Skip to main content
ARS Home » Pacific West Area » Davis, California » Western Human Nutrition Research Center » Obesity and Metabolism Research » Research » Publications at this Location » Publication #221133

Title: Twenty-four Hour Endocrine and Metabolic Profiles Following Consumption of High Fructose Corn Syrup-, Sucrose- Fructose-, and Glucose-Sweetened Beverages with Meals

Author
item STANHOPE, KIMBER - UC DAVIS, NUTR. DEPT.
item GRIFFEN, STEVEN - UCDMC SCHOOL OF MEDICINE
item BAIR, BRANDI - UC DAVIS, NUTR. DEPT.
item SWARBRICK, MICHAEL - POST DOC FELLOW, UCD NUTR
item Keim, Nancy
item HAVEL, PETER - UC DAVIS DETP. NUTR. PROF

Submitted to: The American Journal of Clinical Nutrition
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 1/4/2008
Publication Date: 7/10/2008
Citation: Stanhope, K.L., Griffen, S.C., Bair, B.R., Swarbrick, M.M., Keim, N.L., Havel, P.J. 2008. Twenty-four Hour Endocrine and Metabolic Profiles Following Consumption of High Fructose Corn Syrup-, Sucrose- Fructose-, and Glucose-Sweetened Beverages with Meals. American Journal of Clinical Nutrition. Amer. J. Clin. Nutr., 87:1194-1203, 2008.

Interpretive Summary: The amount of added sweeteners, such as high-fructose corn syrup and sucrose (table sugar), consumed in the United States has increased in recent years, along with the increase in obesity and other diseases associated with obesity. We studied the effect of consuming a large quantity of high-fructose corn syrup, sucrose, and their simple sugars—fructose and glucose—in the form of sweetened beverages taken with mixed meals at breakfast, lunch and dinner on blood glucose and blood lipid levels in adults. We found men displayed a more pronounced increase in blood triglycerides in response to the sweeteners, compared to women. The consumption of HFCS and table sugar produced increases in blood triglycerides that were comparable to that of pure fructose, even though the fructose content of the beverages with these sweeteners was only half that delivered in the pure fructose-sweetened beverage. Overall, ingestion of sucrose- or HFCS-sweetened beverages produced similar metabolic and hormonal effects. In males, HFCS-, sucrose-, and fructose-sweetened beverages led to significantly elevated levels of triglycerides following meals, a finding that is concerning considering that high levels of lipids circulating in the blood pose a significant risk for cardiovascular disease

Technical Abstract: We have reported that compared with glucose-sweetened beverages, consuming fructose-sweetened beverages with meals results in lower 24-h circulating glucose, insulin and leptin concentrations, and elevated triacylglycerol (TG). However, pure fructose and glucose are not commonly used as sweeteners. High fructose corn syrup (HFCS) has replaced sucrose as the predominant sweetener in beverages in the U.S. We compared the metabolic/endocrine effects of HFCS with sucrose, and in a subset of subjects with pure fructose and glucose. Thirty-four men and women consumed 3 isocaloric meals with either sucrose- or HFCS-sweetened beverages, and blood samples were collected over 24 hours. Eight of the male subjects were also studied when fructose- or glucose-sweetened beverages were consumed. In 34 subjects, 24-h glucose, insulin, leptin, ghrelin and TG profiles were similar between days that sucrose or HFCS were consumed. Postprandial TG excursions after HFCS or sucrose were larger in men than women. In the 8 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. In conclusion, sucrose and HFCS do not have substantially different short-term endocrine/ metabolic effects. However, in male subjects, short-term consumption of sucrose, HFCS, and fructose all significantly elevate postprandial TG exposure, a risk factor for atherogenesis and cardiovascular disease.