Effect of chronic stress on gastric emptying and plasma ghrelin levels in rats

Ochi, Masahiro; Tominaga, Kazunari; Tanaka, Fumio; Tanigawa, Tetsuya; Shiba, Masatsugu; Watanabe, Toshio; Fujiwara, Yasuhiro; Oshitani, Nobuhide; Higuchi, Kazuhide; Arakawa, Tetsuo

doi:10.1016/j.lfs.2008.01.020

Cited by 118 publications

(109 citation statements)

References 33 publications

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“…In our fatigued model, the rat was kept in a water cage for 5 d to induce psychological and physical exhaustion, during which energy consumption would be increased. Indeed, an increase in plasma ghrelin levels has been reported in these fatigued rats (27). These observations suggest that an increase in gastric aromatase might be involved in energy homeostasis via regulation of gastric ghrelin production.…”

Section: Discussionmentioning

confidence: 79%

“…Ghrelin, an endogenous ligand for the growth hormone secretagogue receptor, is predominantly produced in the stomach (25), and its expression and release are thought to be regulated by gastric estrogen in a paracrine fashion (26). Recently, ghrelin levels have been observed to be upregulated in a chronic stress model in rats (27), which was originally developed by our group as a comprehensive fatigue model (21). To confirm whether gastric aromatase is also upregulated in such a fatigued condition, we performed 11 C-vorozole PET studies in these fatigued rats.…”

Section: Pet Studies In Fatigued Ratsmentioning

confidence: 99%

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PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole

Ozawa¹,

Takahashi²,

Akazawa³

et al. 2011

J Nucl Med

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Aromatase is a rate-limiting enzyme for estrogen biosynthesis and has been implicated in pathophysiological states of various diseases via estrogen production. This enzyme is known to be widely distributed in extragonadal and gonadal tissues including the stomach. In contrast to circulating estrogen, the functional role of gastric aromatase/estrogen has not been elucidated in detail, because there is no efficient methodology to investigate spatiotemporal changes of gastric aromatase/ estrogen in vivo. Recently, (S)-11 C-6-[(4-chlorophenyl)(1H-1,2,4-triazole-1-yl)methyl]-1-methyl-1H-benzotriazole ( 11 Clabeled vorozole), based on a potent nonsteroidal aromatase inhibitor, has been developed as a tracer to investigate aromatase distribution in living animals and humans using a noninvasive PET technique. In the present study, we investigated gastric aromatase expression by means of PET with 11 C-vorozole. Methods: After bolus injection of 11 C-vorozole into the tail vein, emission scans were obtained for 90 min on male and female rats under isoflurane anesthesia. Displacement studies with unlabeled vorozole and autoradiographic analysis were conducted for demonstration of specific binding. Immunohistochemistry was performed to confirm aromatase expression. Results: PET scans revealed that 11 C-vorozole highly accumulated in the stomach and adrenal glands. Displacement studies and autoradiography demonstrated that aromatase was expressed in the stomach but that the accumulation of 11 C-vorozole in the adrenal glands might be through nonspecific binding. Immunohistochemical analysis revealed that aromatase is expressed in gastric parietal cells but not in adrenal glands. Moreover, the accumulation of 11 C-vorozole in the stomach was significantly increased in fatigued rats. Conclusion: These results suggest that the 11 C-vorozole PET technique is a useful tool for evaluation of gastric aromatase dynamics in vivo, which may provide important information for understanding the molecular mechanisms of gastric aromatase/estrogenrelated pathophysiological processes and for the development of new drugs.

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Section: Discussionmentioning

confidence: 79%

Section: Pet Studies In Fatigued Ratsmentioning

confidence: 99%

PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole

Ozawa¹,

Takahashi²,

Akazawa³

et al. 2011

J Nucl Med

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“…Leptin and ghrelin are involved in hypothalamo-pituitaryadrenal (HPA) responses to stressful stimuli (Spinedi & Gaillard 1998, Kristenssson et al 2006, Patterson-Buckendahl et al 2007, Ochi et al 2008. Here, restriction stress decreased plasma ghrelin levels and increased leptin levels.…”

Section: Discussionmentioning

confidence: 97%

Nutritional and environmental factors affecting plasma ghrelin and leptin levels in rats

Nakahara¹,

Okame²,

Katayama³

et al. 2010

Journal of Endocrinology

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We examined which factors suppress the rise of ghrelin secretion under hunger in 16-h-starved rats, and compared the responses of plasma ghrelin and leptin levels to various exogenous and endogenous stimuli in intact rats. Although an acute expansion of the stomach by infusion of 6 ml air or 3 ml water in rats starved for 16 h did not change the level of plasma acyl-ghrelin 3 ml corn starch solution, corn oil, or 20% ethanol significantly decreased it. Vagotomy inhibited suppression by nutrients but not by ethanol. Chronic infusion of ethanol into the stomach for 3 weeks in free-feeding rats caused widespread injury of the stomach mucosa, and increased both plasma ghrelin levels and the number of ghrelin cells. In intact rats, low temperature did not change ghrelin levels, but increased leptin levels. On the other hand, restriction stress decreased plasma ghrelin levels, but had the reverse effect on plasma leptin levels. Although insulin decreased and 20% glucose increased plasma glucose levels, they both decreased plasma ghrelin levels. Insulin elevated plasma leptin levels, but glucose had no effect. These results indicate that 1) acyl-ghrelin secretion from the stomach under fasting condition is suppressed by nutrients but not by mechanical expansion of the stomach; 2) high and low environmental temperature, stress, or administration of insulin reciprocally affect plasma levels of ghrelin and leptin; and 3) an increase of stomach ghrelin cell number and plasma ghrelin levels after chronic ethanol treatment may be involved in restoration of gastric mucosae.

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“…Regarding a potential role for ghrelin in stress-based eating, elevations of ghrelin have been observed in several animal and human stress models (26)(27)(28)(29)(30)(31). For instance, human subjects subjected to the standardized trier social stress test display increased plasma ghrelin (30).…”

Section: Introductionmentioning

confidence: 99%

Ghrelin mediates stress-induced food-reward behavior in mice

Chuang¹,

Perelló²,

Sakata³

et al. 2011

J. Clin. Invest.

303

344

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The popular media and personal anecdotes are rich with examples of stress-induced eating of calorically dense "comfort foods." Such behavioral reactions likely contribute to the increased prevalence of obesity in humans experiencing chronic stress or atypical depression. However, the molecular substrates and neurocircuits controlling the complex behaviors responsible for stress-based eating remain mostly unknown, and few animal models have been described for probing the mechanisms orchestrating this response. Here, we describe a system in which food-reward behavior, assessed using a conditioned place preference (CPP) task, is monitored in mice after exposure to chronic social defeat stress (CSDS), a model of prolonged psychosocial stress, featuring aspects of major depression and posttraumatic stress disorder. Under this regime, CSDS increased both CPP for and intake of high-fat diet, and stress-induced food-reward behavior was dependent on signaling by the peptide hormone ghrelin. Also, signaling specifically in catecholaminergic neurons mediated not only ghrelin's orexigenic, antidepressant-like, and food-reward behavioral effects, but also was sufficient to mediate stress-induced food-reward behavior. Thus, this mouse model has allowed us to ascribe a role for ghrelin-engaged catecholaminergic neurons in stress-induced eating. IntroductionMost humans experience altered feeding behaviors upon stress, with approximately 40% eating more and 40% eating less than usual (1). Furthermore, upon stress, most people report an increase in the intake of highly palatable foods, independent of hyperphagia or hypophagia (2, 3). Altered eating is also a frequent finding in individuals with major depressive disorder, with the "atypical" subtype even containing hyperphagia as a possible distinguishing characteristic (4). In one study, 46% of study subjects who met DSM-IV criteria for major depressive disorder with atypical features reported increased appetite (5). Of the remaining depressed patients without atypical features, 18% reported increased appetite, while 50% reported decreased appetite (5). The complex eating behaviors that are associated with and/or stimulated by stress and major depression undoubtedly contribute to the increased number of overweight and obese individuals who experience or have experienced stress and depression. For example, a longitudinal study from New Zealand showed that major depression in late-adolescent girls was associated with a 2.3-fold increased risk of obesity in adulthood and, furthermore, that the prevalence of obesity in adulthood was positively correlated with the number of major depressive episodes during adolescence in these girls (6). In another study, 47% of a large cohort of subjects with atypical depression reported increased body weight (5). Also, the combined overweight and obesity prevalence in a sample of US veterans with posttraumatic stress disorder was found in a chart review study to exceed that within the US general population by 20% (7).

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Effect of chronic stress on gastric emptying and plasma ghrelin levels in rats

Cited by 118 publications

References 33 publications

PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole

PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole

Nutritional and environmental factors affecting plasma ghrelin and leptin levels in rats

Ghrelin mediates stress-induced food-reward behavior in mice

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Effect of chronic stress on gastric emptying and plasma ghrelin levels in rats

Cited by 118 publications

References 33 publications

PET of Aromatase in Gastric Parietal Cells Using 11C-Vorozole

PET of Aromatase in Gastric Parietal Cells Using 11C-Vorozole

Nutritional and environmental factors affecting plasma ghrelin and leptin levels in rats

Ghrelin mediates stress-induced food-reward behavior in mice

Contact Info

Product

Resources

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PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole

PET of Aromatase in Gastric Parietal Cells Using ¹¹C-Vorozole