astressin and Body-Weight

Effects of intracerebroventricular (ICV) injection of corticotrophin releasing factor (CRF) on feed intake were evaluated in two lines of White Plymouth Rock chickens that have been selected from a common base population for high (HWS) or low (LWS) juvenile body weight. Both lines responded with reduced feed intake after ICV CRF; however, the threshold of response was lower in line LWS than HWS. Additionally, the effects of two receptor antagonists, astressin and alpha-helical CRF (9-41; alpha-CRF), and the effect of CRF fragment 6-33, (which displaces CRF from its binding protein), were evaluated in these lines. Although all three antagonists increased feed intake in line LWS but not line HWS, they attenuated the appetite-reducing effects of CRF only in line HWS. Peripheral plasma corticosterone concentrations after an acute stressor were higher in line LWS than in line HWS. These data support the thesis of correlated responses in the CRF system to selection for high or low juvenile body weight. These differences may contribute to differential feed intake, and hence altered body weights.

Topics: Animals; Body Weight; Carrier Proteins; Chickens; Corticosterone; Corticotropin-Releasing Hormone; Feeding Behavior; Injections, Intraventricular; Peptide Fragments; Receptors, Corticotropin-Releasing Hormone; Sheep

Corticotropin-releasing factor (CRF) modulates the activity of the hypothalamic-pituitary-adrenal axis, and has a key role in mediating neuroendocrine effects that occur in response to stressful stimuli. We have recently shown that exposure of neonatal chicks to low-temperature resulted in increased oxidative damage to the brain and i.c.v. injection of CRF increased homeothermy that was associated with tissue specific enhancement of mitochondrial fatty acid oxidation enzyme activities. These observations prompted an investigation into the potential role of CRF in a state of oxidative damage in the brain and other vital organs in low-temperature-exposed chicks. In the first experiment, neonatal chicks (Gallus gallus) were given i.c.v. injection of CRF (42 pmol) or saline and were then exposed to low-temperature (20 degrees C) for 3 h. Malondialdehyde (MDA) levels were measured in the plasma, brain, heart and skeletal muscle. In the second experiment, to confirm the modulatory role of CRF in the brain oxidative damage, as observed in the first experiment, neonatal chicks were given the i.c.v. injection of CRF (42 pmol), astressin (6 nmol, CRF receptor antagonist), or CRF (42 pmol) plus astressin (6 nmol) in combination, and were then exposed to low-temperature (20 degrees C) for 3 h. CRF significantly decreased the weight gain and feed consumption of chicks that were recovered by astressin. In the plasma, significantly higher MDA levels were observed in i.c.v. CRF chicks exposed to low-temperature, but this pattern was not observed in the brain, heart and skeletal muscle. Brain MDA levels in i.c.v. CRF chicks were decreased as compared with that of i.c.v. saline chicks on low-temperature exposure while i.c.v. astressin increased the MDA levels. In conclusion, CRF plays a putative neuroprotective role in the brain of low-temperature-exposed neonatal chicks.

Topics: Animals; Animals, Newborn; Body Temperature; Body Weight; Brain; Chickens; Cold Temperature; Corticotropin-Releasing Hormone; Eating; Hypothermia; Injections, Intraventricular; Male; Malondialdehyde; Muscle, Skeletal; Myocardium; Neuroprotective Agents; Peptide Fragments

The effects of the corticotropin-releasing factor (CRF) receptor antagonists, alpha-helical CRF-(9-41), [D-Phe12,Nle21,38, CalphaMe-Leu37]humanCRF-(12-41) (D-PheCRF-(12-41)) and astressin ([cyclo(30-33)[D-Phe12,Nle21,38,Glu30,Lys33]h umanCRF-(12-41) upon hypophagic and motor activation response to human/ratCRF (h/rCRF) were investigated. All three antagonists (100 microg intracerebroventricular (i.c.v.)) blocked the effects of h/rCRF (1 microg i.c.v.) upon food intake and body weight change in food-deprived rats. In contrast, alpha-helical CRF-(9-41) and astressin (both at 100 microg i.c.v., but not lower doses), but not D-PheCRF-(12-41) (up to 100 microg i.c.v.), blocked h/rCRF (0.3 microg i.c.v.)-induced motor activation in rats in a familiar environment. The ability of D-PheCRF-(12-41) to block CRF-induced hypophagia, but not motor activation, suggests a selective action of this antagonist upon the behavioural effects of centrally administered h/rCRF.

Topics: Animals; Behavior, Animal; Body Weight; Corticotropin-Releasing Hormone; Eating; Food Deprivation; Habituation, Psychophysiologic; Hormone Antagonists; Humans; Motor Activity; Peptide Fragments; Rats; Rats, Sprague-Dawley; Receptors, Corticotropin-Releasing Hormone