Effects of consuming sugar-sweetened beverages for 2 weeks on 24-h circulating leptin profiles, ad libitum food intake and body weight in young adults

Authors: SIGALA, DESIREE - University Of California, Davis; WIDAMAN, ADRIANNE - San Jose State University; HERIONIMUS, BETTINA - University Of California, Davis; NUNEZ, MARINELLE - University Of California, Davis; LEE, VIVIEN - University Of California, Davis; BENYAM, YANET - University Of California, Davis; BREMER, ANDREW - National Institutes Of Health (NIH); MEDICI, VALENTINA - University Of California, Davis; HAVEL, PETER - University Of California, Davis; STANHOPE, KIMBER - University Of California, Davis; Keim, Nancy

Submitted to: Nutrients
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 12/16/2020
Publication Date: 12/19/2020
Citation: Sigala, D.M., Widaman, A., Herionimus, B., Nunez, M., Lee, V., Benyam, Y., Bremer, A.A., Medici, V., Havel, P., Stanhope, K.L., Keim, N.L. 2020. Effects of consuming sugar-sweetened beverages for 2 weeks on 24-h circulating leptin profiles, ad libitum food intake and body weight in young adults. Nutrients. 12(2). Article 3893. https://doi.org/10.3390/nu12123893.
DOI: https://doi.org/10.3390/nu12123893

Interpretive Summary: There is substantial evidence to suggest that drinking large quantities of sugar-sweetened beverages contributes to an unhealthy body weight. A popular theory is that beverage calories are ‘invisible’ to food intake control mechanisms, however, little is known about why this occurs. To better understand the body’s failure to regulate food intake with sugar-sweetened beverages, under controlled conditions, we studied food intake of young adults who consumed one of three different sugar-sweetened beverages or a non-caloric beverage sweetened by aspartame. In addition, we measured a circulating hormone, leptin, that is known to influence food intake. We found that the sugar sweetened beverages were indeed partially invisible and that including these beverages with meals led to increased calorie intake. However, leptin levels, measured continuously throughout the day when food intake was measured, did not explain this increase in calorie intake. Other biological signals affecting food intake may be involved, and this needs further study.

Technical Abstract: Background: Sugar-sweetened beverage (sugar-SB) consumption may significantly contribute to overweight and obesity through excess energy intake. We hypothesized that this effect may be mediated by the effect of fructose to decrease in 24-h leptin concentrations. We examined the effects of consuming beverages sweetened with aspartame, glucose, fructose, sucrose, or high-fructose corn syrup (HFCS), for two weeks on body weight, ad libitum energy intake and day-long leptin concentrations. Methods: 131 young adults (normal- and overweight 18-35 kg/m2, males and females, 18-40yrs) participated in a parallel, double-blinded, intervention study. Body weight was monitored and ad libitum food intake trials were conducted during breakfast, lunch, and dinner on the first day of a 3.5-d baseline inpatient period. 24-h serial blood samples were collected while standardized meals were consumed on the third day. Participants were then assigned to consume three sweetened beverages (SB)/day containing aspartame (n=23) or 25% of their energy requirement as glucose- (n=28), fructose- (n=28), sucrose- (n=24) or HFCS-SB (n=28) for a 12-day outpatient period. This was followed by a 3.5-d intervention inpatient period, during which participants consumed SB during follow-up ad libitum food intake trials and 24-h serial blood collections. On the 9th day of intervention, fructose malabsorption was assessed before and following SB consumption by measurements of breath hydrogen. Serial plasma samples were assayed for leptin and 24-h area under the curve (AUCs) were calculated. Results: There were no significant differences in body weight gain among beverage groups. Subjects consuming glucose- (0.5 kg, P=0.02) and HFCS-SB (0.8 kg, P=0.0008) had significantly increased body weight compared to baseline and subjects consuming fructose did not (0.1 kg, P=0.8). Compared to energy intake during the baseline ad libitum food intake trial and to subjects consuming aspartame-SB (-4%, P=0.27), subjects consuming sucrose- (+14%, P<0.001 vs baseline; P=0.002 vs aspartame-SB) and fructose-SB (+9%, P=0.002 vs baseline; P=0.03 vs aspartame-SB) had significantly increased energy intake during the intervention trial. However, compared to baseline, subjects consuming glucose- (6%, P=0.056 vs baseline) and HFCS-SB (8%, P=0.01) also consumed more energy during the intervention ad libitum food intake trials. Thus, all sugar-SB groups failed to fully compensate for beverage energy. Fructose-SB consumption caused a significant decrease in 24-h leptin AUC compared to baseline (-14 ng/mLx24h, P=0.0317) and compared to consumption of sucrose-SB (+26 ng/mLx24h, P=0.0006 vs baseline; P=0.0008 vs fructose-SB). The changes in leptin did not explain the changes in ad libitum energy intake or body weight. Breath hydrogen was significantly increased in subjects consuming fructose-SB compared to all other groups. Conclusion: The addition of sugar-SB, but not aspartame-SB, to ad libitum meals led to increased energy intake. These results support the evidence that suggest consuming sugar-SB leads to failure to fully compensate for beverage energy and contributes to weight gain. The results do not support our hypothesis that effects of sugar-SB consumption on energy intake and body weight gain are mediated by the fructose-induced reduction in circulating leptin. Energy intake and weight gain in subjects consuming fructose-SB may be affected by fructose malabsorption.