Fructose had no effect on LDL-C , non-HDL-C , apolipoprotein B , triglycerides , or HDL-C in isocaloric trials .
Conclusions Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories ( + 21 % to 35 % energy ) .
When isocalorically exchanged for other carbohydrates , fructose had no adverse effects on blood lipids .
Background Debate over the role of fructose in mediating  cardiovascular  risk remains active .
To up date the evidence on the effect of fructose on established therapeutic lipid targets for cardiovascular disease ( low-density lipoprotein cholesterol [LDL]-C , apolipoprotein B , non-high-density lipoprotein cholesterol [ HDL-C ] ) , and metabolic syndrome ( triglycerides and HDL-C ) , we conducted a systematic review and meta- analysis of controlled feeding trials .
Effects of a short-term overfeeding with fructose or glucose in healthy young males.
Consumption of simple carbohydrates has markedly increased over the past decades , and may be involved in the increased prevalence in metabolic diseases . Whether an increased intake of fructose is specifically related to a dysregulation of glucose and lipid metabolism remains controversial . We therefore compared the effects of hypercaloric diets enriched with fructose ( HFrD ) or glucose ( HGlcD ) in healthy men . Eleven subjects were studied in a r and omised order after 7 d of the following diets : ( 1 ) weight maintenance , control diet ; ( 2 ) HFrD ( 3.5 g fructose/kg fat-free mass ( ffm ) per d , + 35 % energy intake ) ; ( 3 ) HGlcD ( 3.5 g glucose/kg ffm per d , + 35 % energy intake ) . Fasting hepatic glucose output ( HGO ) was measured with 6,6 - 2H2-glucose . Intrahepatocellular lipids ( IHCL ) and intramyocellular lipids ( IMCL ) were measured by 1H magnetic resonance spectroscopy . Both fructose and glucose increased fasting VLDL-TAG ( HFrD : + 59 % , P < 0.05 ; HGlcD : + 31 % , P = 0.11 ) and IHCL ( HFrD : + 52 % , P < 0.05 ; HGlcD : + 58 % , P = 0.06 ) . HGO increased after both diets ( HFrD : + 5 % , P < 0.05 ; HGlcD : + 5 % , P = 0.05 ) . No change was observed in fasting glycaemia , insulin and alanine aminotransferase concentrations . IMCL increased significantly only after the HGlcD ( HFrD : + 24 % , NS ; HGlcD : + 59 % , P < 0.05 ) . IHCL and VLDL-TAG were not different between hypercaloric HFrD and HGlcD , but were increased compared to values observed with a weight maintenance diet . However , glucose led to a higher increase in IMCL than fructose
Fructose had no effect on LDL-C , non-HDL-C , apolipoprotein B , triglycerides , or HDL-C in isocaloric trials .
Conclusions Pooled analyses showed that fructose only had an adverse effect on established lipid targets when added to existing diets so as to provide excess calories ( + 21 % to 35 % energy ) .
When isocalorically exchanged for other carbohydrates , fructose had no adverse effects on blood lipids .
Background Debate over the role of fructose in mediating  cardiovascular  risk remains active .
To up date the evidence on the effect of fructose on established therapeutic lipid targets for cardiovascular disease ( low-density lipoprotein cholesterol [LDL]-C , apolipoprotein B , non-high-density lipoprotein cholesterol [ HDL-C ] ) , and metabolic syndrome ( triglycerides and HDL-C ) , we conducted a systematic review and meta- analysis of controlled feeding trials .