***TASK*** the task is to summarize an input biomedical literature in six sentences 
    ***INPUT*** the input is a biomedical literature 
    ***OUTPUT*** the output is the summary of an input biomedical literature in six sentences 
    ***DOCUMENTATION*** 
    ***EXAMPLES*** 
    Input: OBJECTIVE To evaluate the effect of sodium and fructose restriction on mitochondrial DNA ( mtDNA ) content and systemic oxidative stress in a sample of overweight and pre hypertensive subjects . MATERIAL / METHODS Data and blood sample s were collected from 36 overweight and pre hypertensive patients r and omly assigned to either an isocaloric ( with respect to baseline ) low sodium-fructose diet or an isocaloric low sodium diet . Patients were followed for 8 weeks . We measured mitochondrial DNA ( mtDNA ) content from peripheral blood white cells by Real-time PCR and plasma malondialdehyde ( MDA ) and 2,4-dinitrophenylhydrazine ( DNPH ) as markers of reactive oxygen species ( ROS ) . RESULTS Compared to baseline , at week 8 there was a continued and significant increase in mtDNA in both the low sodium diet group [ 2.4 vs. 13.1 ( relative copy number ) , p<0.05 ] and the low sodium diet-fructose group ( 1.9 vs. 147.2 , p<0.05 ) . By week 8 there was a continued decrease in plasma DNPH levels in the low sodium diet group ( 4.6 vs. 2.6 , p<0.05 ) and in the low sodium diet-fructose group ( 5.8 vs. 2.2 , p<0.05 ) . No significant differences were found with MDA . CONCLUSION Our studies suggest that simple dietary measures such as reducing salt with or without restricting fructose can increase mtDNA and improve markers of oxidative stress 
    Output:
    
The combination of low sodium and low fructose did increase mtDNA but it did not increase it more than the low sodium diet alone without fructose restriction .
This suggests that the eff ect appears dependent on sodium but not fructose .
Conversely , in isocaloric comparisons where energy intake is matched , these eff ects are not observed .
That is , fructose behaves no worse than any other carbohydrate [ 4 – 8 ] , although there may be a dosethreshold for some fasting lipid eff ects [ 4 , 10 – 12 ] .
This lack of eff ect remains true even under conditions of fructose overfeeding ( positive energy balance ) , as long as the comparison is matched for the excess calories .
Taken together , the main driver mediating any harm attributable to fructose appears to be excess energy .
In conclusion , there is insuffi cient evidence to conclude that fructose restriction has a signifi ca nt eff ect on mtDNA and oxidative stress when holding energy equal .
Energy imbalance appears to be a prerequisite for eliciting an eff ect .