Effects of the CRF1 receptor antagonist SSR125543 on energy balance and food deprivation-induced neuronal activation in obese Zucker rats

Doyon, Christian; Samson, Pierre; Lalonde, Josée; Richard, Denis

doi:10.1677/joe.1.07064

Cited by 11 publications

(8 citation statements)

References 56 publications

(59 reference statements)

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“…Moreover, several other minor effects of CRF were also noticed in the abundance mRNAs for neuropeptides, such as the increase noticed for POMC in the hypothalamus. The slight amount of changes observed in abundance of mRNAs for peptides due to CRF treatment agrees with results obtained in mammals (Doyon et al, 2007), reinforcing the view that the main action of CRF on peptide expression is altering the pattern of response to changes in glucose levels. In general, it seems that CRF treatment altered the normal response to increased glucose concentration in the medium of mRNA abundance of several neuropeptides in the hypothalamus and hindbrain, resulting in a similar response that became independent of glucose concentration.…”

Section: Discussion the Effects Of Crf On Glucosensing-related Paramesupporting

confidence: 85%

“…Moreover, members of the CRF family of peptides are known to produce a global negative energy profile by reducing food intake and increasing energy expenditure, and the effects on energy expenditure are thought to depend on the activation of thermogenesis mediated by corticotropin-releasing factor receptor type 1 (CRF-R-1, also known as CRHR1) (Doyon et al, 2007). Moreover, CRF has been suggested to change the sensitivity of hypothalamic glucosensing neurons to glucose (McCrimmon et al, 2006) and to regulate the glucosensing machinery (Evans et al, 2004).…”

Section: Introductionmentioning

confidence: 99%

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CRF treatment induces a readjustment in glucosensing capacity in the hypothalamus and hindbrain of rainbow trout

Conde-Sieira

Librán-Pérez

López‐Patiño

et al. 2011

Journal of Experimental Biology

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SUMMARYStress conditions induced in rainbow trout a readjustment in the glucosensing response of the hypothalamus and hindbrain such that those sensors did not respond properly to changes in glucose levels, as demonstrated in previous studies. To evaluate the hypothesis that corticotropin-releasing factor (CRF) could be involved in that response, we have incubated the hypothalamus and hindbrain of rainbow trout at different glucose concentrations in the presence of different concentrations of CRF. Under those conditions, we evaluated whether parameters related to glucosensing [the levels of glucose, glycogen and glucose 6-phosphate, the activities of glucokinase (GK), glycogen synthase (GSase) and pyruvate kinase (PK), and mRNA abundance of transcripts for GK, Glut2, Kir.6-like and sulfonylurea receptor (SUR)-like] are modified in the presence of CRF in a way comparable to that observed under stress conditions. We obtained evidence allowing us to suggest that CRF could be involved in the interaction between stress and glucosensing as CRF treatment of the hypothalamus and hindbrain in vitro induced a readjustment in glucosensing parameters similar to that previously observed under stress conditions in vivo. We had also previously demonstrated that stress elicits alterations in food intake in parallel with the readjustment of glucosensing systems. Here, we provide evidence that the mRNA abundance of several of the neuropeptides involved in the regulation of food intake, such as neuropeptide Y (NPY) or cocaine-and amphetamine-regulated transcript (CART), is affected by CRF treatment, in such a way that their expression does not respond to changes in glucose levels in the same way as controls, allowing us to suggest that the food intake response that is integrated by changes in those peptides and known to be reduced by stress could be also mediated by CRF action in glucosensing areas.

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Section: Discussion the Effects Of Crf On Glucosensing-related Paramesupporting

confidence: 85%

Section: Introductionmentioning

confidence: 99%

CRF treatment induces a readjustment in glucosensing capacity in the hypothalamus and hindbrain of rainbow trout

Conde-Sieira

Librán-Pérez

López‐Patiño

et al. 2011

Journal of Experimental Biology

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“…To estimate carcass energy, fat, and protein contents, carcasses were processed as previously described . To calculate energy gain, initial contents were estimated from the live body weight of KO and WT mice with reference to a baseline group of initials (six per phenotype) sacrificed at the beginning of the experimental period.…”

Section: Methodsmentioning

confidence: 99%

Trefoil factor family member 2 (Tff2) KO mice are protected from high‐fat diet‐induced obesity

Giorgio

Yoshioka

Riedl

et al. 2013

Obesity

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Introduction: Trefoil factor family member 2 (Tff2) is a small gut peptide, mainly known for its protective and healing functions. As previously demonstrated, high-fat (HF) feeding can rapidly and specifically modulate Tff2 transcription in key tissues of mice, including the duodenum and mesenteric adipose tissue, therefore suggesting a novel role for this gene in energy balance. Design and Methods: To explore whether and how Tff2 can influence feeding behavior and energy metabolism, Tff2 knock-out (KO) mice were challenged with HF diet for 12 weeks, hence food and energy intakes, body composition, as well as energy excretion and serum lipid and hormonal levels were analyzed. Finally, energy efficiency was estimated. Results: Tff2 KO mice showed a greater appetite and higher energy intake compared to wild-type (WT). Consistently, they presented lower levels of serum leptin, and increased transcription of agouti-related protein (Agrp) in the hypothalamus. Though energy and triglyceride fecal excretion were augmented in Tff2 KO mice, digestible energy intake was superior. However, KO mice were finally protected from HF diet-induced obesity, and accumulated less weight and fat depots than WT animals, while keeping a normal lean mass. Energy efficiency was lower in HF-KO mice, while energy expenditure and locomotor activity were globally increased. Conclusions: The present work demonstrates previously unsuspected roles for Tff2 and suggests it to be a mastermind in the control of energy balance and a promising therapeutic target for obesity.

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“…glucose; 15) or nutrient derivatives (e.g. malonyl-CoA; 209), but CRH (210) and glucocorticoids also have an influence. Some of the most important MSH forms bind to melanocortin receptors (211) in the hypothalamus and brainstem, mainly to types MC3R and MC4R (alpha-MSH to both, gamma-MSH to MC3R: the two receptors exhibit similarities as well as differences; 212, 213).…”

Section: Catabolic Peptides 421 the Pomc-melanocortin Systemmentioning

confidence: 99%

Thermoregulation energy balance regulatory peptides recent developments

Székely

Pétervári

Balaskó³

2010

Front Biosci

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Energy balance of the body is determined mainly by the function of various hypothalamic and brainstem nuclei, according to a complex interaction between the regulation of body temperature (actual metabolic rate vs. heat loss) and regulation of body weight (metabolic rate vs. food intake). The direct effect of central anabolic neuropeptides (neuropeptide Y, orexins, melanin concentrating hormone, etc.) is to enhance food intake and suppress metabolic rate with a tendency to cause hypothermia, while central catabolic neuropeptides (melanocortins, corticotropin releasing factor, cocaine-amphetamine regulated peptide, etc.) suppress food intake and enhance energy expenditure with a tendency to induce hyperthermia. Many other neuropeptides are neither clearly anabolic, nor clearly catabolic, but still influence these complex hypothalamic/brainstem functions. Some peripheral peptides (e.g. leptin, insulin, ghrelin) acting at either peripheral or cerebral sites also contribute to the regulation of energy balance. The prevailing thermoregulatory status, the substances or neural signals representing actual feeding vs. established nutritional states, and the aging process may modify the expression and/or activity of peripheral and central peptides and peptide receptors.

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Effects of the CRF1 receptor antagonist SSR125543 on energy balance and food deprivation-induced neuronal activation in obese Zucker rats

Cited by 11 publications

References 56 publications

CRF treatment induces a readjustment in glucosensing capacity in the hypothalamus and hindbrain of rainbow trout

CRF treatment induces a readjustment in glucosensing capacity in the hypothalamus and hindbrain of rainbow trout

Trefoil factor family member 2 (Tff2) KO mice are protected from high‐fat diet‐induced obesity

Thermoregulation energy balance regulatory peptides recent developments

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