Potential link between excess added sugar intake and ectopic fat: a systematic review of randomized controlled trials

Abstract

Context: The effect of added sugar intake on ectopic fat accumulation is a subject of debate. Objective: A systematic review and meta-analysis of randomized controlled trials (RCTs) was conducted to examine the potential effect of added sugar intake on ectopic fat depots. Data Sources: MEDLINE, CAB Abstracts, CAB Global Health, and EBM (Evidence-Based Medicine) Reviews -Cochrane Central Register of Controlled Trials databases were searched for studies published from 1973 to September 2014. Data Extraction: RCTs with a minimum of 6 days' duration of added sugar exposure in the intervention group were selected. The dosage of added sugar intake as a percentage of total energy was extracted or calculated. Means and standard deviations of pre-and post-test measurements or changes in ectopic fat depots were collected. Data Synthesis: Fourteen RCTs were included. Most of the studies had a medium to high risk of bias. Meta-analysis showed that, compared with eucaloric controls, subjects who consumed added sugar under hypercaloric conditions likely increased ectopic fat, particularly in the liver (pooled standardized mean difference ¼ 0.9 [95%CI, 0.6-1.2], n ¼ 6) and muscles (pooled SMD ¼ 0.6 [95%CI, 0.2-1.0], n ¼ 4). No significant difference was observed in liver fat, visceral adipose tissue, or muscle fat when isocaloric intakes of different sources of added sugars were compared. Conclusions: Data from a limited number of RCTs suggest that excess added sugar intake under hypercaloric diet conditions likely increases ectopic fat depots, particularly in the liver and in muscle fat. There are insufficient data to compare the effect of different sources of added sugars on ectopic fat deposition or to compare intake of added sugar with intakes of other macronutrients. Future well-designed RCTs with sufficient power and duration are needed to address the role of sugars on ectopic fat deposition.

Isocaloric Dietary Changes and Non-Alcoholic Fatty Liver Disease in High Cardiometabolic Risk Individuals

“…Briefly, the first meta-analysis reported that, in healthy subjects, using high doses of fructose in terms of 104–220 g/day in a hypercaloric diet increased both liver fat content and serum ALT levels, while it did not produce any effect in isocaloric conditions [ 108 ]. Similar findings were reported by the second meta-analysis where it was observed that the excess of added sugar intake in a hypercaloric diet compared with a eucaloric control diet increased liver fat content [ 109 ].…”

“…Many clinic trials have investigated the effect of simple sugars mainly fructose, glucose and sucrose on NAFLD in healthy individuals and in those at high cardiometabolic risk [ 100 , 101 , 102 , 103 , 104 , 105 , 106 , 107 ], and two meta-analyses on this issue were carried out [ 108 , 109 ]. Briefly, the first meta-analysis reported that, in healthy subjects, using high doses of fructose in terms of 104–220 g/day in a hypercaloric diet increased both liver fat content and serum ALT levels, while it did not produce any effect in isocaloric conditions [ 108 ].…”

The twin white herrings: Salt and sugar

“…[ 33 54 55 ] Excess sugar intake in hypercaloric diet have postprandial triglyceride-raising effect, may increase ectopic fat depots particularly in the liver and in muscle fat which may further cause fatty liver disease and increase cardiometabolic risk. [ 18 56 57 ] Fructose is metabolized primarily in the liver and enhances lipogenesis and the production of uric acid. [ 17 18 58 ] Short-term mechanistic studies have shown that excess fructose ingestion can result in additional cardiometabolic effects due to increased hepatic de novo lipogenesis (DNL), accumulation of visceral adiposity and ectopic fat, and production of uric acid.…”

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

“…However, because DNL in rodents differs from that in humans , it is not clear how relevant these findings are for humans. Recent meta‐analyses have identified several limitations in clinical studies investigating the adverse metabolic effects of fructose (such as small sample sizes, short intervention periods, variable doses of fructose intake and studies in healthy lean subjects with low baseline liver fat content) . These limitations may explain the discrepant conclusions of the trials studying the effect of fructose consumption on liver fat content .…”