Stress and eating: a dual role for bombesin-like peptides

Abstract

The current obesity “epidemic” in the developed world is a major health concern; over half of adult Canadians are now classified as overweight or obese. Although the reasons for high obesity rates remain unknown, an important factor appears to be the role stressors play in overconsumption of food and weight gain. In this context, increased stressor exposure and/or perceived stress may influence eating behavior and food choices. Stress-induced anorexia is often noted in rats exposed to chronic stress (e.g., repeated restraint) and access to standard Chow diet; associated reduced consumption and weight loss. However, if a similar stressor exposure takes place in the presence of palatable, calorie dense food, rats often consume an increase proportion of palatable food relative to Chow, leading to weight gain and obesity. In humans, a similar desire to eat palatable or “comfort” foods has been noted under stressful situations; it is thought that this response may potentially be attributable to stress-buffering properties and/or through activation of reward pathways. The complex interplay between stress-induced anorexia and stress-induced obesity is discussed in terms of the overlapping circuitry and neurochemicals that mediate feeding, stress and reward pathways. In particular, this paper draws attention to the bombesin family of peptides (BBs) initially shown to regulate food intake and subsequently shown to mediate stress response as well. Evidence is presented to support the hypothesis that BBs may be involved in stress-induced anorexia under certain conditions, but that the same peptides could also be involved in stress-induced obesity. This hypothesis is based on the unique distribution of BBs in key cortico-limbic brain regions involved in food regulation, reward, incentive salience and motivationally driven behavior.

The behavior of larval zebrafish reveals stressor-mediated anorexia during early vertebrate development

“…In adult zebrafish, pre-exposure to either aversive stimuli or alarm cues caused reduced feeding (Oswald and Robison, 2008 ). Also, just as in humans, where the effect of stress on food intake can be either positive or negative, models of both stress-induced anorexia and stress-induced obesity are being advanced (Merali et al, 2013 ), highlighting the complexity of the link between stress and metabolic disorders. It has been shown, for example, that adult zebrafish exposed to alarm signals gained weight (as compared to non-exposed individuals) only if they were on a high-fat diet (Nguyen et al, 2013 ).…”

Insights into bombesin receptors and ligands: Highlighting recent advances

“…Manipulation of BnRs could potentially have an important therapeutic role in obesity, food intake and energy/glucose metabolism (Table 3) [129,193,214,215,279,370,386,387]. This has occurred because of the demonstrated role of each of the three human BnRs, the GRPR, the NMBR and BRS-3, in regulating satiety, with evidence from both receptor knockout studies [163,249,259,370,387] and from pharmacological studies using Bn receptor agonists and antagonists [50,161,169,170,311].…”

Anorexia in human and experimental animal models: physiological aspects related to neuropeptides

“…Various types of physiological and pathophysiological anorexia models have been proposed, although these models are not the same model as human anorexia because of its complexities of biological, psychological and/or environmental abnormalities. The typical models of physiological anorexia are dehydrationinduced anorexia and stress-induced anorexia [9][10][11][12]. On the other hand, the typical models of pathophysiological anorexia are drug-induced anorexia, lipopolysaccharides (LPS)-induced anorexia, anti-cancer drug-induced anorexia as a side effect and cancer-induced cachexia-anorexia [13][14][15].…”