Models of anorexia

Avraham, Yosefa; Dagon, Yossi; Magen, Iddo; Berry, Elliot M.

doi:10.1016/j.ddmod.2005.08.010

Cited by 4 publications

(4 citation statements)

References 63 publications

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“…Anorexia is caused by many factors stemming from psychology, physiology and genetics (Avraham et al, 2005). Considerable research has been conducted in an attempt to explain the physiology of anorexia, with several studies conducted at the hypothalamic level (Kaye, 1996;Bergh and Södersten, 1998;Fetissov et al, 2002).…”

Section: Introductionmentioning

confidence: 99%

Differential feeding responses to central alpha-melanocyte stimulating hormone in genetically low and high body weight selected lines of chickens

et al. 2008

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Section: Introductionmentioning

confidence: 99%

Differential feeding responses to central alpha-melanocyte stimulating hormone in genetically low and high body weight selected lines of chickens

et al. 2008

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“…Second, diet restriction does not model the antecedents of this devastating disease. Despite these limitations, many of the changes in neuroendocrine function and other phenotypes found in AN patients can be mimicked by DR in mice, thus giving it some face validity as a model of certain aspects of the disease [2]. Indeed, restricted caloric intake models key phenotypes presented by an anorexia nervosa patient, including profound weight loss, cognitive deficits, alterations in hormones and neurotransmitters, and increased mortality and morbidity.…”

Section: Discussionmentioning

confidence: 99%

“…AN models include the following aspects: adolescent onset of the disease, predominance in females, decreased food intake and body weight, increased activity and abnormal neuoroendocrine function. In the present study, we employed the DR model because it results in several phenotypes presented by AN patients, including profound weight loss, cognitive deficits, alterations in hormones and neurotransmitters, and increased mortality and morbidity [2, 10]. …”

Section: Introductionmentioning

confidence: 99%

Fish oil promotes survival and protects against cognitive decline in severely undernourished mice by normalizing satiety signals

Avraham

Saidian

Burston

et al. 2011

The Journal of Nutritional Biochemistry

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Severe malnutrition resulting from anorexia nervosa or involuntary starvation leads to low weight, cognitive deficits, and increased mortality rates. In the present study, we examined whether fish oil supplementation, compared with canola oil, would ameliorate the morbidity and mortality associated with these conditions by normalizing endocannabinoid and monoaminergeric systems as well as other systems involved in satiety and cognitive function within the hypothalamus and hippocampus. Female Sabra mice restricted to 40% of their daily food intake exhibited decreased body weight, were sickly in appearance, displayed cognitive deficits, and had increased mortality rates. Strikingly, fish oil supplementation that contains high omega-3 fatty acids levels decreased mortality and morbidity, and normalized the expression of genes and neurotransmitters in the hippocampus and hypothalamus. Fish oil supplementation, but not canola oil, increased survival rates, improved general appearance, and prevented cognitive decline, despite the facts that both diets contained an equivalent number of calories and that there were no differences in weight between mice maintained on the two diets in 100% but decrease in the 40%. In the hypothalamus, the beneficial effects of fish oil supplementation were related to normalization of the endocannabinoid 2-arachidonylglycerol (2-AG), serotonin (5-HT) (p<0.056), dopamine (DA), neuropeptide Y (NPY), and Ca2+/calmodulin (CaM)-dependent protein kinase (Camkk2). In the hippocampus, fish oil supplementation normalized 5-HT, Camkk2, silent mating type information regulation 1 (SIRT-1), and brain-derived neurotrophic factor (BDNF). In conclusion, dietary supplements of fish oil, as source of omega-3 fatty acids, may alleviate cognitive impairments associated with severe diet restriction and prolong survival independently of weight gain by normalizing neurochemical systems.

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“…In the quantitative food restriction models, the severity of the restriction generates various levels of weight loss associated with modifications of energy expenditure and respiratory quotient ( 145 , 147 – 150 ). Indeed, long-term 30% FR in mice leads to a significant shift to carbohydrate metabolism during the meal ( 145 ).…”

Section: Inputs Of Animal Models Of Anmentioning

confidence: 99%

The Use of Animal Models to Decipher Physiological and Neurobiological Alterations of Anorexia Nervosa Patients

2015

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Extensive studies were performed to decipher the mechanisms regulating feeding due to the worldwide obesity pandemy and its complications. The data obtained might be adapted to another disorder related to alteration of food intake, the restrictive anorexia nervosa. This multifactorial disease with a complex and unknown etiology is considered as an awful eating disorder since the chronic refusal to eat leads to severe, and sometimes, irreversible complications for the whole organism, until death. There is an urgent need to better understand the different aspects of the disease to develop novel approaches complementary to the usual psychological therapies. For this purpose, the use of pertinent animal models becomes a necessity. We present here the various rodent models described in the literature that might be used to dissect central and peripheral mechanisms involved in the adaptation to deficient energy supplies and/or the maintenance of physiological alterations on the long term. Data obtained from the spontaneous or engineered genetic models permit to better apprehend the implication of one signaling system (hormone, neuropeptide, neurotransmitter) in the development of several symptoms observed in anorexia nervosa. As example, mutations in the ghrelin, serotonin, dopamine pathways lead to alterations that mimic the phenotype, but compensatory mechanisms often occur rendering necessary the use of more selective gene strategies. Until now, environmental animal models based on one or several inducing factors like diet restriction, stress, or physical activity mimicked more extensively central and peripheral alterations decribed in anorexia nervosa. They bring significant data on feeding behavior, energy expenditure, and central circuit alterations. Animal models are described and criticized on the basis of the criteria of validity for anorexia nervosa.

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Models of anorexia

Cited by 4 publications

References 63 publications

Differential feeding responses to central alpha-melanocyte stimulating hormone in genetically low and high body weight selected lines of chickens

Differential feeding responses to central alpha-melanocyte stimulating hormone in genetically low and high body weight selected lines of chickens

Fish oil promotes survival and protects against cognitive decline in severely undernourished mice by normalizing satiety signals

The Use of Animal Models to Decipher Physiological and Neurobiological Alterations of Anorexia Nervosa Patients

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