosis. Hepatic de novo lipogenesis (fatty acid and triglyceride synthesis) is increased in patients with NAFLD. Stable-isotope studies showed that increased de novo lipogenesis (DNL) in patients with NAFLD contributed to fat accumulation in the liver and the development of NAFLD. Specifically, DNL was responsible for 26% of accumulated hepatic triglycerides and 15%-23% of secreted very low-density lipoprotein triglycerides in patients with NAFLD compared to an estimated less than 5% DNL in healthy subjects and 10% DNL in obese people with hyperinsulinemia. In conclusion, understanding the underlying causes of NAFLD forms the basis for rational preventive and treatment strategies of this major form of chronic liver disease.
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Poor quality carbohydrates are associated with long-term weight gain, diabetes, and CVD.
“Consistent with this constellation of adverse effects, poor quality carbohydrates are associated with long-term weight gain, diabetes, and CVD.29, 89, 158, 167”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [164]
This rapid digestion may induce multiple adverse effects, potentially stimulating reward/craving areas in the brain, activating hepatic de novo lipogenesis, increasing uric acid production, and promoting visceral adiposity.
“This rapid digestion may induce multiple adverse effects, potentially stimulating reward/craving areas in the brain, activating hepatic de novo lipogenesis, increasing uric acid production, and promoting visceral adiposity.49, 162-166”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [164]
High doses of rapidly digested fructose have little influence on blood glucose or insulin levels, but more directly stimulate hepatic de novo lipogenesis, hepatic and visceral adiposity, and uric acid production.
“In comparison, high doses of rapidly digested fructose have little influence on blood glucose or insulin levels, but more directly stimulate hepatic de novo lipogenesis, hepatic and visceral adiposity, and uric acid production.164-166”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [164]
High doses of rapidly digested glucose induce postprandial hyperglycemia, hyperinsulinemia, and related metabolic disturbances.
“High doses of rapidly digested glucose induce postprandial hyperglycemia, hyperinsulinemia, and related metabolic disturbances.”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [164]
There are important metabolic differences between glucose and fructose.
“In contrast, there are important metabolic differences between glucose and fructose – each equally present in both high-fructose corn syrup and natural sugar (sucrose).”
From Dietary and Policy Priorities for Cardiovascular Disease, Diabetes, and Obesity: A Comprehensive Review (2016) · cites this paper as [164]
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- Authors
- Basaranoglu, M.
- Venue
- World Journal of Gastroenterology
- Publisher
- Baishideng Publishing Group Inc.
- Published
- 2013
- Volume
- 19
- Issue
- 8
- Pages
- 1166
- ISSN
- 1007-9327 (ISSN-L)
- PMC
- PMC3587472
- OpenAlex
- W1982998620
- Cited by
- 235
- References
- 63
- Citations by year
- 2026: 5 · 2025: 11 · 2024: 10 · 2023: 15 · 2022: 11 · 2021: 23 · 2020: 24 · 2019: 24 · 2018: 21 · 2017: 13 · 2016: 23 · 2015: 24 · 2014: 22 · 2013: 8
- FWCI
- 3.79
- Type
- journal article
- Language
- en
- Open access
- hybrid
- doi.org
- Licence
- cc-by-nc
- Locations
- World Journal of Gastroenterology (publishedVersion, cc-by-nc)
- Europe PMC (PubMed Central) (publishedVersion)
- PubMed Central (publishedVersion)
- PubMed (publishedVersion)
- Topics
- Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Diet, Metabolism, and Disease
- Health Sciences › Medicine › Epidemiology › Liver Disease Diagnosis and Treatment
- Health Sciences › Medicine › Pathology and Forensic Medicine › Alcohol Consumption and Health Effects
- Keywords
- fructose, non-alcoholic fatty liver disease, nonalcoholic steatohepatitis, high fructose corn syrup, obesity, insulin resistance, hepatic insulin signaling, c-Jun N-terminal kinase, liver fibrosis, endoplasmic reticulum stress, lipoapoptosis, de novo lipogenesis, hepatic triglycerides, very low density lipoprotein secretion, liver inflammation, type 2 diabetes, plasma lipid profile, fast food diet
- MeSH terms
- Animals, Dietary Carbohydrates, Dietary Fats, Fatty Liver, Fructose, Humans, Insulin Resistance, Liver, Obesity, Risk Factors, Sweetening Agents, Signal Transduction, Inflammation Mediators, Lipogenesis, Fast Foods, Epidemics, Non-alcoholic Fatty Liver Disease
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