The corticotropin-releasing hormone system in the regulation of energy balance in obesity

Richard, Denis; Huang, Qingling; Timofeeva, Elena

doi:10.1038/sj.ijo.0801275

Cited by 101 publications

(51 citation statements)

References 47 publications

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“…In addition to binding to the CRF 1 R, CRF also binds to the CRF 2 R, which could be involved in the anorectic effects of CRF (Vaughan et al 1995, Richard et al 2000, 2002. The present study demonstrates an increased expression of CRF 2 R mRNA in the VMH after leptin infusion into the brain.…”

Section: Discussionsupporting

confidence: 55%

Regulation of corticotropin-releasing factor and its types 1 and 2 receptors by leptin in rats subjected to treadmill running-induced stress

Huang¹,

Timofeeva²,

Richard³

2006

Journal of Endocrinology

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The present study was conducted to investigate the long-term effects of subchronic elevation of central leptin levels on the expression of corticotropin-releasing factor (CRF) and its types 1 and 2 receptors in the brain of rats subjected to treadmill running-induced stress. PBS or recombinant murine leptin was infused continuously for a period of 5 days into the third ventricle of rats with the aid of osmotic minipumps at a delivery rate of 2 mg/day. On the fifth day of infusion, rats were killed under resting conditions or after a session of treadmill running, which is known to induce a stress response in rats. Leptin treatment significantly decreased food intake, body weight, white adipose tissue weight, glucose and insulin plasma contents, and blunted the treadmill runninginduced elevation in plasma levels of corticosterone. Leptin infusion prevented stress-induced de novo synthesis of CRF in the paraventricular hypothalamic nucleus (PVN), which was measured using the intronic probe for CRF heteronuclear RNA. The induction of the type 1 CRF receptor (CRF 1 R) in the PVN and supraoptic nucleus in running rats was also significantly blunted by leptin. In contrast, leptin treatment strongly increased the expression of type 2 CRF receptor (CRF 2 R) in the ventromedial hypothalamic nucleus (VMH). The present results suggest that subchronic elevation of central levels of leptin blunts treadmill running-induced activation of the hypothalamic-pituitary-adrenal axis through the inhibition of activation of the CRFergic PVN neurons, and potentially enhances the anorectic CRF effects via the stimulation of expression of CRF 2 R in the VMH.

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Section: Discussionsupporting

confidence: 55%

Regulation of corticotropin-releasing factor and its types 1 and 2 receptors by leptin in rats subjected to treadmill running-induced stress

Huang¹,

Timofeeva²,

Richard³

2006

Journal of Endocrinology

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“…† p<0.05; † † † p<0.001 compared with the pair-fed group. Bars are SEs (for food intake in lean mice where n=2, the bar also indicates the higher of the two values) in corticotrophin-releasing-factor activity not only decreases food intake but also increases sympathetic activity [6]. In the present study, BVT.2733 may have prevented a reduction in sympathetic activity in response to reduced energy intake by preventing an increase in plasma corticosterone (Fig.…”

Section: Discussionmentioning

confidence: 57%

Inhibition of 11β-hydroxysteroid dehydrogenase type 1 reduces food intake and weight gain but maintains energy expenditure in diet-induced obese mice

et al. 2006

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Aims/hypothesis: The 11β-hydroxysteroid dehydrogenase type-1 inhibitor BVT.2733 lowers blood glucose and insulin in mutant mouse models of obesity and diabetes. Its effects on energy balance and body composition, and their contribution to improved glucose homeostasis have received little attention. Materials and methods: BVT.2733 (100 mg/kg, orally) was given twice daily to lean and diet-induced obese mice for 16 or 17 days. A group of obese mice was pair-fed to the amounts consumed by BVT.2733-treated mice. Results: In both obese and lean mice, BVT.2733 reduced food intake and weight gain, but increased water intake. Pair-feeding caused almost as great a decrease in body weight as BVT.2733. Energy expenditure was 38±8% higher in the BVT.2733-treated obese mice than in the pair-fed mice. Terminal plasma corticosterone was raised, lean body weight reduced and percentage fat unchanged in the pairfed mice (control, 47.8±2.6%; pair-fed, 47.1±1.9%), whereas BVT.2733 did not reduce lean mass, but did reduce percentage fat (40.9±2.0%). BVT.2733 but not pairfeeding reduced both the glucose tolerance AUC and the plasma insulin concentration 30 min after giving glucose. Conclusions/interpretation: BVT.2733 reduced food intake but prevented a concomitant reduction in lean body mass and energy expenditure. The latter effects may have contributed to improved glucose tolerance.

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“…Like NPY and galanin, CRH and its closely related peptide urocortin (19) can alter feeding behavior when administered centrally. However, CRH and urocortin are potent inhibitors of food intake, while also stimulating metabolism and energy expenditure (20,21). In addition to sharing a role in the control of feeding, NPY, galanin, and CRH are closely related anatomically.…”

mentioning

confidence: 99%

Interplay Between Galanin and Leptin in the Hypothalamic Control of Feeding via Corticotropin-Releasing Hormone and Neuropeptide Y

Bergonzelli¹,

Pralong²,

Glauser³

et al. 2001

Diabetes

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Over long periods, feeding and metabolism are tightly regulated at the central level. The total amount of nutrients ingested is thought to result from a delicate balance between orexigenic and anorexigenic factors expressed and secreted by specialized hypothalamic neuronal populations. We have developed a system of perifused hypothalamic neurons to characterize the relationships existing between the orexigenic peptide galanin and two other physiological modulators of feeding: neuropeptide Y (NPY) and corticotropin-releasing hormone (CRH). We demonstrated that galanin stimulates CRH and NPY secretion from hypothalamic neurons in a dose-dependent manner. Exposure to leptin for 24 h before galanin stimulation decreased NPY secretion by 30%, leaving the responsiveness of CRH neurons intact. These results suggest that CRH and NPY neurons participate to the intrahypothalamic signaling pathway of galanin, an observation that can explain the lower potency of galanin to stimulate food intake in vivo compared with NPY. The differential effects exerted by leptin on CRH and NPY suggest that there exists a subset of NPY neurons that are exquisitely sensitive to marked variations in leptin levels, and that the CRH neurons are less responsive to increases in leptin concentrations. Diabetes 50:2666 -2672, 2001 R ecent evidence suggests that the central nervous system plays a key role in controlling food intake and metabolic adaptations (1). A delicate interplay seems to exist between the activities of highly specialized neuronal subpopulations involved in the regulation of feeding and energy storage, or of satiety and energy expenditure. Overall, these regulations, operating at the level of the central nervous system, achieve the tight control of energy balance observed in mammals (2). The neurons involved are mainly located within the hypothalamus, where they serve as central integrators of peripheral metabolic signals. One important function of leptin (3) seems to be informing these neurons about levels of energy stored in the body (4). Changes in circulating leptin levels can therefore trigger an appropriate response of the central nervous system to modulate food intake and metabolism according to the total amount of body fat (5) as well as the variations of energy balance (6).However, the relations between the different hypothalamic neuronal subpopulations seem to be extremely complex (1). The systems involved are redundant, and thus they are most difficult to individualize in vivo. Neuropeptide Y (NPY) and galanin can both elicit strong feeding behavior when injected centrally (7-10) and are expressed in hypothalamic areas associated with feeding and metabolic regulations (10 -12). NPY is one of the most abundant peptides of the hypothalamus (11) and remains among the most potent orexigenic factors (13). In addition, it has also been implicated in the control of neuroendocrine adaptations to fasting or unfavorable metabolic conditions (14,15). Like NPY, galanin plays a physiologically important role in the regulation of ne...

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The corticotropin-releasing hormone system in the regulation of energy balance in obesity

Cited by 101 publications

References 47 publications

Regulation of corticotropin-releasing factor and its types 1 and 2 receptors by leptin in rats subjected to treadmill running-induced stress

Regulation of corticotropin-releasing factor and its types 1 and 2 receptors by leptin in rats subjected to treadmill running-induced stress

Inhibition of 11β-hydroxysteroid dehydrogenase type 1 reduces food intake and weight gain but maintains energy expenditure in diet-induced obese mice

Interplay Between Galanin and Leptin in the Hypothalamic Control of Feeding via Corticotropin-Releasing Hormone and Neuropeptide Y

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