OBJECTIVE: Previous studies have reported that individuals with obesity have reduced taste perception, but the relationship between obesity and taste is poorly understood. Earlier work has demonstrated that diet-induced obesity directly impairs taste. Currently, it is not clear whether these changes to taste are due to obesity or to the high-fat diet exposure. The goal of the current study was to determine whether diet or excess weight is responsible for the taste deficits induced by diet-induced obesity. METHODS: C57BL/6 mice were placed on either high-fat or standard chow in the presence or absence of captopril. Mice on captopril did not gain weight when exposed to a high-fat diet. Changes in the responses to different taste stimuli were evaluated using live cell imaging, brief-access licking, immunohistochemistry, and real-time polymerase chain reaction. RESULTS: Diet and weight gain each affected taste responses, but their effects varied by stimulus. Two key signaling proteins, α-gustducin and phospholipase Cβ2, were significantly reduced in the mice on the high-fat diet with and without weight gain, identifying a potential mechanism for the reduced taste responsiveness to some stimuli. CONCLUSIONS: Our data indicate that, for some stimuli, diet alone can cause taste deficits, even without the onset of obesity.
OBJECTIVE: Previous studies have reported that individuals with obesity have reduced taste perception, but the relationship between obesity and taste is poorly understood. Earlier work has demonstrated that diet-induced obesity directly impairs taste. Currently, it is not clear whether these changes to taste are due to obesity or to the high-fat diet exposure. The goal of the current study was to determine whether diet or excess weight is responsible for the taste deficits induced by diet-induced obesity. METHODS: C57BL/6 mice were placed on either high-fat or standard chow in the presence or absence of captopril. Mice on captopril did not gain weight when exposed to a high-fat diet. Changes in the responses to different taste stimuli were evaluated using live cell imaging, brief-access licking, immunohistochemistry, and real-time polymerase chain reaction. RESULTS: Diet and weight gain each affected taste responses, but their effects varied by stimulus. Two key signaling proteins, α-gustducin and phospholipase Cβ2, were significantly reduced in the mice on the high-fat diet with and without weight gain, identifying a potential mechanism for the reduced taste responsiveness to some stimuli. CONCLUSIONS: Our data indicate that, for some stimuli, diet alone can cause taste deficits, even without the onset of obesity.
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