Abstract
Emerging evidence suggest an impaired endocannabinoid activity in the pathophysiology of binge eating disorder (BED). Herein, we investigated whether endocannabinoid tone could be modified as a consequence of dietary-induced binge eating in female rats. For this purpose, brain levels of the endocannabinoids anandamide (AEA) and 2-arachidonoyl glycerol (2-AG), as well as two endocannabinoid-like lipids, oleoylethanolamide (OEA) and palmitoylethanolamide (PEA), were assessed in different brain areas involved in the hedonic feeding (i.e., prefrontal cortex, nucleus accumbens, amygdala, hippocampus, and hypothalamus). The brain density of cannabinoid type-1 receptors (CB1) was also evaluated. Furthermore, we determined plasma levels of leptin, ghrelin, and corticosterone hormones, which are well-known to control the levels of endocannabioids and/or CB1 receptors in the brain. To induce binge eating behavior, rats were subject to an intermittent and limited access to a high fat diet (HFD) (margarine). Three experimental groups were used, all with ad libitum access to chow: control (CTRL), with no access to margarine; low restriction (LR), with 2 h margarine access 7 days/week; high restriction (HR), with 2 h margarine access 3 days/week. Bingeing was established when margarine intake in the HR group exceeded that of the LR group. Our results show that, compared to CTRL, AEA significantly decreased in the caudate putamen, amygdala, and hippocampus of HR group. In contrast, 2-AG significantly increased in the hippocampus while OEA decreased in the hypothalamus. Similar to the HR group, AEA and OEA decreased respectively in the amygdala and hypothalamus and 2-AG increased in the hippocampus of LR group. Moreover, LR group also had AEA decreased in the prefrontal cortex and increased in the nucleus accumbens. In both groups we found the same reduction of CB1 receptor density in the prefrontal cortex compared to CTRL. Also, LR and HR groups showed alterations in both ghrelin and corticosterone levels, while leptin remained unaltered. In conclusion, our findings show a modified endocannabinoid tone due to margarine exposure, in several brain areas that are known to influence the hedonic aspect of food. Even if not uniquely specific to binge eating, margarine-induced changes in endocannabinoid tone could contributes to the development and maintenance of this behavior.
Highlights
Binge eating disorder (BED) is one of the most common eating disorders and is characterized by recurrent and persistent episodes of compulsive overeating of certain foods, typically highly palatable foods rich in calories, that are not inevitably motivated by hunger or metabolic needs (APA, 2013)
With respect to chow consumption during the 2 h limited access period, two-way analysis of variance (ANOVA) revealed a significant effect of dietary group [F(2, 462) = 32.51, P < 0.0001] and subsequent individual one-way ANOVA within each day, showed that both low restriction (LR) and high restriction (HR) groups consumed significantly less chow than CTRL [week 1: [W] F(2, 33) = 5.560, P < 0.01; week 2: [F] F(2, 33) = 9.997, P < 0.001; week 3: [M] F(2, 33) = 3.919, P = 0.0297, [W] F(2, 33) = 6.527, P < 0.05, [F] F(2, 33) = 4.485, P < 0.05; week 4: [M] F(2, 33) = 21.26, P < 0.0001, [W] F(2, 33) = 20.33, P < 0.0001; week 5: [M] F(2, 33) = 5.498, P < 0.01] (Figure 3B)
When looking at the total caloric intake consumed by each dietary group during the 24 h period calculated as 1-block week (M/T, W/Th, F/S), two-way ANOVA detected a significant dietary group x time interaction [F(8, 132) = 2.14, P < 0.05], and post-hoc analysis showed the HR group had a higher total intake than the LR and CTRL groups from the first week of the study (Table 1)
Summary
Binge eating disorder (BED) is one of the most common eating disorders and is characterized by recurrent and persistent episodes of compulsive overeating of certain foods (binge eating), typically highly palatable foods rich in calories, that are not inevitably motivated by hunger or metabolic needs (APA, 2013). Several line of evidence suggest that a dysfunction in the mesocorticolimbic system, that represent the principal neural pathway that drive hedonic feeding, could be a main mechanism associated with development of this disorder (Davis and Carter, 2009; Dichter et al, 2012; Witt and Lowe, 2014) This pathway consist of subpopulations of dopaminergic neurons, originating in the ventral tegmental area and pars compacta of the substantia nigra, which project to the nucleus accumbens, as well as to other limbic structures, such as the amygdala, hippocampus, and prefrontal cortex (Kenny, 2011; Hutson et al, 2018). All these areas are highly connected to the hypothalamus, and many molecules involved in homeostatic hypothalamic regulation of feeding, such as leptin and ghrelin, play an important role in the hedonic and motivational components of food (Monteleone and Maj, 2013; Murray et al, 2014)
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