کد مقاله | کد نشریه | سال انتشار | مقاله انگلیسی | نسخه تمام متن |
---|---|---|---|---|
6261901 | 1613260 | 2013 | 8 صفحه PDF | دانلود رایگان |

- Emotional stress induces anorexia in laboratory animals, and obesity in humans.
- Stress per se does not result in overeating and obesity, only at high caloric diet.
- Glucocorticoids stimulate and stress inhibits food intake in laboratory animals.
- In animals the orexigenic effects of glucocorticoids are overcome by other factors (like CRH) at acute and chronic stresses.
The prevalence of obesity is increasing worldwide with serious consequences such as diabetes mellitus type 2 and cardiovascular diseases. Emotional stress is considered to be one of the main reasons of obesity development in humans. However, there are some contradictory results, which should be addressed. First of all stress induces anorexia, but not overeating in laboratory animals. Glucocorticoids, the effector molecules of the hypothalamo-pituitary-adrenocortical (HPA) axis stimulate and stress inhibits food intake. It is also not clear if stress is diabetogenic or an antidiabetogenic factor. The review will discusses these issues and the involvement of the whole HPA axis and its separate molecules (glucocorticoids, adrenocorticotropin, corticotropin-releasing hormone) in food intake regulation under stress.
Bidirectional effects of stress on eating behavior. We assume that in animals and humans, stress affects food intake in a bidirectional way depending on stress intensity and environmental factors. Any stress activates both anorexigenic and orexigenic pathways. Balance between the pathways shifts to anorexigenic if high calorie food is not available, and shifts to orexigenic if high calorie food is available, obviously due to reduced aversiveness of stressor and rewarding potential of the food. Thus, stress may potentiate the development of obesity and other aspects of metabolic syndrome only in animals and people, which fed a high calorie, fat and sugar diet. Solid lines, direct effects; dashed lines, indirect effects; CRH, corticotropin-releasing hormone; ACTH, adrenocorticotropin; GCs, glucocorticoids; Ucn 3, urocortin 3; CART, cocain-amphetamine related peptide; NPW, neuropeptide W; SSS, sensory specific satiety; NPY, neuropeptide Y; AgRP, agouti-related peptide.
Journal: Brain Research Bulletin - Volume 95, June 2013, Pages 46-53