There was interaction by food source , with specific food sources showing beneficial effects ( fruit and fruit juice ) or harmful effects ( sweetened milk and mixed sources ) in substitution studies and harmful effects ( sugars‐sweetened beverages and fruit juice ) in addition studies on at least one outcome .
Conclusions Energy control and food source appear to mediate the effect of fructose‐containing sugars on glycaemic control .
Although most food sources of these sugars ( especially fruit ) do not have a harmful effect in energy matched substitutions with other macronutrients , several food sources of fructose‐containing sugars ( especially sugars‐sweetened beverages ) adding excess energy to diets have harmful effects .
Objective To assess the effect of different food sources of fructose‐containing sugars  on glycaemic control at different levels of energy control .
High hepatic SCD1 activity is associated with low liver fat content in healthy subjects under a lipogenic diet.
CONTEXT Increased hepatic de novo lipogenesis ( DNL ) in response to dietary sugar is implicated in the pathophysiology of fatty liver . Saturated fatty acids are the product of DNL and exert lipotoxic effects that promote liver fat accumulation . Desaturation of fatty acids by stearoyl-CoA desaturase 1 ( SCD1 ) can prevent these deleterious effects . Here we investigated whether DNL and SCD1 are activated in parallel by dietary sugar and influence liver fat accumulation . METHODS In 20 healthy subjects ( eight females and 12 males , aged 30.5 ± 2.0 yr , body mass index 25.9 ± 0.5 kg/m(2 ) ) who received a 4-wk lipogenic diet supplemented with 150 g/d of monosaccharides  , hepatic SCD1 activity and DNL were determined using vali date d fatty acid ratios ( 16:1n-7/16:0 ; 16:0/18:2n-6 ) in very low-density lipoprotein triglycerides . Liver fat content was measured by localized (1)H-magnetic resonance spectroscopy . RESULTS At baseline , liver fat content was positively associated with the DNL ( r = 0.54 , P = 0.01 ) but not the SCD1 activity index ( r = 0.16 , P = 0.49 ) . Dietary sugar supplementation increased liver fat content and DNL and SCD1 activity indices ( + 33 , + 19 , and + 8 % , respectively ) . The increase of the DNL index was strongly related to the changes in liver fat content  during the sugar supplementation ( r = 0.75 , P = 0.0001 ) but showed no association with changes in the SCD1 activity ( P > 0.35 ) . After the monosaccharide supplementation , the DNL index was still positively associated with liver fat content ( r = 0.52 , P = 0.02 ) , whereas SCD1 activity showed a strong negative correlation with liver fat content ( r = -0.63 , P = 0.002 ) . CONCLUSIONS DNL is closely linked with hepatic steatosis under dietary conditions rich in monosaccharides . Our data suggest that the individual hepatic SCD1 activity is a determinant of liver fat accumulation under lipogenic dietary conditions
There was interaction by food source , with specific food sources showing beneficial effects ( fruit and fruit juice ) or harmful effects ( sweetened milk and mixed sources ) in substitution studies and harmful effects ( sugars‐sweetened beverages and fruit juice ) in addition studies on at least one outcome .
Conclusions Energy control and food source appear to mediate the effect of fructose‐containing sugars on glycaemic control .
Although most food sources of these sugars ( especially fruit ) do not have a harmful effect in energy matched substitutions with other macronutrients , several food sources of fructose‐containing sugars ( especially sugars‐sweetened beverages ) adding excess energy to diets have harmful effects .
Objective To assess the effect of different food sources of fructose‐containing sugars  on glycaemic control at different levels of energy control .