Study Summary of “Adverse effects of fructose on cardiometabolic risk factors and hepatic lipid metabolism in subjects with abdominal obesity”

For your information, a study entitled “Adverse effects of fructose on cardiometabolic risk factors and hepatic lipid metabolism in subjects with abdominal obesity” was recently published in the Journal of Internal Medicine. The purpose of this study by Taskinen et al. was to determine the effects of fructose on liver fat development, body composition, dietary intake, cardiometabolic risk markers, hepatic de novo lipogenesis, and postprandial responses to a standardized oral fat tolerance test (OFTT).

Seventy-one “obese healthy men” between the ages of 20 and 65 for the study at four clinical centers (Helsinki, Finland; Naples, Italy; Quebec, Canada; and Gothenburg, Sweden) completed the study. Inclusion criteria included: large waist circumference (>96 cm), body mass index (BMI) between 27 and 40 kg/m2, stable weight over the preceding 3 months, a low-density lipoprotein (LDL) <4.5 mmol/L, and serum triglycerides (TG) <5.5 mmol/L. Smoking, excessive alcohol consumption, and diagnoses of type 2 diabetes, cardiovascular disease, hepatic and renal diseases, gastroenterological, thyroid, or hematological abnormalities, or any chronic disease requiring medication (other than hypertension) or hormone therapy were considered grounds for exclusion.

The 12-week study intervention required that participants consume 75g of fructose daily, provided as three 330ml bottles of lemon-flavored carbonated beverage. During the intervention, participants were asked to consume their habitual ad libitum diet and were required to keep a 3-day food record prior to the intervention and again within 2 weeks of completing the study. Participants also met with a dietitian weekly to monitor weight and compliance to the study protocol. Prior to the study and within 2 weeks of completing the study, participants were also required to complete 4 separate study visits to include: an oral glucose tolerance test (OGTT), an OFTT, a heparin test, and magnetic resonance examinations.

Researchers report the following results:

  • At baseline, the energy provided by fructose was 2.5±0.2%. At the time of the intervention, energy provided by fructose increased to 14.7±0.3%.
  • Participants compensated for the additional calories provided from the fructose beverages. The total increased energy intake during the intervention was approximately 54kcals and not statistical significance.
  • Intakes of sucrose, protein, total fat, saturated fat, and unsaturated fatty acids was lower during the fructose intervention. Intake of cholesterol, total fiber, and alcohol was not significantly during the intervention.
  • After the fructose intervention, there were small but significant increases in weight (1.1±1.7%) and waist circumference (0.67±2.5%). However, there were large variations in individual weight response to the fructose treatment. Of the participants, 37 gained >1kg, 26 maintained their weight, and 8 lost >1kg.
  • After fructose treatment, liver fat content increased by approximately 10%. There were no changes in subcutaneous or visceral fat.  Changes of liver fat content correlated with:
    • Weight (r=0.26)
    • Subcutaneous fat (r=0.37)
    • Insulin (r=0.25)
    • Homeostatic model assessment (HOMA) (r=.31)
  • Those who gained the most liver fat had slightly lower fructose intake levels at baseline compared to those who lost liver fat (11.0±7.0 versus 16.4±9.1).
  • Analysis of polymorphisms PNPLA3, TM6SF2, and MBOAT7 determined that these polymorphisms did not explain the different responses between those who gained liver fat and those who lost it.
  • Plasma TG and apoB48 following the OFTT were augmented by the fructose intervention demonstrating higher levels for approximately 120 minutes after the meal.  There were no changes in AUCs of TG and apoB48 in chylomicrons, VLDL1 or VLDL2 after the fructose intervention.
  • The fructose intervention also resulted in significantly higher systolic blood pressure, fasting insulin, HOMA index, fasting serum TG levels, and apoC-III.
  • Fructose intervention was not associated with significant changes in heart rate, fasting free fatty acids, FGF-21, uric acid concentrations, or in glucose or insulin AUCs during OGTT.
  • There was a significant increase in DNL following fructose feeding in the fasting state and at 4 and 8 hours postprandially. Conversely, fructose feeding resulted in a significant decrease in fasting levels of β-hydroxybutyrate, a marker of hepatic β-oxidation.
  • Multivariate regression analysis showed that changes in subcutaneous fat, FGF-21, apoC-III, saturated fat intake, fructose intake, DNL and total fat intake accounted for 27% of the variance in liver fat response to the diet intervention but no one single variable explained more than 5% of the variance alone.
  • Multivariate regression analysis showed that changes in apoC-III, DNL, insulin, HOMA, weight, saturated fat intake, and total fat intake accounted for 73.7% of the variance in TG AUC change after fructose intervention. ApoC-III was the strongest predictor for the change in TG AUC, explaining 59% of the variance. DNL explained 16% of the variance.

Taskinen et al. conclude that “a real world daily consumption of fructose-sweetened beverages for 12 weeks had significant but modest adverse effects on multiple cardiometabolic risk factors…Out study also indicates that there are remarkable individual differences in susceptibility to visceral adiposity/liver fat deposition and that such differences play a role in modulating the health hazard associated with chronic consumption of fructose-containing beverages.”


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