December 04, 2013
1 min read
Save

No direct relationship observed between NAFLD, sugar intake

You've successfully added to your alerts. You will receive an email when new content is published.

Click Here to Manage Email Alerts

We were unable to process your request. Please try again later. If you continue to have this issue please contact customerservice@slackinc.com.

Despite studies suggesting fructose contributes more to nonalcoholic fatty liver disease than glucose, recent study results found little difference related to ingestion of the sugars and a far greater relationship between disease progression and caloric intake.

“Overweight men who were on a high-fructose or a high-glucose diet did not develop any significant changes in hepatic concentration of TAGs [triacylglycerols] or serum levels of liver enzymes,” the researchers wrote. “However, in the hypercaloric period, both high-fructose and high-glucose diets produced significant increases … without any significant difference between the two groups.”

Researchers analyzed 32 men (aged 18 to 50 years) with a BMI between 25 and 32 and a waist circumference greater than 94 cm in the randomized, double blind study. Participants were given a moderate high-fructose or high-glucose diet for 2 weeks. After a 6-week washout period, participants were assigned a hypercaloric high-fructose or high-glucose diet for 2 more weeks.

Primary outcome measures were hepatic level of TAG, along with TAG levels in serum and soleus muscle, hepatic levels of adenosine triphosphate and systemic and hepatic insulin resistance.

During the study’s moderate isocaloric portion, body weight and TAG concentration in liver, serum and soleus muscle remained stable in both groups. Uric acid levels, however, increased 22 ± 52 mcmol/L among the high-fructose group and decreased 23 ± 25 mcmol/L in the high-glucose group (P<.01). The high-fructose diet also resulted in an increase of 0.76 ± 0.9 in the homeostasis model assessment of insulin resistance vs. an increase of 0.13 ± 0.7 among high-glucose diet patients (P=.03).

“The lack of change in HTGC [hepatic TAG content] during the isocaloric period and increase in the hypercaloric period suggests an exquisite hepatic sensitivity to excess energy, as opposed to a specific monosaccharide,” the researchers said, concluding that “features of NAFLD including steatosis, and increased serum transaminase and triglyceride levels, occurred during energy overfeeding.”

Researchers suggested additional studies to determine whether the energy overfeeding changes discovered are monosaccharide specific and to learn more about the results of reduced monosaccharide intakes in NAFLD patients.

Disclosure: See the study for a full list of relevant financial disclosures.