Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch

Reiser, Sheldon; Powell, A S; Scholfield, Daniel J.; Panda, P; Fields, Meira; Canary, John J.

doi:10.1093/ajcn/50.5.1008

Cited by 45 publications

(27 citation statements)

References 35 publications

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“…However, increases of fasting TG concentrations have been reported after 2 or more weeks of fructose consumption at 15%-20% of energy requirements (13)(14)(15)(16)(17)(18). The reason for these conflicting results is unclear but may be related to the marked within-group and within-individual variability we observed in fasting TG responses to dietary fructose.…”

Section: Figurementioning

confidence: 87%

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

et al. 2009

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Studies in animals have documented that, compared with glucose, dietary fructose induces dyslipidemia and insulin resistance. To assess the relative effects of these dietary sugars during sustained consumption in humans, overweight and obese subjects consumed glucose-or fructose-sweetened beverages providing 25% of energy requirements for 10 weeks. Although both groups exhibited similar weight gain during the intervention, visceral adipose volume was significantly increased only in subjects consuming fructose. Fasting plasma triglyceride concentrations increased by approximately 10% during 10 weeks of glucose consumption but not after fructose consumption. In contrast, hepatic de novo lipogenesis (DNL) and the 23-hour postprandial triglyceride AUC were increased specifically during fructose consumption. Similarly, markers of altered lipid metabolism and lipoprotein remodeling, including fasting apoB, LDL, small dense LDL, oxidized LDL, and postprandial concentrations of remnant-like particle-triglyceride and -cholesterol significantly increased during fructose but not glucose consumption. In addition, fasting plasma glucose and insulin levels increased and insulin sensitivity decreased in subjects consuming fructose but not in those consuming glucose. These data suggest that dietary fructose specifically increases DNL, promotes dyslipidemia, decreases insulin sensitivity, and increases visceral adiposity in overweight/obese adults. IntroductionStudies investigating the effects of fructose consumption in humans and animals have been comprehensively reviewed (1-4), and while strong evidence exists that consumption of diets high in fructose results in increased de novo lipogenesis (DNL), dyslipidemia, insulin resistance, and obesity in animals, direct experimental evidence that consumption of fructose promotes DNL, dyslipidemia, insulin resistance, glucose intolerance, and obesity in humans is lacking. Thus, we have investigated and compared the biological effects of the 2 major simple sugars in the diet, glucose and fructose, on BW and regional fat deposition and on indices of lipid and carbohydrate metabolism in older, overweight and obese men and women.We sought to answer the following questions: (a) Does consumption of fructose with an ad libitum diet promote greater BW gain and have differential effects on regional adipose deposition and adipose gene expression compared with consumption of glucose with an ad libitum diet? (b) Does consumption of fructose induce dyslipidemia compared with consumption of glucose? (c) Is fructose-induced hypertriglyceridemia the result of increased rates

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Section: Figurementioning

confidence: 87%

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

et al. 2009

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“…Noticeably, type 2 diabetic patients are common with obesity and, 150-225 million people worldwide are affected with type 2 diabetes, according to a recent epidemiologic report (Zimmet, 2003). A diet with high sucrose or fructose has been observed to induce insulin resistance, although without clear mechanisms (Hallfrisch et al, 1983;Israel et al, 1983;Reaven, 1991;Reiser et al, 1989). For instance, an increased blood pressure associated with hyperinsulinemia and hypertriglyceridemia in normal Sprague Dawley rats was observed after only 2 weeks on a high fructose (66%) diet (Hwang et al, 1987).…”

Section: Discussionmentioning

confidence: 99%

“…The consumption of fructose or sucrose (1 glucose + 1 fructose) sweeteners used in beverages and processed foods has increased significantly in the last two decades. It has been shown that a diet high in fructose or sucrose can increase blood pressure and induce insulin resistance although the mechanism is unclear (Hallfrisch et al, 1983;Israel et al, 1983;Reaven, 1991;Reiser et al, 1989). Significant increase of serum fructose to 12 μM in diabetic patients compared with a level of 8.1 μM in healthy subjects has been reported (Kawasaki et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Fructose-induced peroxynitrite production is mediated by methylglyoxal in vascular smooth muscle cells

et al. 2006

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“…After fructose ingestion, several researchers observed blood glucose levels that were reduced compared with levels after starch or sucrose ingestion in diabetic patients (10,(15)(16)(17)(18). Additionally, studies conducted in healthy subjects noted that different amounts of fructose intake did not change HbA 1c levels (19), yet they significantly elevated plasma triglycerides (20).…”

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confidence: 99%

A Prospective Study of Sugar Intake and Risk of Type 2 Diabetes in Women

et al. 2003

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OBJECTIVE -To investigate prospectively whether intake of total or type of sugar is associated with the risk of developing type 2 diabetes. The contribution of sugar intake to the pathogenesis of type 2 diabetes has not been settled in the context of primary prevention because of limited prospective data.RESEARCH DESIGN AND METHODS -The Women's Health Study is a randomized controlled trial of aspirin and vitamin E in the prevention of cardiovascular disease and cancer. A validated semiquantitative food frequency questionnaire was completed by 39,345 women aged 45 years and older. The main outcome was the incidence of type 2 diabetes. The predictor was sugar intake, including sucrose, glucose, fructose, and lactose. Using Cox proportional hazard models, multivariate RRs of type 2 diabetes for increasing quintiles of sugar intake compared with the lowest quintile were estimated.RESULTS -Compared with the lowest quintile of sugar intake, the RRs and 95% CIs for the highest quintiles were 0.84 (0.67-1.04) for sucrose, 0.96 (0.78 -1.19) for fructose, 1.04 (0.85-1.28) for glucose, and 0.99 (0.80 -1.22) for lactose, after adjustment for known risk factors for type 2 diabetes. Similar findings of no association were obtained in subgroup analyses stratified by BMI.CONCLUSIONS -Intake of sugars does not appear to play a deleterious role in primary prevention of type 2 diabetes. These prospective data support the recent American Diabetes Association's guideline that a moderate amount of sugar can be incorporated in a healthy diet. Diabetes Care 26:1008 -1015, 2003P revailing beliefs over the past 20 years regarding sugars and diabetes admonished that added sugar, primarily sucrose, should be avoided and that naturally occurring sugars should be restricted in the diabetic diet (1,2). Support for these beliefs was based largely on results from animal and human studies suggesting that simple sugars would confer a higher postprandial glycemia than starch (3). Consequently, diets for diabetic patients have been sugar restricted for fear of stimulating hyperglycemia (1), exaggerating insulin response to carbohydrates (4,5), and causing possible cardiomyocyte dysfunction (6) and/or accelerated loss of ␤-cells (7).However, several metabolic studies have reported that inclusion of a moderate amount of dietary sucrose within a balanced diabetic diet did not elicit subsequent deleterious effects on glycemic control (2,8 -12). Different types of sugars may have variable metabolic effects on glycemia or lipemia (13-15). After fructose ingestion, several researchers observed blood glucose levels that were reduced compared with levels after starch or sucrose ingestion in diabetic patients (10,(15)(16)(17)(18). Additionally, studies conducted in healthy subjects noted that different amounts of fructose intake did not change HbA 1c levels (19), yet they significantly elevated plasma triglycerides (20).The risks and benefits of sugar ingestion in metabolic studies of diabetes have been controversial, and the data on primary prevention, name...

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Day-long glucose, insulin, and fructose responses of hyperinsulinemic and nonhyperinsulinemic men adapted to diets containing either fructose or high-amylose cornstarch

Cited by 45 publications

References 35 publications

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

Consuming fructose-sweetened, not glucose-sweetened, beverages increases visceral adiposity and lipids and decreases insulin sensitivity in overweight/obese humans

Fructose-induced peroxynitrite production is mediated by methylglyoxal in vascular smooth muscle cells

A Prospective Study of Sugar Intake and Risk of Type 2 Diabetes in Women

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