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Background/objectives: In the absence of consistent clinical evidence, there are concerns that fructose contributes to non-alcoholic fatty liver disease (NAFLD). To determine the effect of fructose on markers of NAFLD, we conducted a systematic review and meta-analysis of controlled feeding trials., Subjects/methods: We searched MEDLINE, EMBASE, CINAHL and the Cochrane Library (through 3 September 2013). We included relevant trials that involved a follow-up of ≥ 7 days. Two reviewers independently extracted relevant data. Data were pooled by the generic inverse variance method using random effects models and expressed as standardized mean difference (SMD) for intrahepatocellular lipids (IHCL) and mean difference (MD) for alanine aminotransferase (ALT). Inter-study heterogeneity was assessed (Cochran Q statistic) and quantified (I(2) statistic)., Results: Eligibility criteria were met by eight reports containing 13 trials in 260 healthy participants: seven isocaloric trials, in which fructose was exchanged isocalorically for other carbohydrates, and six hypercaloric trials, in which the diet was supplemented with excess energy (+21-35% energy) from high-dose fructose (+104-220 g/day). Although there was no effect of fructose in isocaloric trials, fructose in hypercaloric trials increased both IHCL (SMD=0.45 (95% confidence interval (CI): 0.18, 0.72)) and ALT (MD=4.94 U/l (95% CI: 0.03, 9.85))., Limitations: Few trials were available for inclusion, most of which were small, short (≤ 4 weeks), and of poor quality., Conclusions: Isocaloric exchange of fructose for other carbohydrates does not induce NAFLD changes in healthy participants. Fructose providing excess energy at extreme doses, however, does raise IHCL and ALT, an effect that may be more attributable to excess energy than fructose. Larger, longer and higher-quality trials of the effect of fructose on histopathological NAFLD changes are required.

Objective: To investigate the effect of varying the volume of sugar meals on the post-prandial glycemic response (PGR)., Research Design and Methods: On six separate occasions, after an overnight fast, blood glucose concentrations were measured in eight healthy subjects (34 +/- 4 years of age, BMI 22.9 +/- 0.9 kg/m2) after the consumption of 25 g glucose, sucrose, or fructose dissolved in either 200 or 600 ml of water. Blood was obtained at fasting and then at times 15, 30, 45, 60, and 90 min after the start of the test meal., Results: PGR was found to be influenced by carbohydrate type (P < 0.001). Mean response areas (min.mmol.l-1) to the three sugars were statistically different (P < 0.05). Glucose had the highest response area (90.0 +/- 8.1), followed by sucrose (61.3 +/- 5.0) and then fructose (14.7 +/- 2.8). Independent of this effect, PGR was also found to be influenced by volume dose (P < 0.01). By tripling meal volume from 200 to 600 ml, PGR areas were significantly increased for all three sugars, glucose (79.3 +/- 10.3 vs. 100.8 +/- 12.0, P = 0.035), sucrose (52.6 +/- 5.5 vs. 70 +/- 7.4, P = 0.0094), and fructose (11.0 +/- 3.8 vs. 18.4 +/- 3.9, P = 0.012). Where the effects of time (P < 0.05) and dose (P < 0.05) were determined to be independent (interaction nonsignificant) for all three sugars, this increase in volume also significantly increased glycemic concentrations at 15 min, for glucose (P = 0.033) and sucrose (P = 0.026), suggesting that changes in gastric emptying time may be a mechanism of action., Conclusions: Varying the volume of liquid sugar meals alters PGR. Understanding this concept may help to reduce variability both in the glycemic testing of foods and oral glucose tolerance testing.

Sugars containing fructose are emerging as the dominant public health targets for their role in the epidemic of overweight and obesity. This position is largely supported by ecological observations, rodent models of overfeeding and select human trials. Higher level evidence from systematic reviews and meta-analyses of controlled dietary trials has yet to show convincingly that fructose-containing sugars behave differently from any other forms of energy (especially refined starch and fat). Prospective cohort studies, which provide the strongest observational evidence, have shown an association between risk of overweight and obesity and fructose-containing sugars consumed as sugar-sweetened beverages but not as total sugars or other important sources of added sugars such as cakes, pastries and sweets. Comparative analyses show that high intakes of other highly palatable foods such as refined grains, processed meats, red meats, French fries and potato products, as well as physical inactivity may play an equal or greater role in weight gain and the risk of overweight and obesity. The contributions of these factors are also difficult to disentangle from that of sugar-sweetened beverages owing to their collinearity with sugar-sweetened beverages as part of a Western dietary pattern and lifestyle. Attention needs to remain focused on decreasing overconsumption of all foods associated with overweight and obesity. Sugar-sweetened beverages and foods are certainly an important place to start but should not draw attention away from the issue of overconsumption in general. [ABSTRACT FROM AUTHOR]