Although it is widely accepted that obesity results from an imbalance of energy intake and expenditure, the mechanisms underlying this process and effective strategies for prevention and treatment are unclear. Growing evidence suggests excess consumption of sugar may play an important role, yet we showed previously that consuming up to 30% of calories as sucrose in the diet had no impact on weight regulation. Since in humans consumption of sugar-sweetened beverages has been widely implicated, we investigated whether the mode of ingestion (solid or liquid) had different impacts on body weight regulation and glucose homeostasis in mice.


Dietary sucrose was delivered in solid (as part of a standard pelleted rodent chow) and liquid (in drinking water) to male C57BL/6 mice for 8 weeks. Body weight, body composition, energy intake and expenditure were monitored, as well as glucose and insulin tolerance tests. Expression of sweet taste receptors on the tongue, glycogen and fat contents of the liver were measured.


Sucrose consumption in solid form, even when comprising 73% of ingested calories, did not induce adiposity. Consequently, mice fed solid sucrose were leaner and metabolically healthier. However, the same amount of sucrose given in liquid form was responsible for significantly higher energy intake, greater body weight gain and increased adiposity . The expression of the hepatic insulin receptor substrate 2 (Irs2) was repressed, correlated with a higher circulating serum insulin level and impaired glucose homeostasis in liquid sucrose fed mice. The altered metabolic homeostasis was mostly attributable to body fatness rather than directly to energy input from sucrose.


Consumption of sucrose-sweetened water, but not equivalent levels of solid sucrose, led to body fat gain in C57BL/6 mice. These data support the suggestion that consumption of sugar sweetened beverages may be an important contributor to dysregulation of body weight and related metabolic syndromes.