Abstract
Aspartame consumption is implicated in the development of obesity and metabolic disease despite the intention of limiting caloric intake. The mechanisms responsible for this association remain unclear, but may involve circulating metabolites and the gut microbiota. Aims were to examine the impact of chronic low-dose aspartame consumption on anthropometric, metabolic and microbial parameters in a diet-induced obese model. Male Sprague-Dawley rats were randomized into a standard chow diet (CH, 12% kcal fat) or high fat (HF, 60% kcal fat) and further into ad libitum water control (W) or low-dose aspartame (A, 5–7 mg/kg/d in drinking water) treatments for 8 week (n = 10–12 animals/treatment). Animals on aspartame consumed fewer calories, gained less weight and had a more favorable body composition when challenged with HF compared to animals consuming water. Despite this, aspartame elevated fasting glucose levels and an insulin tolerance test showed aspartame to impair insulin-stimulated glucose disposal in both CH and HF, independently of body composition. Fecal analysis of gut bacterial composition showed aspartame to increase total bacteria, the abundance of Enterobacteriaceae and Clostridium leptum. An interaction between HF and aspartame was also observed for Roseburia ssp wherein HF-A was higher than HF-W (P<0.05). Within HF, aspartame attenuated the typical HF-induced increase in the Firmicutes:Bacteroidetes ratio. Serum metabolomics analysis revealed aspartame to be rapidly metabolized and to be associated with elevations in the short chain fatty acid propionate, a bacterial end product and highly gluconeogenic substrate, potentially explaining its negative affects on insulin tolerance. How aspartame influences gut microbial composition and the implications of these changes on the development of metabolic disease require further investigation.
Highlights
Regular consumption of artificially sweetened soft drinks is associated with disorders of the metabolic syndrome, including abdominal obesity, insulin resistance and/or impaired glucose tolerance, dyslipidemia and high blood pressure [1,2,3]
All animals, had access to food and fluid ad libitum for an additional 8 week prior to sacrifice. This resulted in four treatment groups (n = 10–12 per treatment); chow water (CHW), high fat water (HFW), chow aspartame (CHA) and high fat aspartame (HFA)
CHA and HFA consumed 17 and 25% less energy, but more fluid compared to their respective controls (p,0.05)
Summary
Regular consumption of artificially sweetened soft drinks is associated with disorders of the metabolic syndrome, including abdominal obesity, insulin resistance and/or impaired glucose tolerance, dyslipidemia and high blood pressure [1,2,3]. Daily diet soda consumption (primarily sweetened with N-a-L-aspartyl-L-phenylalanine methyl ester, aspartame, APM), is reported to increase the relative risk of type 2 diabetes and the metabolic syndrome by 67% and 36% respectively [3]. Given this data, and the presence of APM in over 6000 food products, there is a need to understand the potential role of APM sweetened products in the development and maintenance of metabolic disease [4]. Microbial metabolites appearing in serum consist of metabolic intermediates, organic acids and bacterial fermentation end products including the short chain fatty acids (SCFA) [12,13,14]
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