Estrogen and the etiology of anorexia nervosa
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Synaptic changes in the hippocampus of adolescent female rodents associated with resilience to anxiety and suppression of food restriction-evoked hyperactivity in an animal model for anorexia nervosa
2017, Brain ResearchCitation Excerpt :and behavioral flexibility, together with its pharmacological attributes (expression of receptors for sex hormones, stress hormones and the growth hormone secretagogue, ghrelin), makes this structure a good candidate as a node that influences an individual׳s vulnerability to anorexia nervosa. Estrogens generally inhibit food intake (Young, 1991), and estrogen receptor beta (ESR2) polymorphism (1082G>A) has been shown to be associated with anorexia nervosa (Eastwood et al., 2002; Rosenkranz et al., 1998). Most reviews consider the role of estrogen in anorexia nervosa, as it interacts with the dopamine, serotonin and neuropeptide systems within brains of individuals with anorexia nervosa (Casper et al., 2008; Kaye et al., 2009).
Exogenous progesterone exacerbates running response of adolescent female mice to repeated food restriction stress by changing α4-GABA<inf>A</inf> receptor activity of hippocampal pyramidal cells
2015, NeuroscienceCitation Excerpt :AN has a very high relapse rate (greater than 30 %) and the highest mortality rate among all psychiatric disorders (10–15%); (Sullivan, 1995; Strober et al., 1997; Herzog et al., 1999; Carter et al., 2004; Birmingham et al., 2005). It has been suggested that P4 could ameliorate the symptoms of AN (Young, 1991). Our data indicate that Young’s proposal should be considered cautiously, to the extent that findings from the animal model could be extrapolated to the human disease.
Sex Hormone, Pituitary, Parathyroid, and Adrenal Disorders and the Nervous System
2014, Aminoff's Neurology and General Medicine: Fifth EditionAnorexia Nervosa and Estrogen Receptors
2013, Vitamins and HormonesCitation Excerpt :AN presents a high heritability, and genetic analysis, in AN families and in case–control studies, also supports an involvement of estrogen pathway in vulnerability to AN (Hinney, Scherag, & Hebebrand, 2010; Ramoz, Versini, & Gorwood, 2007; Rask-Andersen, Olszewski, Levine, & Schiöth, 2010; Versini et al., 2010). The hypothesis of the involvement of estrogen in the control of food intake and in AN has been discussed for a long time (Butera, 2010; Young, 1991, 2010). This chapter focuses on the biological pathway of estrogen receptors and their potential role in the development of AN.
Anorexia nervosa and estrogen: Current status of the hypothesis
2010, Neuroscience and Biobehavioral ReviewsMolecular mechanisms underlying anorexia nervosa: Focus on human gene association studies and systems controlling food intake
2010, Brain Research ReviewsCitation Excerpt :AN predominantly develops in girls around the age of puberty which suggests the involvement of female sex hormones in the development of the disease. Animal studies have shown estrogen to be anorexigenic, potentially via inhibition of NPY expressing neurons in the arcuate nucleus (Young, 1991) and by involvement in the CCK-dependent satiety inducing cascade of events in the hindbrain (Geary et al., 2001). In fact, the proper functioning of the estrogen system is necessary for normal food intake, adiposity and body weight control (Geary et al., 2001).