Upregulated expression of neuropeptide Y in hypothalamic–pituitary system of rats by chronic dexamethasone administration

Konno, Jinko; Yoshida, Shigeo; Ina, Ayuka; Ohmomo, Hideki; Shutoh, Fumihiro; Nogami, Hisashi; Hisano, Setsuji

doi:10.1016/j.neures.2007.11.005

Cited by 21 publications

(16 citation statements)

References 42 publications

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“…However, there are several contradictory reports. Konno et al reported a higher NPY mRNA level in the hypothalamus of Wistar rats after 10 consecutive days of a subcutaneous injection of Dex (2 mg/ kg/day) (22). Makimura et al (26) found that ADX completely blocked the elevation of NPY and AGRP mRNA in diabetic mice.…”

Section: Discussionmentioning

confidence: 99%

“…Zakrzewska et al (19) found that intraperitoneal infusion of dexamethasone (Dex; 0.025 mg/kg/ day) for 3 days in normal rats resulted in a significant decrease in food intake and body weight. Konno et al (22) reported that a 10-day subcutaneous injection of Dex (2 mg/kg/day) resulted in a significant decrease in weight and food intake in Wistar rats. Coll et al (23) reported a significant decrease in body weight and length in Pomc -/-mice after receiving cortisosterone-supplemented drinking water (25 µg/ml final concentration).…”

Section: Discussionmentioning

confidence: 99%

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Glucocorticoids decrease body weight and food intake and inhibit appetite regulatory peptide expression in the hypothalamus of rats

Liu¹,

Shi²,

Du³

et al. 2011

Experimental and Therapeutic Medicine

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Abstract. The aim of the present study was to investigate the effects of glucocorticoids (GCs) on appetite and gene expression of the hypothalamic appetite regulatory peptides, neuropeptide Y (NPY), agouti-related protein (AGRP) and cocaine and amphetamine-regulated transcript (CART), in non-obese and obese rats. Both non-obese and obese rats were randomly assigned to three groups: normal saline, low-and high-dose GC groups (NSG, LDG and HDG, respectively), which received an intraperitoneal injection with normal saline (0.2 ml/100 g) or hydrocortisone sodium succinate at 5 and 15 mg/kg, respectively, for 20 days. The expression levels of NPY, AGRP and CART mRNA in the hypothalamus were measured by real-time quantitative PCR. Non-obese and obese rats were found to undergo weight loss after GC injection, and a higher degree of weight loss was observed in the HDG rats. The average and cumulative food intakes in the obese and nonobese rats injected with high-dose GC were lower compared to that in the NSG (p<0.05). mRNA expression levels of the orexigenic neuropeptides, NPY and AGRP, and the anorexigenic neuropeptide, CART, were significantly lower in the HDG than levels in the NSG for both the obese and non-obese rats (p<0.05). GC treatment decreased appetite and body weight, induced apparent glucolipid metabolic disturbances and hyperinsulinemia, while down-regulated mRNA expression levels of the orexigenic neuropeptides, NPY and AGRP, and anorexigenic neuropeptide, CART, in the hypothalamus in the rats. The mechanism which induces this neuropeptide expression requires further study.

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Section: Discussionmentioning

confidence: 99%

Section: Discussionmentioning

confidence: 99%

Glucocorticoids decrease body weight and food intake and inhibit appetite regulatory peptide expression in the hypothalamus of rats

Liu¹,

Shi²,

Du³

et al. 2011

Experimental and Therapeutic Medicine

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show abstract

“…Glucocorticoids stimulate food intake by interacting with several appetite-regulating targets. They increase AMP-activated protein kinase signaling in the ARC to up-regulate NPY and AGRP expression in this region and stimulate the actions of these orexigenic peptides (Savontaus et al, 2002; Konno et al, 2008; Shimizu et al, 2008). Glucocorticoids also influence the function of leptin, whose normal role is to signal satiety thus suppressing appetite.…”

Section: The Chronic Effects Of Stress On Appetitementioning

confidence: 99%

Eating behavior and stress: a pathway to obesity

2014

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Stress causes or contributes to a huge variety of diseases and disorders. Recent evidence suggests obesity and other eating-related disorders may be among these. Immediately after a stressful event is experienced, there is a corticotropin-releasing-hormone (CRH)-mediated suppression of food intake. This diverts the body’s resources away from the less pressing need to find and consume food, prioritizing fight, flight, or withdrawal behaviors so the stressful event can be dealt with. In the hours following this, however, there is a glucocorticoid-mediated stimulation of hunger and eating behavior. In the case of an acute stress that requires a physical response, such as a predator-prey interaction, this hypothalamic-pituitary-adrenal (HPA) axis modulation of food intake allows the stressful event to be dealt with and the energy used to be replaced afterward. In the case of ongoing psychological stress, however, chronically elevated glucocorticoids can lead to chronically stimulated eating behavior and excessive weight gain. In particular, stress can enhance the propensity to eat high calorie “palatable” food via its interaction with central reward pathways. Activation of this circuitry can also interact with the HPA axis to suppress its further activation, meaning not only can stress encourage eating behavior, but eating can suppress the HPA axis and the feeling of stress. In this review we will explore the theme of eating behavior and stress and how these can modulate one another. We will address the interactions between the HPA axis and eating, introducing a potential integrative role for the orexigenic hormone, ghrelin. We will also examine early life and epigenetic modulation of the HPA axis and how this can influence eating behavior. Finally, we will investigate the clinical implications of changes to HPA axis function and how this may be contributing to obesity in our society.

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“…They stimulate the actions of orexigenic peptides NPY and agouti-related peptide (AGRP) (Savontaus et al 2002;Konno et al 2008), up-regulating gene expression of NPY and AGRP in the arcuate nucleus (ARC) by increasing AMP-activated protein kinase signalling (Shimizu et al 2008). GCs also influence the function of anorexigenic leptin.…”

Section: Glucocorticoid Regulation Of Appetitementioning

confidence: 99%

The glucocorticoid contribution to obesity

Spencer¹,

Tilbrook²

2011

Stress

117

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Obesity is fast becoming the scourge of our time. It is one of the biggest causes of death and disease in the industrialized world, and affects as many as 32% of adults and 17% of children in the USA, considered one of the world's fattest nations. It can also cost countries billions of dollars per annum in direct and indirect care, latest estimates putting the USA bill for obesity-related costs at $147 billion in 2008. It is becoming clear that the pathophysiology of obesity is vastly more complicated than the simple equation of energy in minus energy out. A combination of genetics, sex, perinatal environment and life-style factors can influence diet and energy metabolism. In this regard, psychological stress can have significant long-term impact upon the propensity to gain and maintain weight. In this review, we will discuss the ability of psychological stress and ultimately glucocorticoids (GCs) to alter appetite regulation and metabolism. We will specifically focus on (i) GC regulation of appetite and adiposity, (ii) the apparent sexual dimorphism in stress effects on obesity and (iii) the ability of early life stress to programme obesity in the long term.

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Upregulated expression of neuropeptide Y in hypothalamic–pituitary system of rats by chronic dexamethasone administration

Cited by 21 publications

References 42 publications

Glucocorticoids decrease body weight and food intake and inhibit appetite regulatory peptide expression in the hypothalamus of rats

Glucocorticoids decrease body weight and food intake and inhibit appetite regulatory peptide expression in the hypothalamus of rats

Eating behavior and stress: a pathway to obesity

The glucocorticoid contribution to obesity

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