scholarly journals Meal patterns and hypothalamic NPY expression during chronic social stress and recovery

2010 ◽  
Vol 299 (3) ◽  
pp. R813-R822 ◽  
Author(s):  
Susan J. Melhorn ◽  
Eric G. Krause ◽  
Karen A. Scott ◽  
Marie R. Mooney ◽  
Jeffrey D. Johnson ◽  
...  

In the present study, we examined meal patterns during and after exposure to the visible burrow system (VBS), a rodent model of chronic social stress, to determine how the microstructure of food intake relates to the metabolic consequences of social subordination. Male Long-Evans rats were housed in mixed-sex VBS colonies (4 male, 2 female) for 2 wk, during which time a dominance hierarchy formed [1 dominant male (DOM) and 3 subordinate males (SUB)], and then male rats were individually housed for a 3-wk recovery period. Controls were individually housed with females during the 2-wk VBS period and had no changes in ingestive behavior compared with a habituation period. During the hierarchy-formation phase of VBS housing, DOM and SUB had a reduced meal frequency, whereas SUB also had a reduced meal size. However, during the hierarchy-maintenance phase of VBS housing, DOM meal patterns did not differ from controls, whereas SUB continued to display a reduced food intake via less frequent meals. During recovery, DOM had comparable meal patterns to controls, whereas SUB had an increased meal size. Hypothalamic neuropeptide Y (NPY) mRNA levels were not different between these groups during the experimental period. Together, the results suggest that exposure to chronic social stress alters ingestive behavior both acutely and in the long term, which may influence the metabolic changes that accompany bouts of stress and recovery; however, these differences in meal patterns do not appear to be mediated by hypothalamic NPY.

2010 ◽  
Vol 95 (1) ◽  
pp. 92-99 ◽  
Author(s):  
L.L. Bellinger ◽  
P.J. Wellman ◽  
R.B.S. Harris ◽  
E.W. Kelso ◽  
P.R. Kramer

1993 ◽  
Vol 264 (5) ◽  
pp. R957-R962 ◽  
Author(s):  
V. Lemaire ◽  
M. Le Moal ◽  
P. Mormede

We have shown previously that chronic social stress has differential effects on adrenal weight and on tyrosine hydroxylase (TH) and phenylethanolamine N-methyltransferase (PNMT) specific activity, depending on the experimental design. To determine the role of the sympathetic nervous system and of the hypothalamo-pituitary-adrenocortical axis (HPAA) in these modifications, we studied the mechanisms of regulation of these parameters in basal conditions as well as in response to reserpine treatment and chronic social stress in the Wistar strain of rats. We found that the adrenal weight is mostly dependent on the activity of the HPAA, which is increased in male rats living in mixed-sex colonies. PNMT specific activity is regulated by splanchnic innervation, confirming that its induction by social instability is a consequence of sympathetic nervous system hyperactivity. The increase of TH specific activity, as seen in unstable, mixed-sex colonies, is not under sympathetic control. However, we show that the pituitary may exert a tonic inhibitory influence, dependent on the sympathetic innervation. These data confirm that the HPAA and the sympathetic nervous system may be independently triggered in chronic social stress conditions.


Appetite ◽  
2009 ◽  
Vol 52 (3) ◽  
pp. 857
Author(s):  
K.A. Scott ◽  
S.J. Melhorn ◽  
E.G. Krause ◽  
R.R. Sakai

2008 ◽  
Vol 295 (1) ◽  
pp. R76-R81 ◽  
Author(s):  
Nicholas T. Bello ◽  
Matthew H. Kemm ◽  
Timothy H. Moran

Amylinergic mechanisms are believed to be involved in the control of appetite. This study examined the effects of the amylin agonist, salmon calcitonin, on food intake and meal patterns in adult male rhesus monkeys. Fifteen minutes before the onset of their 6-h daily feeding period, monkeys received intramuscular injections of various doses of salmon calcitonin (0.032, 0.056, 0.1, 0.32, and 1 μg/kg) or saline. Salmon calcitonin dose dependently reduced total daily and hourly food intake, with significant decreases at the 0.1, 0.32, and 1 μg/kg doses. Daily food intake was reduced by ∼35%, 62%, and 96%, at these doses, respectively. An analysis of meal patterns revealed that size of the first meal was significantly reduced across the dose range of 0.056 to 1 μg/kg, while average meal size was reduced with the 0.32 and 1 μg/kg doses. Meal number was only affected at the 1 μg/kg dose. Repeated 5-day administration of the 0.1 μg/kg dose resulted in a reduction in daily food intake only on injection day 2, while significant reductions in food intake were observed on all five injection days with a 0.32 μg/kg dose. Daily food intake was also reduced for 1 day after the termination of the 5-day injections of the 0.32 μg/kg salmon calcitonin dose. These sustained reductions in intake were expressed through decreases in meal size. These data demonstrate that salmon calcitonin acutely and consistently decreases food intake mainly through reductions in meal sizes in nonhuman primates.


Author(s):  
A.M. Liashevych ◽  
I.I. Tubalceva ◽  
Yevdokiya M. Reshetnik ◽  
Oleksandr V. Bondarenko ◽  
Stanislav P. Veselsky ◽  
...  

Endocrinology ◽  
2003 ◽  
Vol 144 (4) ◽  
pp. 1420-1425 ◽  
Author(s):  
Waljit S. Dhillo ◽  
Caroline J. Small ◽  
Preeti H. Jethwa ◽  
Sabina H. Russell ◽  
James V. Gardiner ◽  
...  

Abstract Calcitonin gene-related protein (CGRP) inhibits food intake and stimulates the hypothalamo-pituitary-adrenal (HPA) axis after intracerebroventricular injection in rats. However, the hypothalamic site and mechanism of action are unknown. We investigated the effects of intraparaventricular nucleus administration (iPVN) of CGRP on food intake and the HPA axis in rats and the effect of CGRP on the release of hypothalamic neuropeptides in vitro. In addition, we investigated the effects of food deprivation on hypothalamic CGRP expression. CGRP dose-dependently reduced food intake in the first hour after iPVN injection in fasted male rats (saline, 5.1 ± 0.8 g; 0.3 nmol CGRP, 1.1 ± 0.5 g; P < 0.001 vs. saline). iPVN injection of CGRP8–37 (a CGRP1 receptor antagonist) alone had no effect on food intake. However, the reduction in food intake by iPVN CGRP was attenuated by prior administration of CGRP8–37 [CGRP8–37 (10 nmol)/CGRP (0.3 nmol), 3.0 ± 0.8 g; P < 0.05 vs. 0.3 nmol CGRP]. CGRP (100 nm) stimulated the release of α-melanocyte stimulating hormone, cocaine- and amphetamine-related transcript, corticotropin-releasing hormone, and arginine vasopressin from hypothalamic explants to 127 ± 19%, 148 ± 10%, 158 ± 17%, and 198 ± 21% of basal levels, respectively (P < 0.05 vs. basal), but did not alter the release of either neuropeptide Y or agouti-related protein. Hypothalamic CGRP mRNA levels in 24-h fasted rats were increased to 130 ± 8% of control levels [CGRP mRNA (arbitrary units), 4.75 ± 0.4; controls, 3.65 ± 0.34; P < 0.05]. Our data suggest that CGRP administered to the PVN inhibits food intake and stimulates the HPA axis.


2000 ◽  
Vol 278 (6) ◽  
pp. R1627-R1633 ◽  
Author(s):  
A. A. Ammar ◽  
F. Sederholm ◽  
T. R. Saito ◽  
A. J. W. Scheurink ◽  
A. E. Johnson ◽  
...  

Many studies have indicated that neuropeptide Y (NPY) stimulates and leptin inhibits food intake. In line with this, intracerebroventricular injection of NPY (10 μg) stimulated and leptin (10 μg) inhibited intake of a sucrose solution when female rats were required to obtain the solution from a bottle. However, NPY inhibited and leptin stimulated intake if the solution was infused intraorally. Thus NPY stimulates the responses used to obtain food but inhibits those used to consume food, and leptin has the opposite effects. To test the specificity of these responses the sexual behavior of male rats was examined. NPY-treated males showed minor deficits in sexual behavior but chose to ingest a sucrose solution rather than copulate with a female if offered the choice. By contrast, leptin-treated males ingested little sucrose and displayed an increase in ejaculatory frequency if given the same choice. It is suggested that NPY is not merely an orexigenic peptide, but one that directs attention toward food. Similarly, leptin may not be an anorexic peptide, but one that diverts attention away from food toward alternate stimuli.


Endocrinology ◽  
2003 ◽  
Vol 144 (9) ◽  
pp. 3789-3798 ◽  
Author(s):  
Rekha Pal ◽  
Abhiram Sahu

Abstract Using a rat model of chronic central leptin infusion in which neuropeptide Y neurons develop leptin resistance, we examined whether leptin signal transduction mechanism in the hypothalamus is altered during central leptin infusion. Adult male rats were infused chronically into the lateral cerebroventricle with leptin (160 ng/h) or vehicle via Alzet pumps for 16 d. In the leptin-infused group, the initial decrease in food intake was followed by a recovery to their preleptin levels by d 16, although food intake remained significantly lower than in artificial cerebrospinal fluid controls; and body weight gradually decreased reaching a nadir at d 11 and remained stabilized at lower level thereafter. Phosphorylated leptin receptor and phosphorylated signal transducer and activator of transcription-3 (p-STAT3) remained elevated in association with a sustained elevation in DNA-binding activity of STAT3 in the hypothalamus throughout 16-d period of leptin infusion. However, phosphorylated Janus kinase-2 was increased during the early part of leptin infusion but remained unaltered on d 16. Although hypothalamic suppressors of cytokine signaling-3 (SOCS3) mRNA levels were increased throughout leptin infusion, SOCS3 protein levels were increased only on d 16. This study demonstrates a sustained elevation in hypothalamic leptin receptor signaling through Janus kinase-STAT pathway despite an increased expression of SOCS3 during chronic central leptin infusion. We propose that an alteration in leptin signaling in the hypothalamus through pathways other than STAT3 and/or a defect in downstream of STAT3 signaling may be involved in food intake recovery seen after an initial decrease during chronic central leptin infusion.


2021 ◽  
Vol 6 (4) ◽  
pp. 186-192
Author(s):  
A. M. Liashevych ◽  
◽  
І. S. Lupaina ◽  
M. Yu. Makarchuk ◽  
◽  
...  

The creation of universally effective and safe correctors of biliary secretion disorders is becoming more timely. There is an urgent need for scientists to find drugs that would correct blood cholesterol levels and metabolism in liver effectively and without limiting side effects. The purpose of the study was to investigate the possibility of using corvitin to correct stress-induced biliary disorders of the liver of male rats. Materials and methods. The article looks at recent research dealing with changes in the bile acid composition of outbred male rats’ bile under chronic social stress (social defeat in daily male confrontations, 14 days) when using Corvitin (1 mg/kg, intragastrically, 7 days). Chronic social stress was created by daily agonistic interactions between animals. The state of memory and the level of research activity in the object recognition test (cognitive test) were also studied. The main fractions of conjugated bile acids (taurocholic, taurohenodeoxycholic and taurodeoxycholic, glycocholic, glycochenodeoxycholic and glycodeoxycholic and free ones – cholic, chenodeoxycholic and deoxycholic) were determined by the method of thin layer chromatography of bile. Results and discussion. Chronic social stress leads to a slight increase in the overall activity of the experimental animals, but significantly impairs the processes of recognition and memory. Social stress significantly inhibits the processes that ensure the synthesis, biotransformation and transport of bile acids in the bile. Also, chronic social stress causes changes in bile production, which reduce the solubilization properties of bile and increase the risk of lithogenesis. Conclusion. The use of Corvitin simultaneously with the simulation of experimental social stress normalized the biliary secretory function of the liver, which indicates a high potential for the use of Corvitin as a corrective factor in chronic social stress. Corvitin used by us in the conditions of experimental social stress to some extent corrected the content of bile acids in the liver of male rats, which indicates the ability of this drug to interfere with the metabolism of cholate in liver cells, in the mechanisms of bile acid transport. Correction of stress-induced pathologies of liver bile-secretory function by Corvitin requires further thorough experimental studies


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