Prevention of stress-induced weight loss by third ventricle CRF receptor antagonist

1999 ◽  
Vol 276 (5) ◽  
pp. R1461-R1468 ◽  
Author(s):  
Gennady N. Smagin ◽  
Leigh Anne Howell ◽  
Stephen Redmann ◽  
Donna H. Ryan ◽  
Ruth B. S. Harris
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Receptor Antagonist ◽  
Acute Stress ◽  
Third Ventricle ◽  
Corticotropin Releasing Factor ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Sustained Reduction ◽  
Acute Responses

We previously reported that rats exposed to repeated restraint (3 h/day for 3 days) experience temporary hypophagia and a sustained reduction in body weight compared with nonrestrained controls. Studies described here determined the involvement of central corticotropin-releasing factor (CRF) receptors in the initiation of this chronic response to acute stress. In experiment 1, Sprague-Dawley rats were fitted with cannulas in the lateral ventricle and infused with 50 μg of αhCRF-(9—41) or saline immediately before restraint on each of the 3 days of restraint. The receptor antagonist inhibited hypophagia and weight loss on day 1 of restraint but not on days 2 and 3. In experiment 2, 10 μg of αhCRF-(9—41) or saline were infused into the third ventricle immediately before each restraint. The receptor antagonist totally blocked stress-induced hypophagia and weight loss. These results demonstrate that CRF receptors located in or near the hypothalamus mediate the acute responses to stress that lead to a permanent change in the hormonal or metabolic processes that determine body weight and body composition.

scholarly journals Antagonism of specific corticotropin-releasing factor receptor subtypes selectively modifies weight loss in restrained rats

2008 ◽  
Vol 295 (6) ◽  
pp. R1762-R1773 ◽  
Author(s):  
Christina Chotiwat ◽  
Ruth B. S. Harris
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Third Ventricle ◽  
Corticotropin Releasing Factor ◽  
Receptor Subtypes ◽  
Mild Stress ◽  
Sustained Reduction ◽  
Corticosterone Response ◽  
Poststress Period ◽  
Corticosterone Release

Rats exposed to 3 h of restraint stress on each of 3 days (RRS) lose weight on the days of RRS and gain weight at the same rate as controls after stress ends, but do not return to the weight of controls. RRS rats also show an exaggerated endocrine response to subsequent novel stressors. Studies described here tested the effects of corticotropin-releasing factor receptor (CRFR) antagonism on RRS-induced weight loss, hypophagia, and corticosterone release during mild stress in the postrestraint period. Weight loss was not prevented by either peripheral or third-ventricle administration of a CRFR1 antagonist, antalarmin, before each restraint. Antalarmin did, however, allow recovery of body weight in the poststress period. Third-ventricle administration of a CRFR2 antagonist, antisauvagine 30, had no effect in RRS rats but caused sustained weight loss in control animals. Surprisingly, third-ventricle administration of the nonselective CRFR antagonist, astressin, caused hypophagia and reversible weight loss in control rats. It had no effect in RRS rats. None of the antagonists modified the corticosterone response to RRS or to mild stress in the post-RRS period, but antalarmin suppressed corticosterone during the period of restraint in Control rats. These results suggest that CRFR1 activation is required for the initiation of events that lead to a prolonged down-regulation of body weight in RRS rats. The sustained reduction in body weight is independent of the severity of hypophagia on the days of restraint and of RRS-induced corticosterone release.

scholarly journals Dietary Exposure to Oxidized Frying Oil from Fetus to Adulthood Suppresses Male Reproductive Development by Altering Testicular Cholesterol and Testosterone Homeostasis in Sprague Dawley Rats

2020 ◽  
Vol 150 (7) ◽  
pp. 1713-1721
Author(s):  
Hai-Ping Wu ◽  
Yu-Shun Lin ◽  
Chi-Fen Chang ◽  
Shui-Yuan Lu ◽  
Pei-Min Chao
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Soybean Oil ◽  
Body Weight Loss ◽  
Reproductive Development ◽  
Frying Oil ◽  
Female Rats ◽  
Male Rats ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

ABSTRACT Background Dietary frying oil may have endocrine-disrupting effects, as a feminization effect was observed in cohorts of C57BL/6J male mice fetuses from dams consuming oxidized frying oil (OFO) during pregnancy. Objective The aim of present study was to test the hypothesis that OFO is an anti-androgen. Methods In experiment 1, male progeny of Sprague Dawley female rats fed fresh oil or an OFO diet (10 g fat/100 g, from fresh or 24-h–fried soybean oil; [control diet (C) and OFO groups, respectively] from midgestation through lactation were studied. Pups were weaned at 3 wk of age and then consumed their mothers’ diet until 9 wk of age. In addition, a group of dams and pups that consumed a high-fat diet (HF; 10 g fried and 20 g fresh soybean oil/100 g) was included to counteract body-weight loss associated with OFO ingestion. Indices of male reproductive development and testosterone homeostasis were measured. In experiment 2, male rats were allocated to C and OFO groups (treated as above) and indices of male fertility compared at 9–10 wk of age. Results In experiment 1, final body weights of the HF group were lower (17%) than the C group but higher (14%) than the OFO group (P < 0.0001 for each). In addition to abnormalities in seminiferous tubules, HF and OFO groups did not differ from one another, but, compared with the C group, had delayed preputial separation (4.9 d) and reductions in serum testosterone concentrations (17–74%), anogenital distance (8–20%), weights of androgen-dependent tissues (8–30%), testicular testosterone and cholesterol concentrations (30–40%), and mRNA levels of genes involved in steroidogenesis and cholesterol homeostasis (30–70%). In experiment 2, OFO-exposed males had 20% lower sperm motility (P < 0.05); however, when mated to normal females, pregnancy rates and litter sizes did not differ between OFO and C groups. Conclusions The anti-androgenic effect of OFO in Sprague Dawley rats was attributed to decreased testicular concentrations of cholesterol (testosterone precursor) and not body-weight loss.

Energy balance and regulation of body weight after intestinal bypass surgery in rats

1983 ◽  
Vol 245 (5) ◽  
pp. R658-R663 ◽  
Author(s):  
R. L. Atkinson ◽  
E. L. Brent ◽  
B. S. Wagner ◽  
J. H. Whipple
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Energy Balance ◽  
Energy Expenditure ◽  
Bypass Surgery ◽  
Calorie Intake ◽  
Intestinal Bypass ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Body Weights

This study evaluated the possibility that intestinal bypass surgery alters energy balance and regulation of body weight. In two sets of experiments, male Sprague-Dawley rats underwent bypass or sham bypass surgery. In experiment 1, half of each group was overfed and half was underfed. Bypass reduced net calorie intake (intake - fecal loss) at 2 wk but not at 6 wk. Body weights were maintained at a much lower level in the bypass rats, yet apparent energy expenditure was greater. In experiment 2, bypass rats were compared with sham bypass and sham bypass who were food restricted for paired-weight-loss to bypass (PWL sham). Net calorie intake and body weights of bypass and sham bypass followed a similar pattern as in experiment 1. At similar levels of body weight postoperatively, bypass rats required more calories per kilogram than did the PWL shams, suggesting that bypass resets downward the level at which body weight is regulated. Calorie requirements correlated with food intake better than with absolute body weight. Further studies to determine the mechanism of altered energy expenditure may provide methods for weight loss without extensive surgery.

scholarly journals Orexigenic response to tail pinch: role of brain NPY1 and corticotropin releasing factor receptors

2014 ◽  
Vol 306 (3) ◽  
pp. R164-R174 ◽  
Author(s):  
Miriam Goebel-Stengel ◽  
Andreas Stengel ◽  
Lixin Wang ◽  
Yvette Taché
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Receptor Antagonist ◽  
Body Weight Gain ◽  
The Body ◽  
Corticotropin Releasing Factor ◽  
Sprague Dawley ◽  
Tail Pinch ◽  
Acute Response

Tail pinch stimulates food intake in rats. We investigated brain mechanisms of this response and the influence of repeated exposure. Sprague-Dawley rats received acute (5 min) or repeated (5 min/day for 14 days) tail pinch using a padded clip. Acute tail pinch increased 5-min food intake compared with control (0.92 ± 0.2 vs. 0.03 ± 0.01 g, P < 0.01). This response was inhibited by 76% by intracerebroventricular injection of BIBP-3226, a neuropeptide Y1 (NPY1) receptor antagonist, increased by 48% by astressin-B, a corticotropin-releasing factor (CRF) receptor antagonist, and not modified by S-406-028, a somatostatin subtype 2 antagonist. After the 5-min tail pinch without food, blood glucose rose by 21% ( P < 0.01) while changes in plasma acyl ghrelin (+41%) and adrenocorticotropic hormone (+37%) were not significant. Two tail pinches (45 min apart) activate pontine and hindbrain catecholaminergic and hypothalamic paraventricular CRF neurons. After 14 days of repeated tail pinch, the 5-min orexigenic response was not significantly different from days 2 to 11 but reduced by 50% thereafter ( P < 0.001). Simultaneously, the 5-min fecal pellet output increased during the last 5 days compared with the first 5 days (+58%, P < 0.05). At day 14, the body weight gain was reduced by 22%, with a 99% inhibition of fat gain and a 25% reduction in lean mass ( P < 0.05). The orexigenic response to acute 5-min tail pinch is likely to involve the activation of brain NPY1 signaling, whereas that of CRF tends to dampen the acute response and may contribute to increased defecation and decreased body weight gain induced by repeated tail pinch.

scholarly journals Maternal low-protein diet causes body weight loss in male, neonate Sprague–Dawley rats involving UCP-1-mediated thermogenesis

2015 ◽  
Vol 26 (7) ◽  
pp. 729-735 ◽  
Author(s):  
Kate J. Claycombe ◽  
Emilie E. Vomhof-DeKrey ◽  
James N. Roemmich ◽  
Turk Rhen ◽  
Othman Ghribi
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Protein Diet ◽  
Low Protein Diet ◽  
Sprague Dawley ◽  
Low Protein ◽  
Sprague Dawley Rats ◽  
Male Neonate

Daily CCK injection enhances reduction of body weight by chronic intracerebroventricular leptin infusion

2002 ◽  
Vol 282 (5) ◽  
pp. R1368-R1373 ◽  
Author(s):  
Claire A. Matson ◽  
Dana F. Reid ◽  
Robert C. Ritter
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Daily Injection ◽  
Bolus Administration ◽  
Sucrose Intake ◽  
Sprague Dawley ◽  
Sprague Dawley Rats ◽  
Main Effect ◽  
Daily Intraperitoneal Injection

In the present study, we tested the hypothesis that a single daily injection of the gut peptide CCK, together with continuous leptin infusion, would produce significantly greater loss of body weight than leptin alone. We found that a single daily intraperitoneal injection of CCK-8 (0.5 μg/kg) significantly enhanced the weight-reducing effects of 0.5 μg/day leptin infused continuously into the lateral ventricle of male Sprague-Dawley rats by osmotic minipump. However, CCK and leptin together did not enhance reduction of daily chow intake. Furthermore, there was no synergistic reduction of 30-min sucrose intake, although a significant main effect of both leptin and CCK was observed on sucrose intake. These results 1) confirm our previous reports of synergy between leptin and CCK on body weight, 2) demonstrate that enhancement of leptin-induced weight loss does not require bolus administration of leptin, and 3) suggest that enhanced body weight loss following leptin and CCK does not require synergistic reduction of food intake by leptin and CCK.

scholarly journals Body weight loss, effective satiation and absence of homeostatic neuropeptide compensation in male Sprague Dawley rats schedule fed a protein crosslinked diet

Appetite ◽  
2017 ◽  
Vol 117 ◽  
pp. 234-246 ◽  
Author(s):  
Nikki Cassie ◽  
Richard L. Anderson ◽  
Dana Wilson ◽  
Anne Pawsey ◽  
Julian G. Mercer ◽  
...  
Keyword(s):  
Weight Loss ◽  
Body Weight ◽  
Body Weight Loss ◽  
Sprague Dawley ◽  
Sprague Dawley Rats

Chronic intravenous administration of V1 arginine vasopressin agonist results in sustained hypertension

1994 ◽  
Vol 267 (2) ◽  
pp. H751-H756 ◽  
Author(s):  
A. W. Cowley ◽  
E. Szczepanska-Sadowska ◽  
K. Stepniakowski ◽  
D. Mattson
Keyword(s):  
Body Weight ◽  
Arginine Vasopressin ◽  
Plasma Catecholamines ◽  
Plasma Osmolality ◽  
Sprague Dawley ◽  
Prolonged Administration ◽  
Chronic Stimulation ◽  
Sustained Hypertension ◽  
Sprague Dawley Rats

Despite the well-recognized vasoconstrictor and fluid-retaining actions of vasopressin, prolonged administration of arginine vasopressin (AVP) to normal animals or humans fails to produce sustained hypertension. The present study was performed to elucidate the role of the V1 receptor in determining the ability of AVP to produce sustained hypertension. Conscious Sprague-Dawley rats with implanted catheters were infused with the selective V1 agonist, [Phe2,Ile3,Orn8]vasopressin (2 ng.kg-1.min-1), for 14 days in amounts that were acutely nonpressor. Blood pressure (MAP), heart rate (HR), body weight, and water intake (WI) were determined daily. Plasma AVP, plasma catecholamines norepinephrine and epinephrine, plasma osmolality, and electrolyte concentration were determined before and on days 1 and 7 of infusion. MAP increased significantly by 10.4 +/- 4.5 mmHg on day 1 and rose to 22 +/- 5 mmHg above control by day 14 (transient decrease on days 6-9) and then fell to control levels after the infusion was stopped. HR did not change significantly. Plasma AVP immunoreactivity increased from 2.5 +/- 0.3 to 10.9 +/- 2.1 pg/ml, whereas norepinephrine tended to fall only on day 1, with epinephrine only slightly elevated on day 7. No evidence of fluid retention was found, and rats lost sodium only on the first day of V1 agonist infusion. Body weight increased throughout the study but was unrelated to the changes of MAP. We conclude that chronic stimulation of V1 receptors results in sustained hypertension in rats.

scholarly journals Renal haemodynamic and tubular actions of urotensin II in the rat

2008 ◽  
Vol 198 (3) ◽  
pp. 617-624 ◽  
Author(s):  
Alaa E S Abdel-Razik ◽  
Ellen J Forty ◽  
Richard J Balment ◽  
Nick Ashton
Keyword(s):  
Body Weight ◽  
Renal Medulla ◽  
Fractional Excretion ◽  
Haemodynamic Effects ◽  
Urotensin Ii ◽  
Sprague Dawley ◽  
Minimal Impact ◽  
Sprague Dawley Rats ◽  
Fractional Excretion Of Sodium ◽  
Excretion Rates

Urotensin II (UTS) is a potent vasoactive peptide that was originally identified in teleost fish. Mammalian orthologues of UTS and its receptor (UTSR) have been described in several species, including humans and rats. We have shown previously that bolus injections of UTS caused a decrease in urine flow and sodium excretion rates in parallel with marked reductions in renal blood flow (RBF) and glomerular filtration rate (GFR). The aim of this study was to determine the effect of UTS infusion at a dose that has minimal impact upon renal haemodynamics in order to identify a potential direct tubular action of UTS. Infusion of rat UTS (rUTS) at 0.6 pmol/min per 100 g body weight in male Sprague–Dawley rats, which had no effect on RBF and caused a 30% reduction in GFR, resulted in a significant increase in the fractional excretion of sodium (vehicle 2.3±0.6 versus rUTS 0.6 pmol 4.5±0.6%, P<0.05) and potassium. At the higher dose of 6 pmol/min per 100 g body weight, haemodynamic effects dominated the response. rUTS induced a marked reduction in RBF and GFR (vehicle 1.03±0.06 versus rUTS 6 pmol 0.31±0.05 ml/min per 100 g body weight, P<0.05) resulting in an anti-diuresis and anti-natriuresis, but no change in fractional excretion of sodium or potassium. Uts2d and Uts2r mRNA expression were greater in the renal medulla compared with the cortex. Together, these data support an inhibitory action of Uts2d on renal tubule sodium and potassium reabsorption in the rat, in addition to its previously described renal haemodynamic effects.

Sign in / Sign up

Export Citation Format

Share Document