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Review
. 2012 Aug;1264(1):36-48.
doi: 10.1111/j.1749-6632.2012.06573.x. Epub 2012 May 22.

Food reward in the obese and after weight loss induced by calorie restriction and bariatric surgery

Hans-Rudolf Berthoud  1 , Huiyuan Zheng, Andrew C Shin
Affiliations
Free PMC article
Review

Food reward in the obese and after weight loss induced by calorie restriction and bariatric surgery

Hans-Rudolf Berthoud et al. Ann N Y Acad Sci. 2012 Aug.
Free PMC article

Abstract

Increased availability of tasty, energy-dense foods has been blamed as a major factor in the alarmingly high prevalence of obesity, diabetes, and metabolic disease, even in young age. A heated debate has started as to whether some of these foods should be considered addictive, similar to drugs and alcohol. One of the main arguments for food addiction is the similarity of the neural mechanisms underlying reward generation by foods and drugs. Here, we will discuss how food intake can generate reward and how behavioral and neural reward functions are different in obese subjects. Because most studies simply compare lean and obese subjects, it is not clear whether predisposing differences in reward functions cause overeating and weight gain, or whether repeated exposure or secondary effects of the obese state alter reward functions. While studies in both rodents and humans demonstrate preexisting differences in reward functions in the obese, studies in rodent models using calorie restriction and gastric bypass surgery show that some differences are reversible by weight loss and are therefore secondary to the obese state.

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Figures

Figure 1
Figure 1
Brief access lick performance as a test of taste-guided liking of sucrose (A) and corn oil (B) in lean and obese rats. Lick performance was first compared between separate groups of chow-fed lean rats (n = 7) and high fat–fed obese rats (n = 7). Obese rats fed a high-fat diet throughout (n = 6) were then subjected to a cycle of weight loss (∼20% in three weeks by means of calorie restriction) and regain (two weeks, as shown in Fig. 3). During the weight-reduced state they received either saline or leptin (1 mg/kg, ip, 1 h before test). In another experiment, lick performance was assessed three to five months after sham surgery (n = 6) or RYGB surgery (n = 5). Note that the significantly reduced response performance to low concentrations of both sucrose and corn oil in the obese versus lean, weight-reduced + leptin versus weight-reduced, and weight-regain versus weight-reduced groups (*P < 0.05 compared with the same concentration). Also note the significantly increased response to the two low concentrations of sucrose and the three low concentrations of corn oil, but the significantly reduced response to the highest concentration of sucrose in RYGB rats compared to sham-operated rats (*P < 0.05, compared with the same concentration). Statistics are based on two separate ANOVAs for each taste stimulant, one for the sham-operated and RYGB rats and one for all other conditions, and Bonferroni-corrected multiple comparisons.
Figure 2
Figure 2
Body weight of rats used for testing reward behaviors. (A) Outbred Sprague–Dawley rats were either fed chow throughout (lean controls, n = 6) or were made obese by 12–16 weeks of high-fat feeding. One cohort of obese rats was then calorie restricted on a high-fat diet for three weeks and kept at a 20% lower body weight for four weeks, before the full amount of high-fat diet was restored and most of the lost body weight was regained. Arrows indicate the time of behavioral testing. (B) Outbred Sprague–Dawley rats made obese with a choice diet consisting of high-fat chow, Ensure, and chow were subjected to RYGB surgery (n = 6) or sham surgery (n = 8), and compared with age-matched, chow-fed lean controls. Behavioral testing was performed three to five months after surgery. Body composition was monitored throughout each experiment to verify the designations “lean” and “obese.”
Figure 3
Figure 3
Regression analysis showing relationship between brief access lick performance and adiposity (as measured by NMR) across rats of all lean and obese conditions as shown in Figure 1. Note that lick performance for 0.01M sucrose (A) and 1% corn oil (B) was negatively correlated with adiposity.
Figure 4
Figure 4
Number of positive hedonic orofacial reactions (Grill & Norgren's taste reactivity test) as a measure of liking of sucrose in Sprague–Dawley rats five months after RYGB or sham surgery and in age-matched, chow-fed lean rats (A), and in genetic lines of obesity-prone rats five months after RYGB or sham surgery (B). Bars that do not share the same letters are significantly (P < 0.05) different from each other (based on Bonferroni-corrected multiple comparisons following separate ANOVAs).
Figure 5
Figure 5
Gastric bypass surgery reduces fat preference in rats. (A, B) Gradual development of reduced fat preference after RYGB surgery in Sprague–Dawley rats as assessed with a choice of two complete solid diets low (13%) or high (60%) in fat. (C) Reduced fat preference measured three months after RYGB or sham surgery in Sprague–Dawley rats given 12-h access to two complete liquid diets, one low (10%) and one high (60%). Bars that do not share the same letter are significantly (P < 0.05) different from each other (based on Bonferroni-corrected multiple comparisons after appropriate ANOVA). (D) Almost complete avoidance of solid high-fat (60%) diet in chow-fed, nonobese Sprague–Dawley rats, three months after RYGB. *P < 0.05 compared to sham-operated rats.
Figure 6
Figure 6
Motivation to obtain food reward (wanting) as measured in the incentive runway and progressive ratio lever press tests. (A) A wanting index was calculated as the mean completion speed averaged over trials 4–7. Note that in outbred Sprague–Dawley rats, high fat–fed obese rats showed reduced wanting compared to chow-fed lean rats and that wanting was restored after weight loss induced by RYGB surgery. Also, genetic lines of young obesity-prone rats exhibited reduced wanting compared to obesity-resistant rats. Eight weeks of high-fat feeding in these genetic lines did not produce further significant changes in wanting (B) Break point in the progressive ratio paradigm was significantly lower in obesity-prone versus obesity-resistant rats both in the fed and fasted condition. Bars that do not share the same letter are significantly (P < 0.05) different from each other (based on Bonferroni-corrected multiple comparisons after appropriate ANOVA).
Figure 7
Figure 7
Schematic diagram showing the relationship between food reward and obesity.
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References

    1. Rosenbaum M, et al. Leptin reverses weight loss-induced changes in regional neural activity responses to visual food stimuli. J. Clin. Invest. 2008;118:2583–2591. - PMC - PubMed
    1. Sjostrom L, et al. Effects of bariatric surgery on mortality in Swedish obese subjects. N. Engl. J. Med. 2007;357:741–752. - PubMed
    1. Ravussin E, Bogardus C. Energy balance and weight regulation: genetics versus environment. Br. J. Nutr. 2000;83(Suppl 1):S17–S20. - PubMed
    1. Gluckman PD, Hanson MA, Beedle AS. Early life events and their consequences for later disease: a life history and evolutionary perspective. Am. J. Hum. Biol. 2007;19:1–19. - PubMed
    1. Corwin RL, Hajnal A. Too much of a good thing: neurobiology of non-homeostatic eating and drug abuse. Physiol. Behav. 2005;86:5–8. - PMC - PubMed