Abstract
The association between the amount and sources of fructose intake with insulin sensitivity and liver fat needs further elucidation. This study aimed at examining whether habitual intake of sucrose plus non-sucrose bound as well as of non-sucrose bound fructose (total fructose, fruit-derived, juice-derived, sugar sweetened beverages (SSB)-derived fructose) is cross-sectionally associated with insulin sensitivity and fatty liver index (FLI). Fructose intake was estimated using the EPIC food frequency questionnaire from 161 participants with type 2 diabetes (T2D) in the ongoing German Diabetes Study (GDS) (age 53 ± 9 years; HbA1c 6.4 ± 0.9%) and 62 individuals without diabetes (CON) (47 ± 14 years; 5.3 ± 0.3%). Peripheral (M-value) and hepatic insulin resistance were assessed by hyperinsulinemic-euglycemic clamps with stable isotope dilution. FLI was calculated based on body mass index, waist circumference, triglyceride and gamma glutamyl transferase concentrations. Multivariable linear regression analyses were performed. A doubling of SSB-derived sucrose plus non-sucrose bound as well as of non-sucrose bound fructose intake was independently associated with a reduction of the M-value by −2.6% (−4.9; −0.2) and −2.7% (−5.2; −0.1) among T2D, respectively, with an increase in the odds of fatty liver by 16% and 17%, respectively among T2D (all p < 0.05). Doubling fruit-derived sucrose plus non-sucrose bound fructose intake independently related to a reduction in the odds of fatty liver by 13% (p = 0.033) among T2D. Moderate SSB-derived fructose intake may detrimentally affect peripheral insulin sensitivity, whereas fruit-derived fructose intake appeared beneficial for liver fat content.
Highlights
There is increasing concern that dietary fructose may be a key contributor to the rising prevalence of metabolic disorders [1]
Disaccharide, sucrose and sucrose plus non-sucrose bound fructose intake was higher among CON compared to type 2 diabetes (T2D), total non-sucrose bound fructose intake was comparable between groups (Table 2)
Sucrose plus non-sucrose bound fructose intake from fruits accounted for about 29%
Summary
There is increasing concern that dietary fructose may be a key contributor to the rising prevalence of metabolic disorders [1]. Fructose intake may affect the liver due to its mainly hepatic metabolism [2]. The addition of fructose to diets in isocaloric exchange for other macronutrients does not affect hepatic fat content and insulin sensitivity [3,4]. Fructose intake exceeding 250 g/day and providing an excess of calories may reduce hepatic insulin sensitivity in healthy, obese or genetically at-risk individuals for diabetes [4]. Fructose overconsumption increased hepatocellular fat content in some, but not all intervention studies [5,6]. The effect of fructose intake on hepatic insulin sensitivity and hepatocellular fat content seems to critically depend on its energy contribution to the diet. The role of moderate or high fructose intake on peripheral insulin sensitivity remains uncertain [4]
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