title: Blood lipids, lipoproteins, apoproteins, and uric acid in men fed diets containing fructose or high-amylose cornstarch. Effects of a short-term overfeeding with fructose or glucose in healthy young males. Soft drinks, fructose consumption, and the risk of gout in men: prospective cohort study Fructose overconsumption causes dyslipidemia and ectopic lipid deposition in healthy subjects with and without a family history of type 2 diabetes. A measure to aid in the interpretation of published clinical trials.
abstract: Ten hyperinsulinemic and 11 nonhyperinsulinemic men consumed for 5 wk each in a cross-over design a diet , similar to one currently consumed in the United States , with 20 % of the kilocalories from either fructose or high-amylose cornstarch to determine the effects of the two diets on various blood metabolites considered to be risk factors associated with heart disease . In the hyperinsulinemic men the intake of fructose as compared with cornstarch significantly increased total triglycerides and their lipoprotein distribution ; total and very-low-density lipoprotein cholesterol ; apoproteins B-100 , C-II , C-III ; and uric acid . In the nonhyperinsulinemic men  total triglycerides , total and low-density lipoprotein cholesterol and uric acid were significantly greater after the consumption of fructose than after cornstarch . The results indicate that in a diet high in saturated fatty acids and cholesterol , fructose increases the levels of risk factors associated with heart disease , especially in hyperinsulinemic men 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 Objective To examine the relation between intake of sugar sweetened soft drinks and fructose and the  risk of incident gout in men . Design Prospect i ve cohort over 12 years . Setting Health professionals follow-up study . Participants 46 393 men with no history of gout at baseline who provided information on intake of soft drinks and fructose through vali date d food frequency question naires . Main outcome measure Incident cases of gout meeting the American College of Rheumatology survey criteria for gout . Results During the 12 years of follow-up 755 confirmed incident cases of gout were reported . Increasing intake of sugar sweetened soft drinks was associated with an increasing risk of gout . Compared with consumption of less than one serving of sugar sweetened soft drinks a month the multivariate relative risk of gout for 5 - 6 servings a week was 1.29 ( 95 % confidence interval 1.00 to 1.68 ) , for one serving a day was 1.45 ( 1.02 to 2.08 ) , and for two or more servings a day was 1.85 ( 1.08 to 3.16 ; P for trend=0.002 ) . Diet soft drinks were not associated with risk of gout ( P for trend=0.99 ) . The multivariate relative risk of gout according to increasing fifths of fructose intake were 1.00 , 1.29 , 1.41 , 1.84 , and 2.02 ( 1.49 to 2.75 ; P for trend < 0.001 ) . Other major contributors to fructose intake such as total fruit juice or fructose rich fruits ( apples and oranges ) were also associated with a higher risk of gout ( P values for trend < 0.05 ) . Conclusions Prospect i ve data suggest that consumption of sugar sweetened soft drinks and fructose is strongly associated with an increased  risk of gout in men . Furthermore , fructose rich fruits and fruit juices may also increase the risk .  Diet soft drinks were not associated with the risk of gout BACKGROUND Both nutritional and genetic factors are involved in the pathogenesis of nonalcoholic fatty liver disease and insulin resistance . OBJECTIVE The aim was to assess the effects of fructose , a potent stimulator of hepatic de novo lipogenesis , on intrahepatocellular lipids ( IHCLs ) and insulin sensitivity in healthy offspring of patients with type 2 diabetes (OffT2D)--a subgroup of individuals prone to metabolic disorders . DESIGN Sixteen male OffT2D and 8 control subjects were studied in a crossover design after either a 7-d isocaloric diet or a hypercaloric high-fructose diet ( 3.5 g x kg FFM(-1 ) x d(-1 ) , + 35 % energy intake ) . Hepatic and whole-body insulin sensitivity were assessed with a 2-step hyperinsulinemic euglycemic clamp ( 0.3 and 1.0 mU x kg(-1 ) x min(-1 ) ) , together with 6,6-[2H2]glucose . IHCLs and intramyocellular lipids ( IMCLs ) were measured by 1H-magnetic resonance spectroscopy . RESULTS The OffT2D group had significantly ( P < 0.05 ) higher IHCLs ( + 94 % ) , total triacylglycerols ( + 35 % ) , and lower whole-body insulin sensitivity ( -27 % ) than did the control group . The high-fructose diet significantly increased IHCLs ( control : + 76 % ; OffT2D : + 79 % ) , IMCLs ( control : + 47 % ; OffT2D : + 24 % ) , VLDL-triacylglycerols ( control : + 51 % ; OffT2D : + 110 % ) , and fasting hepatic glucose output ( control : + 4 % ; OffT2D : + 5 % ) . Furthermore , the effects of fructose on VLDL-triacylglycerols were higher in the OffT2D group ( group x diet interaction : P < 0.05 ) . CONCLUSIONS A 7-d high-fructose diet increased ectopic lipid deposition in liver and muscle and fasting VLDL-triacylglycerols and decreased hepatic insulin sensitivity . Fructose-induced alterations in VLDL-triacylglycerols appeared to be of greater magnitude in the OffT2D group , which suggests that these individuals may be more prone to developing dyslipidemia when challenged by high fructose intakes . This trial was registered at clinical trials.gov as NCT00523562 The published literature contains numerous reports of clinical studies . A problem in their interpretation is that studies in which the observed efficacy of the treatment is high are much more likely to be reported than those in which the observed efficacy is average or poor . This phenomenon has had the consequence of generally discrediting the reliability of the literature , especially that of non-r and omized studies . In this paper a model is developed which permits estimation of the potential magnitude by which the reported efficacy of a treatment might be inflated . This quantity is termed the publication bias . The magnitude of the bias depends on the sample size of the study and the number of similar studies conducted concurrently . Tabulated values of the bias are presented , permitting easy computation . The new measure may have potential use for physicians in clinical decision making in that it characterizes the reliability of results from a specific published study , especially when there are no definitive r and omized studies . However , correction of publication bias in this manner is not a substitute for a well controlled or a r and omized study . The technique merely assists in the interpretation of available evidence from the literature . Moreover , it must be used with due caution in recognition of the assumptions and approximations involved in the calculation
target: These analyses do not support a uric acid-increasing effect  of isocaloric fructose intake in nondiabetic and diabetic participants .
  Hypercaloric fructose intake may , however , increase uric acid concentrations .
background: Hyperuricemia is linked to gout and features of metabolic syndrome .
  There is concern that dietary fructose may increase uric acid concentrations .