Effect of Activation of the Serotoninergic System During Prolonged Starvation on Subsequent Caloric Intake and Macronutrient Selection in the Zucker Rat

Duhault, J; Lacour, F.; Espinal, J.; Rolland, Y.

doi:10.1006/appe.1993.1015

Cited by 10 publications

(6 citation statements)

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“…In ABA rats, the initiation of food‐anticipatory behaviour failed to increase accumbal 5‐HT release, the levels of 5‐HT remained low and their circadian activity was blunted (Verhagen et al ., ). In spite of low 5‐HT levels, rats starved for 4 days showed post‐fasting anorexia, suggesting an up‐regulation of satiety signals (Duhault et al ., ). The enhanced satiety and suppression of appetite may result from a compensatory up‐regulation of 5‐HT receptors that occurs after restricted diet‐induced reduction of brain 5‐HT content (Haleem and Haider, ).…”

Section: Bridging An To Its Animal Models With 5‐htmentioning

confidence: 97%

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Gestel

Kostrzewa

Adan

et al. 2014

British J Pharmacology

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Eating disorders, such as anorexia nervosa (AN), bulimia nervosa (BN) and binge eating disorders (BED), are described as abnormal eating habits that usually involve insufficient or excessive food intake. Animal models have been developed that provide insight into certain aspects of eating disorders. Several drugs have been found efficacious in these animal models and some of them have eventually proven useful in the treatment of eating disorders. This review will cover the role of monoaminergic neurotransmitters in eating disorders and their pharmacological manipulations in animal models and humans. Dopamine, 5‐HT (serotonin) and noradrenaline in hypothalamic and striatal regions regulate food intake by affecting hunger and satiety and by affecting rewarding and motivational aspects of feeding. Reduced neurotransmission by dopamine, 5‐HT and noradrenaline and compensatory changes, at least in dopamine D2 and 5‐HT2C/2A receptors, have been related to the pathophysiology of AN in humans and animal models. Also, in disorders and animal models of BN and BED, monoaminergic neurotransmission is down‐regulated but receptor level changes are different from those seen in AN. A hypofunctional dopamine system or overactive α2‐adrenoceptors may contribute to an attenuated response to (palatable) food and result in hedonic binge eating. Evidence for the efficacy of monoaminergic treatments for AN is limited, while more support exists for the treatment of BN or BED with monoaminergic drugs. Linked Articles This article is part of a themed section on Animal Models in Psychiatry Research. To view the other articles in this section visit http://dx.doi.org/10.1111/bph.2014.171.issue-20

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Section: Bridging An To Its Animal Models With 5‐htmentioning

confidence: 97%

Pharmacological manipulations in animal models of anorexia and binge eating in relation to humans

Gestel

Kostrzewa

Adan

et al. 2014

British J Pharmacology

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“…The process of glycogenolysis is observed in the first 24 hours of fasting [20, 39, 46–49]. Thereafter, gluconeogenesis from amino acid precursors and lipolysis from glycerol, as well as from lactate through the Cori cycle, maintain a regular supply of glucose.…”

Section: Stressmentioning

confidence: 99%

Oxidative Stress, Prooxidants, and Antioxidants: The Interplay

Rahal

Kumar

Singh³

et al. 2014

BioMed Research International

1,355

917

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Oxidative stress is a normal phenomenon in the body. Under normal conditions, the physiologically important intracellular levels of reactive oxygen species (ROS) are maintained at low levels by various enzyme systems participating in the in vivo redox homeostasis. Therefore, oxidative stress can also be viewed as an imbalance between the prooxidants and antioxidants in the body. For the last two decades, oxidative stress has been one of the most burning topics among the biological researchers all over the world. Several reasons can be assigned to justify its importance: knowledge about reactive oxygen and nitrogen species production and metabolism; identification of biomarkers for oxidative damage; evidence relating manifestation of chronic and some acute health problems to oxidative stress; identification of various dietary antioxidants present in plant foods as bioactive molecules; and so on. This review discusses the importance of oxidative stress in the body growth and development as well as proteomic and genomic evidences of its relationship with disease development, incidence of malignancies and autoimmune disorders, increased susceptibility to bacterial, viral, and parasitic diseases, and an interplay with prooxidants and antioxidants for maintaining a sound health, which would be helpful in enhancing the knowledge of any biochemist, pathophysiologist, or medical personnel regarding this important issue.

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“…Although we have a lot of therapeutic experiences on this treatment [9,10], the precise therapeutic mechanisms have not been clarified so far. However, several interpretations have been considered for the treatment.…”

Section: Therapeutic Mechanism Of the Ftmentioning

confidence: 95%

“…There is evidence that FT is capable of increasing a-power and of decreasing h-power of the EEG [6]. During starvation, the brain shifts the major energy source from glucose to h-hydroxy butylic acid and acetoacetate which change the neurotransmission [7][8][9][10]. Interestingly, h-hydroxy butylic acid is a precursor of g-amino butylic acid (GABA) [7], which receptors are strongly related to anxiety.…”

Section: Therapeutic Mechanism Of the Ftmentioning

confidence: 99%