European Journal of Nutrition

, Volume 57, Issue 6, pp 2171–2187 | Cite as

Chronic consumption of fructose in combination with trans fatty acids but not with saturated fatty acids induces nonalcoholic steatohepatitis with fibrosis in rats

  • Sugeedha Jeyapal
  • Uday Kumar Putcha
  • Venkata Surekha Mullapudi
  • Sudip Ghosh
  • Anil Sakamuri
  • Suryam Reddy Kona
  • Sai Santosh Vadakattu
  • Chandana Madakasira
  • Ahamed IbrahimEmail author
Original Contribution



Consumption of Western diet high in fat and fructose has been attributed to the recent epidemic of nonalcoholic fatty liver disease (NAFLD). However, the impact of specific fatty acids on the progression of NAFLD to nonalcoholic steatohepatitis (NASH) is poorly understood. In the present study, we investigated the chronic effects of consumption of fructose in combination with saturated fatty acids (SFA) or trans fatty acids (TFA) on the development of NAFLD.


Male Sprague–Dawley rats were randomly assigned to six isocaloric starch/high fructose (44% of calories), high fat (39% calories) diet containing either starch–peanut oil, fructose–peanut oil, fructose–palmolein, fructose–clarified butter, fructose–coconut oil or fructose–partially hydrogenated vegetable oil and fed for 24 weeks. Palmolein, clarified butter and coconut oil were used as the source of SFA whereas partially hydrogenated vegetable oil was used as the source of TFA. Peanut oil was used as the reference oil.


Long-term feeding of fructose in combination with SFA or TFA induced hepatic steatosis of similar extent associated with upregulation of stearoyl CoA desaturase-1. In contrast, fructose in combination with TFA induced NASH with fibrosis as evidenced by upregulation of hepatic proinflammatory cytokine and fibrogenic gene expression, increased hepatic oxidative stress and adipocytokine imbalance. Histopathological analysis revealed the presence of NASH with fibrosis. Further, peanut oil prevented the development of NAFLD in fructose-fed rats.


Fructose in combination with TFA caused NASH with fibrosis by inducing oxidative stress and inflammation, whereas, fructose in combination with SFA caused simple steatosis, suggesting that the type of fatty acid is more important for the progression of NAFLD.


Western diet High fructose High fat Saturated fatty acids Trans fatty acids Inflammation Oxidative stress Gene expression Nonalcoholic fatty liver disease Nonalcoholic steatohepatitis Fibrosis 



Acetyl CoA carboxylase alpha


Alanine aminotransferases


Aspartate aminotransferases


Area under the curve


Clarified butter


Carbohydrate responsive element binding protein


Coconut oil


Carnitine palmotyl tranferase 1


Enzyme linked immunosorbent assay


Fatty acid methyl ester


Fatty acid synthase


Fructose–peanut oil




Fructose–clarified butter


Fructose–coconut oil


Fructose–partially hydrogenated vegetable oil


Glutathione peroxidase


Reduced glutathione


Hematoxylin and eosin


High-density lipoprotein


Homeostasis model assessment-insulin resistance


Hepatic stellate cells


Interleukin-1 beta




Intraperitoneal glucose tolerance test


Nonalcoholic fatty liver disease


NAFLD Activity score


Nonalcoholic steatohepatitis


Plasminogen activator inhibitor-1


Polymerase chain reaction


Partially hydrogenated vegetable oil


Peanut oil




Peroxisome proliferator-activated receptor alpha


Peroxisome proliferator-activated receptor gamma


Stearoyl CoA desaturase-1


Saturated fatty acid


Superoxide dismutase


Sterol regulatory element binding protein 1c


Thiobarbituric acid reactive substances


Trans fatty acid


Tumor necrosis factor alpha



This study was funded by Grants in aid (5/4/3-7/TF/2011/NCD-II) from Indian Council of Medical Research, Government of India to AI. JS was supported by a fellowship from Indian Council of Medical Research, Government of India.

Author contributions

AI and JS designed the study, analyzed the data and wrote the manuscript. JS, AS, KSR and VSS conducted the animal experiment and prepared the experimental diets. PUK and MVS carried out histopathological analysis of liver and NAS scoring. SG and JS involved in mRNA expression studies by RT-qPCR. JS, KSR and CM carried out biochemical estimations. All the authors read and approved the manuscript.

Compliance with ethical standards

Conflict of interest

All the authors declare no conflict of interest.


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Copyright information

© Springer-Verlag GmbH Germany 2017

Authors and Affiliations

  • Sugeedha Jeyapal
    • 1
  • Uday Kumar Putcha
    • 2
  • Venkata Surekha Mullapudi
    • 2
  • Sudip Ghosh
    • 3
  • Anil Sakamuri
    • 1
  • Suryam Reddy Kona
    • 1
  • Sai Santosh Vadakattu
    • 1
  • Chandana Madakasira
    • 1
  • Ahamed Ibrahim
    • 1
    Email author
  1. 1.Department of Lipid ChemistryNational Institute of NutritionHyderabadIndia
  2. 2.Department of PathologyNational Institute of NutritionHyderabadIndia
  3. 3.Department of Molecular BiologyNational Institute of NutritionHyderabadIndia

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