title: Mechanisms for the acute effect of fructose on postprandial lipemia. Acute fructose administration improves oral glucose tolerance in adults with type 2 diabetes. Fructose and insulin sensitivity in patients with type 2 diabetes.
abstract: BACKGROUND A high fructose intake can lead to postpr and ial hypertriacylglycerolemia . The underlying mechanism is unclear . OBJECTIVE The objective of the study was to investigate the mechanisms involved in fructose-induced hypertriacylglycerolemia and the contribution of de novo lipogenesis in an acute setting . DESIGN In a r and omized , crossover study , 14 subjects were given a fructose or glucose test meal after an overnight fast . [(2)H2]Palmitate and [U(13)C]d-fructose or [U(13)C]d-glucose were added to trace the h and ling of dietary fats and the fate of dietary sugars in the body . Blood sample s were taken before and after the meal . Respiratory exchange ratio was measured by using indirect calorimetry , and breath sample s were collected . RESULTS Plasma triacylglycerol and VLDL-triacylglycerol concentrations were significantly higher ( P = 0.001 for both ) , whereas the concentrations of insulin and [(2)H2]palmitate in nonesterified fatty acids were significantly lower after fructose than after glucose ( P = 0.002 and 0.03 , respectively ) . The respiratory exchange ratio was higher after fructose ( P = 0.04 ) ; significantly ( P = 0.003 ) more carbon from sugars was recovered in breath carbon dioxide over 6 h after fructose ( 30.5 % ) than after glucose ( 24.5 % ) . At 240 min , newly synthesized fatty acids from fructose made up approximately 0.4 % of circulating VLDL-triacylglycerol , whereas newly synthesized triacylglycerol-glycerol made up 38 % . Newly synthesized fatty acids and triacylglycerol-glycerol from glucose contributed almost none of VLDL-triacylglycerol ( P = 0.002 and 0.007 for glucose and fructose , respectively ) . CONCLUSIONS The lower insulin excursion after fructose may result in less activation of adipose tissue lipoprotein lipase , which led to impaired triacylglycerol clearance . The contribution of de novo lipogenesis to fructose-induced hypertriacylglycerolemia is small , but its effect on altering the partitioning of fatty acids toward esterification may be considerable OBJECTIVE In normal adults , a small ( catalytic ) dose of fructose administered with glucose decreases the glycemic response to a glucose load , especially in those with the poorest glucose tolerance . We hypothesized that an acute catalytic dose of fructose would also improve glucose tolerance in individuals with type 2 diabetes . RESEARCH DESIGN AND METHODS Five adults with type 2 diabetes underwent an oral glucose tolerance test ( OGTT ) on two separate occasions , at least 1 week apart . Each OGTT consisted of 75 g glucose with or without the addition of 7.5 g fructose ( OGTT + F or OGTT - F ) , in r and om order . Arterialized blood sample s were collected from a heated dorsal h and vein twice before ingestion of the carbohydrate and every 15 min for 3 h afterward . RESULTS The area under the curve ( AUC ) of the plasma glucose response was reduced by fructose administration in all subjects ; the mean AUC during the OGTT + F was 14 % less than that during the OGTT - F ( P < 0.05 ) . The insulin AUC was decreased 21 % with fructose administration ( P = 0.2 ) . Plasma glucagon concentrations declined similarly during OGTT - F and OGTT + F. The incremental AUC of the blood lactate response during the OGTT - F was approximately 50 % of that observed during the OGTT + F ( P < 0.05 ) . Neither nonesterified fatty acid nor triglyceride concentrations differed between the two OGTTs . CONCLUSIONS Low-dose fructose improves the glycemic response to an oral glucose load in adults with type 2 diabetes , and this effect is not a result of stimulation of insulin secretion The effect of dietary fructose ( 20 % of carbohydrate calories , 45 - 65 g day-1 for 4 weeks ) on glycaemic control , serum lipid , lipoprotein and apoprotein A-I and A-II concentrations and on insulin sensitivity was studied in 10 type 2 diabetic patients . The study was done in a r and omized , double-blind fashion with crystalline fructose or placebo administered evenly during 4 meals or snacks per day . The patients were hospitalized throughout the study periods . The fasting plasma glucose concentration decreased during the fructose ( from 10.7 + /- 1.4 mmol l-1 to 8.0 + /- 0.8 mmol l-1 , P < 0.02 ) and the control diet ( from 10.1 + /- 0.9 mmol l-1 to 8.0 + /- 0.7 mmol l-1 , P < 0.05 ) . The mean diurnal blood glucose concentration also fell both during the fructose ( from 10.8 + /- 0.5 mmol l-1 to 8.4 + /- 0.3 mmol l-1 , P < 0.001 ) and the control diet ( from 10.3 + /- 0.3 mmol l-1 to 8.8 + /- 0.9 mmol l-1 , P < 0.01 ) . The HbA1 concentration improved ( P < 0.02 ) only during the fructose diet . Insulin sensitivity increased by 34 % ( P < 0.05 ) during the fructose diet , but remained unchanged during the control period . Serum insulin , triglyceride , apoprotein A-I and A-II concentrations , body weight , blood pressure and blood lactate remained unchanged during both diets . In conclusion , substitution of moderate amounts of fructose for complex carbohydrates can improve glycaemic control and insulin sensitivity in patients with type 2 diabetes
target: Pooled analyses demonstrated conditional triglyceride-raising and total cholesterol – lowering  effects of isocaloric fructose exchange for carbohydrate in type 2 diabetes .
background: OBJECTIVE Because of blood lipid concerns , diabetes associations discourage fructose at high intakes .
  To quantify the effect of fructose  on blood lipids in diabetes , we conducted a systematic review and meta- analysis of experimental clinical trials investigating the effect of isocaloric fructose exchange for carbohydrate on triglycerides , total cholesterol , LDL cholesterol , and HDL cholesterol in type 1 and 2 diabetes .