Production and heart rate responses of chickens beak-trimmed at hatch or at 10 or 42 days of age

1994 ◽  
Vol 34 (4) ◽  
pp. 443 ◽  
Author(s):  
PC Glatz ◽  
CA Lunam

Heart rate was monitored before and after beak trimming in restrained chickens to measure responses to beak trimming at hatch and at 10 and 42 days of age. Immediately after trimming chickens sham-trimmed (control) and trimmed at 10 and 42 days of age had an increase in heart rate, with the 42-day-old chickens showing the greater change. Chickens sham-trimmed and trimmed at hatch showed no change in heart rate. No difference between trimmed and sham-trimmed chickens occurred at any age for heart rate response. These data indicate that heart rate at trimming may be inadequate as a measure of the stress response associated with beak trimming, especially with the concurrent stressors of handling and restraint. Beak trimming and handling of chickens at hatch is either less stressful than trimming at 10 and 42 days of age, as indicated by the lack of a heart rate response, or heart rate is already at a maximum in chickens at hatch, due to stress associated with hatching. Food intake and body weight were measured for 3-4 weeks after trimming to assess the longer term effects of age and level of trimming on performance of the chicken. Removal of 3 mm of beak at hatch or 4.5 mm at 10 days of age depressed feeding levels and a reduced body weight, indicative of a chronic stress associated with beak trimming.

2019 ◽  
Vol 316 (4) ◽  
pp. R338-R351 ◽  
Author(s):  
Zhen Wang ◽  
Jussara M. do Carmo ◽  
Alexandre A. da Silva ◽  
Kandice C. Bailey ◽  
Nicola Aberdein ◽  
...  

Suppressor of cytokine signaling 3 (SOCS3) is a negative regulator of leptin signaling. We previously showed that the chronic effects of leptin on blood pressure (BP) and glucose regulation are mediated by stimulation of proopiomelanocortin (POMC) neurons. In this study we examined the importance of endogenous SOCS3 in POMC neurons in control of metabolic and cardiovascular function and potential sex differences. Male and female SOCS3flox/flox/POMC-Cre mice in which SOCS3 was selectively deleted in POMC neurons and control SOCS3flox/flox mice were studied during a control diet (CD) or a high-fat diet (HFD) and during chronic leptin infusion. Body weight was lower in male and female SOCS3flox/flox/POMC-Cre than control mice fed the CD, despite similar food intake. Male SOCS3flox/flox/POMC-Cre mice exhibited increased energy expenditure. BP and heart rate were similar in male and female SOCS3flox/flox/POMC-Cre and control mice fed the CD. HFD-fed male and female SOCS3flox/flox/POMC-Cre mice showed attenuated weight gain. HFD-induced elevations in baseline BP and BP responses to an air-jet stress test were greater in female SOCS3flox/flox/POMC-Cre than control mice. Chronic leptin infusion produced similar responses for food intake, body weight, oxygen consumption, blood glucose, BP, and heart rate in all groups. Thus SOCS3 deficiency in POMC neurons influences body weight regulation in the setting of CD and HFD and differentially affects BP and energy balance in a sex-specific manner but does not amplify the dietary, glycemic, or cardiovascular effects of leptin.


Endocrinology ◽  
2006 ◽  
Vol 147 (12) ◽  
pp. 5855-5864 ◽  
Author(s):  
Jonathan D. Roth ◽  
Heather Hughes ◽  
Eric Kendall ◽  
Alain D. Baron ◽  
Christen M. Anderson

Effects of amylin and pair feeding (PF) on body weight and metabolic parameters were characterized in diet-induced obesity-prone rats. Peripherally administered rat amylin (300 μg/kg·d, 22d) reduced food intake and slowed weight gain: approximately 10% (P < 0.05), similar to PF. Fat loss was 3-fold greater in amylin-treated rats vs. PF (P < 0.05). Whereas PF decreased lean tissue (P < 0.05 vs. vehicle controls; VEH), amylin did not. During wk 1, amylin and PF reduced 24-h respiratory quotient (mean ± se, 0.82 ± 0.0, 0.81 ± 0.0, respectively; P < 0.05) similar to VEH (0.84 ± 0.01). Energy expenditure (EE mean ± se) tended to be reduced by PF (5.67 ± 0.1 kcal/h·kg) and maintained by amylin (5.86 ± 0.1 kcal/h·kg) relative to VEH (5.77 ± 0.0 kcal/h·kg). By wk 3, respiratory quotient no longer differed; however, EE increased with amylin treatment (5.74 ± 0.09 kcal/·kg; P < 0.05) relative to VEH (5.49 ± 0.06) and PF (5.38 ± 0.07 kcal/h·kg). Differences in EE, attributed to differences in lean mass, argued against specific amylin-induced thermogenesis. Weight loss in amylin and pair-fed rats was accompanied by similar increases arcuate neuropeptide Y mRNA (P < 0.05). Amylin treatment, but not PF, increased proopiomelanocortin mRNA levels (P < 0.05 vs. VEH). In a rodent model of obesity, amylin reduced body weight and body fat, with relative preservation of lean tissue, through anorexigenic and specific metabolic effects.


1982 ◽  
Vol 8 (1-2) ◽  
pp. 147-159 ◽  
Author(s):  
M.J. Gentle ◽  
B.O. Hughes ◽  
R.C. Hubrecht

2019 ◽  
Vol 316 (5) ◽  
pp. G653-G667 ◽  
Author(s):  
Kamal Albarazanji ◽  
Matthew Jennis ◽  
Cassandre R. Cavanaugh ◽  
Wensheng Lang ◽  
Bhanu Singh ◽  
...  

Trypsin is the major serine protease responsible for intestinal protein digestion. An inhibitor, camostat (CS), reduced weight gain, hyperglycemia, and dyslipidemia in obese rats; however, the mechanisms for these are largely unknown. We reasoned that CS creates an apparent dietary protein restriction, which is known to increase hepatic fibroblast growth factor 21 (FGF21). Therefore, metabolic responses to CS and a gut-restricted CS metabolite, FOY-251, were measured in mice. Food intake, body weight, blood glucose, branched-chain amino acids (LC/MS), hormone levels (ELISA), liver pathology (histology), and transcriptional changes (qRT-PCR) were measured in ob/ob, lean and diet-induced obese (DIO) C57BL/6 mice. In ob/ob mice, CS in chow (9–69 mg/kg) or FOY-251 (46 mg/kg) reduced food intake and body weight gain to a similar extent as pair-fed mice. CS decreased blood glucose, liver weight, and lipidosis and increased FGF21 gene transcription and plasma levels. In lean mice, CS increased liver FGF21 mRNA and plasma levels. Relative to pair feeding, FOY-251 also increased plasma FGF21 and induced liver FGF21 and integrated stress response (ISR) transcription. In DIO mice, FOY-251 (100 mg/kg po) did not alter peak glucose levels but reduced the AUC of the glucose excursion in response to an oral glucose challenge. FOY-251 increased plasma FGF21 levels. In addition to previously reported satiety-dependent (cholecystokinin-mediated) actions, intestinal trypsin inhibition engages non-satiety-related pathways in both leptin-deficient and DIO mice. This novel mechanism improves metabolism by a liver-integrated stress response and increased FGF21 expression levels in mice. NEW & NOTEWORTHY Trypsin inhibitors, including plant-based consumer products, have long been associated with metabolic improvements. Studies in the 1980s and 1990s suggested this was due to satiety hormones and caloric wasting by loss of protein and fatty acids in feces. This work suggests an entirely new mechanism based on the lower amounts of digested protein available in the gut. This apparent protein reduction may cause beneficial metabolic adaptation by the intestinal-liver axis to perceived nutrient stress.


2006 ◽  
Vol 291 (2) ◽  
pp. R367-R375 ◽  
Author(s):  
Niels Vrang ◽  
Andreas Nygaard Madsen ◽  
Mads Tang-Christensen ◽  
Gitte Hansen ◽  
Philip Just Larsen

The gut hormone peptide YY (PYY) was recently proposed to comprise an endogenous satiety factor. We have studied acute anorectic functions of PYY(3–36) in mice and rats, as well as metabolic effects of chronic PYY(3–36) administration to diet-induced obese (DIO) mice and rats. A single intraperitoneal injection of PYY(3–36) inhibited food intake in mice, but not in rats. We next investigated the effects of increasing doses (100, 300, and 1,000 μg·kg−1·day−1) of PYY(3–36) administered subcutaneously via osmotic minipumps on food intake and body weight in DIO C57BL/6J mice. Whereas only the highest dose (1,000 μg·kg−1·day−1) of PYY(3–36) significantly reduced food intake over the first 3 days, body weight gain was dose dependently reduced, and on day 28 the group treated with 1,000 μg·kg−1·day−1 PYY(3–36) weighed ∼10% less than the vehicle-treated group. Mesenteric, epididymal, retroperitoneal, and inguinal fat pad weight was dose dependently reduced. Subcutaneous administration of PYY(3–36) (250 and 1,000 μg·kg−1·day−1) for 28 days reduced body weight and improved glycemic control in glucose-intolerant DIO rats. Neither 250 nor 1,000 μg/kg PYY(3–36) elicited a conditioned taste aversion in male rats.


Development ◽  
1962 ◽  
Vol 10 (4) ◽  
pp. 471-475
Author(s):  
Donald F. Caldwell

A paucity of experimental data exists relating the effect of chronic stress experienced throughout gestation to the incidence of stillbirths. Dornhorst & Young (1952) demonstrated that low, pressor dosages of epinephrine and norepinephrine administered intravenously to gravid rabbits and guinea-pigs produced vigorous uterine contractions with concomitant cyanosis of the placenta and decreases in both foetal heart-rate and blood-pressure. They interpreted their findings as indicating the action of these hormones to be on the placental vasculature and not the blockage of uterine vessels supplying the placenta. Since the secretion of the adrenal medullary hormones is part of the organism's stress response, the findings of the Dornhorst & Young investigation provide evidence for a mechanism which might be used to account, in part or whole, for the deleterious effects to prenatal development arising from maternal stress. The present investigation undertook to test this hypothesis by determining the incidence of stillbirths from adrenal demedullated and non-adrenal demedullated mice subjected to stress throughout gestation or allowed a stress-free gestation.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Angela L. McDowell ◽  
Kathryn M. H. Fransen ◽  
Kevin S. Elliott ◽  
Alhasan Elghouche ◽  
Polina V. Kostylev ◽  
...  

We have previously shown that 21-day chronic restraint stress impacts instrumental learning, but overall few studies have examined sex differences on the impact of stress on learning. We further examined sex differences in response to extended 42-day chronic stress on instrumental learning, as well as recovery from chronic stress. Rats were tested in aversive training tasks with or without prior appetitive experience, and daily body weight data was collected as an index of stress. Relative to control animals, reduced body weight was maintained from day 22 through day 42 across the stress period for males, but not for females. Stressed males had increased response speed and lower learning efficiency during appetitive acquisition and aversive learning. Males overall showed slower escape shaping times and more shock exposure. In contrast, stressed females showed slower appetitive response speeds and higher appetitive and aversive efficiency but overall reduced avoidance rates during acquisition and maintenance for transfer animals and during maintenance for aversive-only animals. These tasks reveal important nuances on the effect of stress on goal-directed behavior and further highlight sexually divergent effects on appetitive versus aversive motivation. Furthermore, these data underscore that systems are temporally impacted by chronic stress in a sexually divergent pattern.


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