Test of the hypothesis that eating high-salt food leads to obesity by stimulating sugar-solution consumption

Abstract

High salt intake has been linked to obesity in humans and rodents, although the direction of causation and underlying mechanisms are unclear. One hypothesis suggests that consuming salt stimulates thirst, which is assuaged by drinking sugar-sweetened beverages, leading to excess energy intake and thus obesity. We attempted to test this hypothesis using a mouse model. Adult male C57BL/6J mice ate semi-synthetic diets with either low (0.56 g Na+/kg diet) or high (5.62 g Na+/kg diet) salt content for 8 weeks. Half the mice fed each diet could drink water; the other half could drink both water and a 16% sucrose solution. Mice fed the high-salt diet with water to drink ingested ~25% more water than did those fed the low-salt diet with water to drink, demonstrating that salt stimulated thirst. However, there was no influence of dietary salt on water or sucrose intake in the groups with access to both water and sucrose. This was probably because sucrose intakes were near-maximal in both groups; mice apparently do not require salt to encourage them to drink sucrose. Dietary salt level had no effect on body weight. Relative to mice that drank only water, those that drank sucrose had a net increase in energy intake but, surprisingly, gained less body weight, perhaps because they consumed too little protein to thrive. In sum, our results do not support the hypothesis that salt increases sugar-sweetened beverage consumption, leading to obesity; however, the simple mouse model used here may not provide a competent test of this hypothesis.