Induced weight loss by caloric restriction or bariatric surgery in
humans and rodents demonstrates that alterations in the fat (and
sweet)tasteresponsivenessarereversible
[46,47]
.Inobesesubjects,
dietary restriction reduced the spontaneous consumption of foods
high in fat and/or sugar
[48]
, while patients with a gastric bypass
fi
nd fatty (and sweet) meals less pleasant
[47]
. Animal studies yield
similar observations. Reversibility of obesity-associated alterations
of oro-sensory perceptions of fat and sweet during weight loss in-
dicates that the size of fat mass plays a signi
fi
cant role in the
regulation of these taste modalities in rodents
[45,46]
. For instance,
an inverse correlation between fat preference and adipose tissue
size was found by using calorie-restricted DIO mice
[45]
. An endo-
crine in
fl
uence is likely. Consistent with this assumption, the in-
crease in sweet taste sensitivity observed during weight loss in
obese women appears to be correlated with the decrease in plasma
leptin levels
[37]
. In rodents, the increased detection threshold (
¼
lower sensitivity) for corn oil or sucrose found in obese rats is
reproduced by exogenous leptin administration in weight-reduced
animals
[44]
. Other alternative, but non-exclusive, in
fl
uences
related to adiposity must be explored, including obesity-induced
in
fl
ammation. Indeed, lipopolysaccharide-induced in
fl
ammation
disturbs the physiology of gustatory papilla