Sensory-specific satiety is intact in rats made obese on a high-fat high-sugar choice diet

Abstract

Sensory-specific satiety (SSS) is the temporary decreased pleasantness of a recently eaten food, which inhibits further eating. Evidence is currently mixed whether SSS is weaker in obese people, and whether such difference precedes or follows from the obese state. Animal models allow testing whether diet-induced obesity causes SSS impairment. Female rats (n = 24) were randomly assigned to an obesogenic high-fat, high-sugar choice diet or chow-only control. Tests of SSS involved pre-feeding a single palatable, distinctively-flavored food (cheese- or cocoa-flavored) prior to free choice between both foods. Rats were tested for short-term SSS (2 h pre-feeding immediately followed by 2 h choice) and long-term SSS (3 day pre-feeding prior to choice on day 4). In both short- and long-term tests rats exhibited SSS by shifting preference towards the food not recently eaten. SSS was not impaired in obese rats. On the contrary, in the long-term tests they showed stronger SSS than controls. This demonstrates that neither the obese state nor a history of excess energy consumption fundamentally causes impaired SSS in rats. The putative impaired SSS in obese people may instead reflect a specific predisposition, properties of the obesogenic diet, or history of restrictive dieting and bingeing.

High Fat/High Glucose Diet Induces Metabolic Syndrome in an Experimental Rat Model

“…As fructose is around twice as sweet as glucose [ 11 ], the reduced caloric intake seems to be caused by a reduced liquid intake due to a sensory-specific satiety. Sensory-specific satiety is defined as the declining pleasure and attraction to the sensory attributes to a specific food eaten in a meal [ 20 ]. Regarding to this, a glucose solution could be more pleasant to drink than a fructose solution, thus reducing the sweet-related satiety, resulting in a major consumption of glucose under same conditions.…”

Trace Amine Associated Receptor 1 (TAAR1) Modulation of Food Reward

“…Compulsive eating behavior is characteristic of certain forms of obesity, BED, BN, certain forms of AN, and food addiction ( de Zwaan, 2001 ; Davis and Carter, 2009 ; Gearhardt et al, 2009 ; American Psychiatric Association, 2013 ; Davis, 2013b ; Volkow et al, 2013 ; Hone-Blanchet and Fecteau, 2014 ). Compulsive eating behavior has been dissected into three functional domains: habitual overeating, eating to alleviate a negative emotional state, and overeating despite negative consequences ( Moore et al, 2017a , b , c ), engendered by maladaptive habit formation ( Furlong et al, 2014 ), the emergence of a negative affect ( Cottone et al, 2009 ; Blasio et al, 2013 ; Iemolo et al, 2013 ), and a failure of inhibitory control systems ( Velazquez-Sanchez et al, 2015 ; Nieh et al, 2015 ; Myers, 2017 ), respectively. ‘Loss of control’ is thought to result from deficits in inhibitory control mechanisms responsible for the suppression of inappropriate actions.…”

Stressing the importance of choice: Validity of a preclinical free‐choice high‐caloric diet paradigm to model behavioural, physiological and molecular adaptations during human diet‐induced obesity and metabolic dysfunction

“…In a recent study, Harris confirmed our initial observations on snacking behaviour by demonstrating that the consumption of sucrose in a fluid but not solid form results in significant sucrose solution snacking behaviour during the light/inactive phase. Finally, it was recently investigated whether fc‐HFHS diet rats show altered sensory‐specific satiety, which refers to the declining pleasure and attraction to the sensory attributes of a specific food eaten in the meal relative to other foods . However, the results demonstrated that female Sprague‐Dawley made obese by long‐term maintenance on a fc‐HFHS had intact sensory‐specific satiety .…”

“…Finally, it was recently investigated whether fc‐HFHS diet rats show altered sensory‐specific satiety, which refers to the declining pleasure and attraction to the sensory attributes of a specific food eaten in the meal relative to other foods . However, the results demonstrated that female Sprague‐Dawley made obese by long‐term maintenance on a fc‐HFHS had intact sensory‐specific satiety . Together, these observations suggest that the inclusion of an individual sucrose solution source drives ‘snacking’ behaviour, especially during the light/inactive phase, and that the consumption of individual fat and sugar components over‐rides the feedback signalling mechanisms normally preventing caloric overconsumption, without affecting sensory‐specific satiety.…”

“…Consumption of a fc-HFHS, for up to 6 months, increases total body weight gain compared to CD controls, and this was associated with profound increases in abdominal and subcutaneous white adipose tissue (WAT) mass. [33][34][35][36][37][38][39][40][41][42] Male Wistar or Sprague-Dawley rats with access to a fc-HF or fc-HS diet consistently show no or very limited effects on total body weight gain compared to CD controls, despite increases in terminal WAT mass. [33][34][35][36][37] When female Sprague-Dawley rats were maintained on a fc-HFHS diet containing a solution with maltodextrin, a polysaccharide composed of chains of glucose, for up to 36 weeks, increases in body weight gain and persistent hyperphagia were also observed.…”