Effects of three intense sweeteners on fat storage in the C. elegans model

Abstract

Beverages sweetened with caloric sweeteners (CS), glucose, sucrose or high-fructose corn syrup, are associated with weight gain. Beverages sweetened with intense sweeteners (IS) are marketed as low-calorie substitutes to prevent beverages-associated weight gain. Using Caenorhabditis elegans, the effects on intestinal fat deposition (IFD) and pharyngeal pumping rate (PPR) of cola beverages sweetened with glucose, aspartame, or aspartame plus acesulfame-potassium (AceK) were compared. Control groups received Escherichia coli (OP50) only. Study I: the nematodes received additional glucose- or IS-sweetened beverages. Study II: the nematodes received additional glucose, aspartame, or aspartame plus AceK (AAK). Beverages containing CS or IS (aspartame or AAK) did not alter IFD in wild type (N2) or in daf-16 deficiency. The CS cola increased IFD in sir-2.1 deficiency (P<0.05). The AAK-cola increased IFD in daf-16/daf-2 deficiency and sir-2.1 deficiency (P<0.05). Glucose increased IFD in N2 and daf-16 deficiency (P<0.05). Aspartame showed a tendency towards reduced IFD in N2 and decreased IFD in daf-16/daf-2 deficiency (P<0.05). AAK increased IFD in daf-16 deficiency and sir-2.1 deficiency (P<0.05), and reversed the aspartame-induced reduction in IFD. The aspartame-sweetened cola increased the PPR in daf-16/daf-2 deficiency and daf-16 deficiency (P<0.05); similar results were obtained in N2 with both IS (P<0.05). AAK increased the PPR in daf-16/daf-2, daf-16, and sir-2.1 deficiencies (P<0.05). Thus, IS increased the PPR, a surrogate marker of lifespan. Aspartame may have an independent effect in reducing IFD to assist humans desiring weight loss. AceK may increase IFD in presence of insulin resistance.