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ORIGINAL RESEARCH COMMUNICATION |
1 From the Department of Molecular Biosciences, School of Veterinary Medicine (KLS, MMS, PJH), the Department of Nutrition (KLS, BRB, MMS, PJH), the Department of Internal Medicine, School of Medicine (SCG), University of California, Davis; and the US Department of Agriculture, Western Human Nutrition Research Center (NLK), Davis, CA
2 Supported in part with funding from Pepsico, Inc. The project also received support from the UC Davis Clinical and Translational Science Center (grant UL1 RR024146) and the US Department of Agriculture. PJH's laboratory also receives support from NIH grants R01 HL075675, 5R21AT2500, 1R21AT002993, and 1R21AT003545 and the American Diabetes Association. 3 Address reprint requests and correspondence to PJ Havel, Department of Molecular Biosciences, School of Veterinary Medicine, University of California, One Shields Avenue, Davis, CA 95616-8669. E-mail: pjhavel{at}ucdavis.edu.
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ABSTRACT |
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 TOP ABSTRACT INTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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Objective:We compared the metabolic/endocrine effects of HFCS with sucrose and, in a subset of subjects, with pure fructose and glucose.
Design:Thirty-four men and women consumed 3 isocaloric meals with either sucrose- or HFCS-sweetened beverages, and blood samples were collected over 24 h. Eight of the male subjects were also studied when fructose- or glucose-sweetened beverages were consumed.
Results:In 34 subjects, 24-h glucose, insulin, leptin, ghrelin, and TG profiles were similar between days that sucrose or HFCS was consumed. Postprandial TG excursions after HFCS or sucrose were larger in men than in women. In the men in whom the effects of 4 sweeteners were compared, the 24-h glucose and insulin responses induced by HFCS and sucrose were intermediate between the lower responses during consumption of fructose and the higher responses during glucose. Unexpectedly, postprandial TG profiles after HFCS or sucrose were not intermediate but comparably high as after pure fructose.
Conclusions:Sucrose and HFCS do not have substantially different short-term endocrine/metabolic effects. In male subjects, short-term consumption of sucrose and HFCS resulted in postprandial TG responses comparable to those induced by fructose.
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INTRODUCTION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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We have reported that consuming fructose-sweetened beverages with meals results in lower 24-h circulating glucose, insulin, and leptin concentrations and decreased postprandial suppression of plasma ghrelin levels when compared with consumption of glucose-sweetened beverages (9). We and others have reported that consuming fructose-sweetened beverages increases postprandial triacylglycerol (TG) concentration compared with glucose-sweetened beverages (9-11). These responses are more pronounced in men compared with women (10, 11) and in overweight/obese subjects compared with normal-weight subjects (11). Because insulin, leptin, and possibly ghrelin function as key signals to the central nervous system in the long-term regulation of energy balance, prolonged consumption of diets high in energy from fructose could lead to increased caloric intake and contribute to weight gain and obesity (2). The sustained elevation of plasma TG concentrations after fructose ingestion suggests that chronic overconsumption of fructose could also contribute to atherogenesis and cardiovascular disease (12, 13). However, pure fructose and pure glucose are not commonly employed as sweeteners. Until a few decades ago, most foods and beverages in the United States were sweetened with the disaccharide sucrose, which is composed of 50% glucose and 50% fructose. In 1970 an enzymatic process to convert corn sugar (composed of glucose) into HFCS was developed. Since then, HFCS, mainly in the form containing 55% fructose and 45% glucose, has replaced sucrose as the predominant sweetener used in soft drinks and represents 
40% of sweeteners added to foods consumed in the United States (14).
Currently, there are few studies comparing the metabolic and endocrine effects of HFCS with sucrose (15, 16), and, to our knowledge, no studies comparing the effects of consuming HFCS with pure fructose or glucose. The objectives of this study, therefore, were to compare the metabolic and endocrine effects of consuming HFCS- and sucrose-sweetened beverages and to determine whether responses are affected by sex and adiposity. A third objective was to compare the effects of consuming HFCS- and sucrose-sweetened beverages with the consumption of beverages sweetened with fructose or glucose.
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SUBJECTS AND METHODS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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Subjects
Thirty-four subjects (18 men and 16 women) with an age range of 20–50 y (
34.7 ± 1.7 y) participated in the study. Participants were recruited through newspaper advertisements and underwent a telephone interview, a complete blood count, and a serum biochemistry panel to assess eligibility. Respondents with anemia, hepatic or renal disease, diabetes mellitus, fasting serum TG levels > 400 mg/dL, hypertension, eating disorders, or who had surgery for weight loss were excluded from the study. Individuals who smoked; who took thyroid, lipid-lowering, glucose-lowering, antihypertensive, antidepressant, or weight-loss medications; or who were pregnant or lactating were also excluded. The Institutional Review Board of the University of California, Davis, CA approved the experimental protocol, and subjects provided informed consent to participate in the study.
Experimental protocol
Each subject participated in 2 experimental trials conducted in random order. The experimental days were spaced 1 mo apart, and each required an overnight stay in the University of California General Clinical Research Center (GCRC). During each experimental day the subjects consumed identical meals based on calculated energy requirements (as described below) that included beverages sweetened with either HFCS or sucrose. The 18 male subjects were invited to extend participation in the study, and, of these, a subset of 8 men completed 2 additional study days during which they consumed the identical meals accompanied by beverages sweetened with either 100% fructose or glucose. Participation in the additional fructose and glucose trials was limited to male subjects because of budgetary constraints.
Percentage of body fat was determined by measurement of bioelectrical impedance (Tanita 310GS Body Composition Analyzer; Tanita Corporation, Tokyo, Japan). Bioelectrical impedance measurements of body fat in healthy adults has been shown to correlate well with body fat measurements by dual-energy X-ray absorptiometry (17, 18). As there is no consensus on the percentage of body fat standards for overweight and obesity (19), we used a statistical approach of dividing subjects of each sex into 2 equal groups based on ranking by percentage of body fat. Therefore, the men and women were divided into 2 groups with lower and higher body adiposity based on a percentage of body fat less than or greater than 22% and 32%, respectively.
The subjects were instructed to maintain their normal dietary intake and level of physical activity during the interval between the GCRC studies. Following a 12-h overnight fast, the subjects checked into the GCRC at 0700. A physical examination was conducted by the study physician, and an intravenous catheter was inserted and kept patent with a slow saline infusion. Blood sampling commenced at 0800 and continued for 24 h. Thirty-six blood samples were collected for substrate and hormone measurements over the 24-h sampling period during which the subjects consumed 3 standardized meals. Each meal was accompanied by a sucrose-, HFCS-, glucose-, or fructose-sweetened beverage.
Meals
The meals consisted of whole foods and were designed by a registered dietitian. The nutrient composition of the diets was determined using the FOOD PROCESSOR SQL, (ESHA Research Inc, Salem, OR). Each subject ingested 3 meals per day. Breakfast consisted of scrambled eggs, ham, potatoes, and asparagus. Lunch consisted of chicken/tortilla soup with corn chips and cheese. Dinner consisted of lasagna with beef and a salad with lettuce, tomato, cucumber, celery, cheese, and vinaigrette dressing. The energy content of the meals was based on each subject's daily energy requirement as estimated by the Mifflin equation with an activity factor of 1.3 (20). The activity factor was low because the subjects remained relatively sedentary while at the GCRC. Twenty percent of the energy requirement was consumed at breakfast, 35% at lunch, and 45% at dinner. The meals contained 30% energy from fat, 15% from protein, 30% from complex carbohydrate, and 25% from sugar. The 25% sugar consisted of sucrose, HFCS, glucose, or fructose in the form of a beverage. It is important to study the effects of sugars at the 25% of energy intake level. The Institute of Medicine of the National Academies, in the 2002 Dietary References Intakes, concluded that there was insufficient evidence to set an upper-intake level for added sugars because there were no specific adverse health outcomes associated with excessive intake (21). Therefore, they suggested a maximal intake level of 25% of energy intake from added sugars. The sucrose and HFCS beverages were provided by the sponsor (PepsiCo Inc, Purchase, NY) as 11% w:w sugar in noncaffeinated carbonated sodas. The fructose and glucose were prepared as 11% w:w solutions in carbonated soda water, flavored with a commercial unsweetened drink mix. The subjects and GCRC study staff were blinded to the sweetener contained in the beverages. The beverages were not matched for sweetness, but, because the trials were spaced approximately 1 mo apart, it is unlikely the subjects would have noticed a difference in the sweetness of the beverages. The only other beverage served during the 24-h study period was water. Breakfast was consumed at 0900, lunch at 1300, and dinner at 1800. The subjects were required to ingest all of the provided food and beverage within 20 min and were observed to ensure compliance.
Blood sampling
Blood samples were drawn from the catheters at 30-min intervals around periods of meal ingestion and during the predicted nocturnal rise of plasma leptin concentrations (ie, 5 h after the evening meal) and at hourly intervals at other times (22). After the 3 baseline samples, which were collected at 0800, 0830, and 0900 before ingestion of the first meal, a total of 33 additional samples were collected 30–60 min apart. Each sample collection involved the removal of 1 mL of blood to clear the catheter tubing, followed by a 5 mL collection into blood-collection tubes containing EDTA. Samples were then centrifuged, divided into aliquots, and stored at –80 °C until assayed.
Assays and data analysis
Plasma glucose and lactate concentrations were measured with an automatic analyzer (YSI 2300 StatPlus Glucose Analyzer; Yellow Springs Instruments, Yellow Springs, OH). Insulin and leptin concentrations were measured by radioimmunoassay (Linco Research Inc, St Charles, MO). Total ghrelin concentrations were measured in unextracted plasma with radioimmunoassay (Phoenix Peptide, Phoenix, AZ). TG concentrations were measured with an automatic analyzer using manufacturer's reagents (PolyChem Analyzer; PolyMedCo Inc, Cortlandt Manor, NY). FFAs were measured with enzymatic colormetric reagents (Wako Chemicals, Richmond, VA). Fasting lipid concentrations were measured at baseline and at 0800 the following morning, and apolipoprotein B100 (ApoB) concentrations were measured at baseline and at 2200 with an automatic analyzer (PolyChem Analyzer).
The area under the curve (AUC) was calculated for glucose, insulin, ghrelin, FFA, and TG with a data spreadsheet program (Microsoft EXCEL; Microsoft, Redmond, WA) using the trapezoidal method. The mean of the 3 baseline values was determined, and net AUC was calculated by subtracting the areas below baseline from AUC values above baseline. AUCs for glucose, insulin, ghrelin, FFA, and TG are expressed as units per 23 h above each subject's fasting baseline levels because the 3 samples taken during the first hour determined the baseline levels. The nadirs for plasma leptin were determined as the 2 lowest consecutive morning values before 1200 h, as described previously (22). The AUCs for leptin are therefore expressed as units above each subject's nadir over 24 h. Data from the 34 subjects were analyzed with the statistical software program SPSS (version 15.0; SPSS Inc. Chicago, IL) by using the general linear model for repeated measures that included a sugar x adiposity group x sex interaction. Age was also included in the analysis, with subjects grouped by 20–29, 30–39, and 40–50 y. Time was included as a within-subject factor to assess change from fasting levels in lipid concentrations. When the general linear model results indicated the presence of a significant sugar effect or sex or body adiposity interaction, paired and unpaired t tests were performed within group, between men and women, or between adiposity groups, respectively. Differences between the responses to the 4 sugars in the subset of 8 male subjects were assessed with GRAPHPAD PRISM (version 4.03; San Diego, CA, USA) using repeated-measures, one-factor ANOVA, and posttests were performed using Tukey's test for multiple comparisons.
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RESULTS |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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. Body weight and baseline fasting plasma concentrations of glucose, hormones, and lipids are shown in Table 2 for the sucrose and HFCS study days. Fasting TG and apoB concentrations were lower in women (–14.1 ± 6.5 and –12.1 ± 4.2 mg/dL, respectively; P < 0.05, paired t test) and higher in men (12.0 ± 5.1 and 6.9 ± 3.4 mg/dL, respectively; P < 0.05, paired t test) on the day of the sucrose feeding compared with the day of the HFCS feeding. There were no differences in baseline concentrations of the other measured parameters on the 2 study days.
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, Table 3). The insulin AUC was slightly but significantly increased by consumption of sucrose-sweetened beverages compared with HFCS-sweetened beverages. This difference was significant in subjects younger than 35 y (n = 17; P < 0.01) but not significant in subjects older than 35 y (n = 17; P = 0.5).
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). Consumption of both sucrose and HFCS significantly increased fasting TG concentrations the following morning (sucrose: +28.3 ± 5.4 mg/dL, P < 0.001; HFCS: +18.9 ± 4.5 mg/dL, P < 0.001) and decreased postprandial ApoB concentrations at 2200 (sucrose: –5.8 ± 1.3 mg/dL, P < 0.001; HFCS: –6.0 ± 1.9 mg/dL, P < 0.01).
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3 times higher than in men (P < 0.01, unpaired t test) during consumption of both HFCS and sucrose (Table 3
, Figure 2A). There was a marked sex difference in 24-h TG AUC, with a mean AUC during sucrose consumption 3 times higher (P < 0.01) and during HFCS consumption 7 times higher (P < 0.001, unpaired t test) in men than in women (Table 3, Figure 2B). The AUC for FFA was less suppressed (ie, less negative) in men compared with women (Table 3), with the effect being statistically significant during HFCS consumption (men: –2.6 ± 0.3 mmol/L23 h; women: –4.5 ± 0.6 mmol/L23 h; P < 0.05) but not during sucrose consumption (men: –2.3 ± 0.3 mmol/L23 h; women: –3.7 ± 0.7 mmol/L23 h; NS, unpaired t test).
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. There were no significant differences in body weight or baseline concentrations of any of the measured parameters across the 4 study days (Table 5).
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, Table 6).
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of the glucose AUCs during fructose and glucose consumption) during sucrose consumption, and 81% of the expected AUC (0.55 x fructose + 0.45 x glucose ) during HFCS consumption. Accordingly, the insulin AUCs during sucrose and HFCS consumption were also lower than expected (84% of the expected value for sucrose; 83% of expected value for HFCS). The 24-h postprandial TG profiles on the days the subjects consumed HFCS or sucrose were not intermediate between those of glucose and fructose as expected but were comparable to the magnitude of the profile following consumption of 100% fructose beverages (Figure 3D). The TG 24-h AUC during HFCS consumption was significantly higher than the AUC during glucose consumption (P < 0.01, Tukey's posttests) (Table 6).
Consumption of all 4 sugar-sweetened beverages with meals also resulted in significant increases in the fasting TG concentrations the following morning (0800 h), but there were no differences among the effects of the 4 sugars. Similarly, all 4 sugars decreased postprandial ApoB concentrations (2200 h); however, the sugar x time interaction was not statistically significant (Table 7).
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DISCUSSION |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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Fasting plasma TG concentrations at 0800 h the following morning were increased compared with baseline levels after both sucrose and HFCS consumption. In the subset of 7 men, consumption of all 4 sugars resulted in significant increases of fasting TG the following morning. These increases in fasting TG induced by 24-h exposure to sugar-sweetened beverages may be transitory. We and other investigators have reported that long-term consumption (
2 wk) of fructose at 20–25% of energy did not increase fasting TG concentrations in healthy subjects (23), in older overweight and obese subjects (24, 25), in hyperinsulinemic female subjects (26), and in patients with type 2 diabetes (27, 28) or hypertriacylglycerolemia (29). However, in other studies, 2 or more weeks of fructose consumption at 15–20% of energy increased fasting TG concentrations in healthy subjects (10, 30-32), in hyperinsulinemic male subjects (32, 33), and in subjects with type 2 diabetes (34). The reasons underlying these conflicting results are not clear. Interestingly, postprandial concentrations of ApoB, measured 4 h after dinner, were significantly decreased compared with baseline levels following consumption of HFCS or sucrose in the 34 subjects and following consumption of all 4 sugars in the subset of 8 male subjects. These data also contrast with results from our 2 long-term studies in which consumption of fructose-sweetened beverages for 10 wk increased both fasting and postprandial ApoB concentrations, whereas consuming glucose-sweetened beverages did not (24, 25). These differences in the effects of short-term and long-term sugar exposure on ApoB and fasting TG concentrations demonstrate the need for long-term studies with both fasting and postprandial measurements to determine the metabolic effects of prolonged daily consumption of sugar-sweetened beverages.
Effects of sex-specific differences
The higher leptin AUC in women compared with men was not unexpected, as sex-specific differences in leptin are well established (35, 36). Men had higher postprandial TG responses than women, and this difference has been demonstrated previously by us (11) in a 24-h study of overweight and obese men and premenopausal women. Bantle et al (10) reported that men had increased postprandial TG levels during consumption of a 6-week, 17%-of-energy fructose diet, but this was not observed in women. Thus, available data suggest that men are more susceptible than women to the effects of sugars containing fructose to increase plasma TG concentrations. Whether this sex-specific difference exists in older males compared with postmenopausal female subjects remains to be determined.
Effects of fructose, glucose, sucrose, and HFCS
As expected, the responses of circulating glucose and insulin induced by consumption of sucrose and HFCS were relative to their glucose and fructose contents, thus intermediate to the larger responses induced by glucose and the lower responses after fructose. We had expected that the TG profiles would be directly related to the fructose content of the beverages consumed. We and Bantle et al (9-11, 25) have demonstrated previously that fructose consumption increases postprandial TG compared with glucose consumption. A likely mechanism is increased hepatic de novo lipogenesis (DNL), which has been reported to increase markedly during fructose ingestion compared with glucose ingestion (37).
In the 7 male subjects who participated in the comparison of all 4 sugars, the 24-h postprandial TG responses to HFCS and sucrose were not intermediate between those induced by fructose and glucose. Sucrose and HFCS resulted in postprandial TG responses that were comparable to pure fructose alone, and consumption of HFCS-sweetened beverages significantly increased 24-h TG AUCs compared with glucose.
It is possible the mechanism by which sucrose and HFCS increase postprandial TG comparably to pure fructose may involve fructose-stimulated hepatic glucose uptake. Low-dose IV infusion of fructose has been reported to increase portal uptake of glucose in dogs (38), and oral fructose has been shown to lower peripheral plasma glucose responses to oral glucose ingestion in humans (39). Data from the present study suggest that additional glucose, when consumed concurrently with fructose, may have been taken up and metabolized in the liver. The consumption of sucrose and HFCS resulted in 24-h glucose and insulin AUCs that were less than would be expected relative to their glucose and fructose content and the AUCs measured during consumption of the beverages sweetened with 100% glucose or fructose.
Activation of sterol receptor element binding protein-1c (SREBP-1c), the major transcriptional regulator of fatty acid synthesis, may also contribute to the larger-than-expected postprandial TG responses during sucrose and HFCS consumption. Matsuzaka et al (40) have reported that glucose, fructose, and sucrose increased hepatic SREBP-1c mRNA expression independently of insulin in streptozotocin-diabetic mice. Interestingly, they found that the timing of the SREBP-1c up-regulation varied following sugar feeding. Glucose and sucrose feeding induced maximal expression of SREBP-1c within 6 h (4- to 7-fold increase), while maximal expression following fructose feeding occurred at 12 h (5-fold increase) (40).
Results from our 2 studies comparing the long-term (10 wk) effects of fructose and glucose consumption demonstrate that the marked postprandial hypertriacylglycerolemia induced by fructose consumption is not a transitory response (24, 25). Similar studies are needed to determine whether the postprandial hypertriacylglycerolemia induced by HFCS and sucrose consumption is also maintained with more prolonged exposure. There is growing evidence to link postprandial lipemia with proatherogenic conditions (12, 13, 41-44). Two recent articles provide clinical evidence to support the association between elevated concentrations of postprandial TG and increased risk of cardiovascular disease. In a prospective cohort study of 7587 women and 6394 men followed for 26 y, elevated nonfasting TG levels were associated with increased risk of myocardial infarction, ischemic heart disease, and death (13). In the Women's Health Study, 26 509 women were followed for 11 y (12). Nonfasting TG levels, but not fasting levels, were associated with incident cardiovascular events independent of traditional cardiac risk factors, levels of other lipids, and markers of insulin resistance (12). In both of these studies there was a significant linear relation between increased nonfasting TG and increased hazard ratio for all outcomes (12, 13).
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Conclusions |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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Comparison of the effects of glucose, fructose, sucrose, and HFCS beverages within the same male subjects demonstrated that postprandial glucose and insulin responses were intermediate between the lower responses induced by pure fructose and the larger responses induced by pure glucose. Unexpectedly, the effects of short-term consumption of HFCS and sucrose on postprandial TG levels were not intermediate to those of fructose and glucose but comparable to fructose alone. Studies to determine whether these high postprandial TG levels are sustained during long-term consumption of sucrose and HFCS are needed. Additional studies in women and in subjects with and without components of the metabolic syndrome, as well as dose-response studies, are needed to more fully understand the metabolic effects of fructose-containing sugars.
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ACKNOWLEDGMENTS |
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The authors' responsibilities were as follows—KLS: responsible for study implementation, organization and analysis of data, and primary preparation of the manuscript; SCG: served as study physician and assisted with manuscript preparation; BRB: responsible for all interactions with human subjects, supervision of dietary staff, and execution of study protocol; MMS: provided assistance with the statistical analysis of the data and manuscript preparation; NLK: assisted with design of the study and the diets and with manuscript preparation; and PJH: responsible for the conception and design of the study, obtaining funding, and preparation of the manuscript. All authors read and approved the submitted manuscript. None of the authors had any financial or personal conflict of interest.
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REFERENCES |
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TOPABSTRACTINTRODUCTIONSUBJECTS AND METHODSRESULTSDISCUSSIONConclusionsREFERENCES |
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) in plasma leptin (C) over the morning nadir and ghrelin concentrations (D) from mean baseline levels (0800–0900) during a 24-h period (0800–0800) in 34 women and men consuming HFCS- or sucrose-sweetened beverages with each meal. Data shown as mean ± SEM.
