31 research outputs found
Influence of the ovarian cycle and estradiol on binge eating evoked in female rats by food restriction followed by frustration stress.
No full textEating disorders show marked gender differences (Klump et al 2008 Psych Med 38:1749-57) and several epidemiologic studies suggest that binge eating episodes are more common in females than in males. To further investigate the mechanisms underlying this sex difference, we used an animal model first described by Cifani et al (2009 Psychopharm 204:113-125), in which binge-eating is evoked in female rats by 3 cycles of food restriction followed by frustration stress (15 min exposure to the sight of the palatable food). We aimed to determine whether binge eating behavior (1) varies across the estrus cycle and (2) is influenced by estradiol (E2) in ovariectomized (OVX) rats. Finally, using immunocytochemistry, we quantified the activation of extracellular signal regulated kinase (ERK) signaling pathway in OVX rats treated with E2 or oil, in basolateral (BLA) and the central (CeA) amygdala, paraventricular nucleus of hypothalamus (PVN) and arcuate nucleus (ARC).
Restricted and stressed rats in estrus and OVX rats treated with E2 did not show binge eating behavior in comparison to the control non-restricted and non-stressed rats. The lack of binge eating behavior in estrous rats was accompanied by a significant decrease in ERK phosphorylation in ARC, PVN and in the CeA, but not in BLA, in comparison to non-estrous rats and to non-restricted and non-stressed animals.
Our findings show that binge eating does not occur during the estrous phase. Because this was recapitulated in OVX rats treated with E2, they suggest that the inhibitory effect of E2 on eating is partly responsible for the lack of bingeing. These results are consistent with reports in women with bulimia nervosa (Edler et al 2007 Psych Med, 37:131-141) and extend our previous findings and increase the validity of our model, that can be used in translational studies of the mechanism of binge eating behavior
Estradiol-dependent decreases in emotional binge-like eating are associated with decreased brain pERK expression in ovariectomized rats.
No full textBulimia nervosa, binge eating disorder and emotional eating occur more commonly in females than in males. To investigate the influence of the ovarian cycle and estradiol (E2) on binge eating, we used an animal model in which binge-like eating is evoked in female rats by three cycles of food restriction followed by “frustration” stress (15 min exposure to the sight and odor of a palatable food). We sought to determine whether binge-like eating behavior varies across the estrus cycle or is influenced by E2 in ovariectomized (OVX) rats, and whether these differences are associated with differences in the neuronal activation pattern using extracellular signal-regulated kinase (ERK) phosphorylation as a marker in the basolateral (BLA) and the central (CeA) amygdala, paraventricular nucleus of hypothalamus (PVN) and arcuate nucleus (ARC). Food restricted and stressed non-estrus rats showed binge-like eating behavior and an increase in ERK phosphorylation in ARC, PVN and in the CeA, but not in BLA, in comparison to the control not restricted and not stressed rats. The binge-like eating response and ERK phosphorylation were not present in restricted and stressed rats in estrus, and in OVX-E2 rats. Stress and food restriction elicited binge-like eating behavior both in non-estrus as well as in OVX rats not treated with E2. These results are consistent with reports in women with bulimia nervosa, and they extend our previous findings and increase the validity of our model that can be used in translational studies of the mechanism of binge eating behavior
Influence of the ovarian cycle and estradiol in frustration stress-induced binge-like palatable food consumption in female rats with a history of food restriction
No full textEating disorders show marked gender differences [1] and several epidemiologic
studies suggest that binge eating episodes are more common in females than in males [2]. To
further investigate the mechanisms underlying this sex difference, we used an animal model first described by Cifani et al. [3], in which binge eating is evoked in female rats by food restriction
followed by frustration stress (15 min exposure to the sight of the palatable food). We aimed to
determine whether binge eating behavior varies across the estrus cycle and is influenced by
estradiol in ovariectomized (OVX) rats. Finally, using immunocytochemistry, we quantified the
activation of extracellular signal regulated kinase (ERK) signaling pathway in OVX rats treated
with estradiol or oil vehicle, in basolateral (BLA) and the central (CeA) nuclei of the amygdala,
paraventricular nucleus of hypothalamus (PVN) and arcuate nucleus (ARC). Restricted and
stressed non-estrus rats showed binge eating behavior in comparison to the control not restricted
and not stressed rats. This response was not present in restricted and stressed rats in estrus, and in
OVX rats treated with estradiol. This lack of binge eating behavior was accompanied by a
significant decrease in ERK phosphorylation in ARC, PVN and in the CeA, but not in BLA, in
comparison to non-estrous rats and to not restricted and not stressed animals. Our behavioral
findings show that binge eating does not occur during the estrous phase. Because this was
recapitulated in OVX rats treated with estradiol, we propose that the inhibitory effect of estradiol
on eating is partly responsible for the lack of bingeing. These findings are consistent with reports
in women with bulimia nervosa [4], in whom the binge frequency decreased during the follicular
phase, a time of the menstrual cycle when eating is also lowest. These results extend our
previous findings and increase the validity of our model, such that it can be used in translational
studies of the mechanism of binge eating behavior. References: [1] Klump et al. 2008 Psych Med
38:1749-57 [2] Cifani et al. 2009 Psychopharmology 204:113-125 [3] Hudson et al. 2007 Biol
Psychiatry 61:348-358 [4] Edler et al. 2007 Psych Med 37:131-14
Estrogenic suppression of binge-like eating elicited by cyclic food restriction and frustrative-nonreward stress in female rats
No full textBecause binge eating and emotional eating vary through the menstrual cycle in human females, we investigated cyclic changes in binge-like eating in female rats and their control by estrogens. Binge-like eating was elicited by three cycles of 4 days of food restriction and 4 days of free feeding followed by a single frustrative nonreward-stress episode (15 min visual and olfactory exposure to a familiar palatable food) immediately before presentation of the palatable food. Intact rats showed binge-like eating during the diestrous and proestrous phases of the ovarian cycle, but not during the estrous (periovulatory) phase. Ovariectomized (OVX) rats not treated with estradiol (E2) displayed binge-like eating, whereas E2-treated OVX rats did not. The procedure did not increase signs of anxiety in an open-field test. OVX rats not treated with E2 that were subjected to food restriction and sacrificed immediately after frustrative nonreward had increased numbers of cells expressing phosphorylated extracellular signal-regulated kinases (ERK) in the central nucleus of the amygdala (CeA), paraventricular nucleus of hypothalamus (PVN), and dorsal and ventral bed nuclei of the stria terminalis (BNST) compared with nonrestricted or E2-treated rats. These data suggest that this female rat model is appropriate for mechanistic studies of some aspects of menstrual-cycle effects on emotional and binge eating in human females, that anxiety is not a sufficient cause of binge-like eating, and that the PVN, CeA, and BNST may contribute to information processing underlying binge-like eating
Comparative effects of intraduodenal amino acid infusions on food intake and gut hormone release in healthy males
No full textIn contrast to the many studies of the effects of individual amino acids (AAs) on eating, no studies have compared the effects of different AAs on eating and underlying preabsorptive gastrointestinal mechanisms. To compare the effects of intraduodenal infusions of l-tryptophan (TRP), l-leucine (LEU), l-phenylalanine (PHE) and l-glutamine (GLN) on appetite, gastrointestinal hormone responses (including ghrelin, cholecystokinin (CCK), peptide YY (PYY) and glucagon-like peptide-1 [GLP-1]), glycemia (glucagon, insulin and glucose) and test meal size in healthy males, we retrospectively analyzed data from four published independent, randomized, double-blind, placebo-controlled studies of 90-min intraduodenal infusions of the individual AAs. The designs of the studies were identical, except the dose of TRP (0.15 kcal/min) was lower than that of the other AAs (0.45 kcal/min) because higher doses of this AA were not well tolerated. TRP and LEU decreased intake more than PHE (reductions relative to control, ~219 ± 68, ~170 ± 48 and ~12 ± 57 kcal, respectively), and TRP decreased intake more than GLN (~31 ± 82 kcal). These effects of TRP and LEU versus GLN, but not versus PHE, were paralleled by greater decreases in plasma ghrelin, and increases in CCK, concentrations. TRP increased PYY more than GLN or LEU, but not PHE. LEU increased PYY less than PHE. No significant differences were detected for GLP-1. PHE increased glucagon more than TRP or LEU, and increased insulin more than TRP. Under our experimental conditions, intraduodenal TRP and LEU were more satiating than PHE and GLN. The greater satiating efficacy of LEU versus PHE was significantly dissociated from the effects of these AAs on PYY, while the greater satiating potency of TRP versus PHE was significantly dissociated from the effects of these AAs on insulin and glucagon. In contrast, ghrelin and CCK, and potentially other mechanisms, including central sensing of individual AAs, appear to be stronger candidate mechanisms for the relative satiating effects obtained.Robert E. Steinert, Sina S. Ullrich, Nori Geary, Lori Asarian, Marco Bueter, Michael Horowitz, Christine Feinle-Bisse
Ghrelin, CCK, GLP-1, and PYY(3-36): secretory controls and physiological roles in eating and glycemia in health, obesity, and after RYGB
No full textThe efficacy of Roux-en-Y gastric-bypass (RYGB) and other bariatric surgeries in the management of obesity and type 2 diabetes mellitus and novel developments in gastrointestinal (GI) endocrinology have renewed interest in the roles of GI hormones in the control of eating, meal-related glycemia, and obesity. Here we review the nutrient-sensing mechanisms that control the secretion of four of these hormones, ghrelin, cholecystokinin (CCK), glucagon-like peptide-1 (GLP-1), and peptide tyrosine tyrosine [PYY(3-36)], and their contributions to the controls of GI motor function, food intake, and meal-related increases in glycemia in healthy-weight and obese persons, as well as in RYGB patients. Their physiological roles as classical endocrine and as locally acting signals are discussed. Gastric emptying, the detection of specific digestive products by small intestinal enteroendocrine cells, and synergistic interactions among different GI loci all contribute to the secretion of ghrelin, CCK, GLP-1, and PYY(3-36). While CCK has been fully established as an endogenous endocrine control of eating in healthy-weight persons, the roles of all four hormones in eating in obese persons and following RYGB are uncertain. Similarly, only GLP-1 clearly contributes to the endocrine control of meal-related glycemia. It is likely that local signaling is involved in these hormones' actions, but methods to determine the physiological status of local signaling effects are lacking. Further research and fresh approaches are required to better understand ghrelin, CCK, GLP-1, and PYY(3-36) physiology; their roles in obesity and bariatric surgery; and their therapeutic potentials.Robert E. Steinert, Christine Feinle-Bisset, Lori Asarian, Michael Horowitz, Christoph Beglinger, Nori Gear
Estradiol (E2) increases the acute eating-inhibitory effect of amylin in ovariectomized (OVX) rats
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Ovariectomy and estradiol treatment affect subcutaneous more than intra-abdominal adipose tissue in rats
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