Effects of long-term administration of clozapine on body weight and food intake in rats

1993 ◽  
Vol 45 (1) ◽  
pp. 51-54 ◽  
Author(s):  
Trino Baptista ◽  
Alejandro Mata ◽  
Luis Teneud ◽  
Mary De Quijada ◽  
Hui-Wan Han ◽  
...  
1994 ◽  
Vol 43 (5) ◽  
pp. 747-754 ◽  
Author(s):  
Masayoshi SAITO ◽  
Masaru TERADA ◽  
Toru R. SAITO ◽  
Kazuaki W. TAKAHASHI

1986 ◽  
Vol 24 (6) ◽  
pp. 1817-1819 ◽  
Author(s):  
R. Iglesias ◽  
M. Llobera ◽  
E. Montoya

1995 ◽  
Vol 268 (1) ◽  
pp. R142-R149 ◽  
Author(s):  
A. M. Strack ◽  
R. J. Sebastian ◽  
M. W. Schwartz ◽  
M. F. Dallman

Signals that regulate long-term energy balance have been difficult to identify. Increasingly strong evidence indicates that insulin, acting on the central nervous system in part through its effect on neuropeptide Y (NPY), inhibits food intake. We hypothesized that corticosteroids and insulin might serve as interacting, reciprocal signals for energy balance, acting on energy acquisition, in part through their effects on hypothalamic NPY, as well as on energy stores. Because glucocorticoids also stimulate insulin secretion, their role is normally obscured. Glucocorticoids and insulin were clamped in adrenalectomized rats with steroid replacement and streptozotocin-induced diabetes. Glucocorticoids stimulated and insulin inhibited NPY mRNA and food intake. Glucocorticoids inhibited and insulin increased energy gain as determined by the change in body weight. When adrenalectomized diabetic rats were treated, corticosterone stimulated and insulin inhibited food intake, and, respectively, inhibited and increased overall energy gain. More than 50% of the variance was explained by regression analysis of the two hormones on food intake and body weight. Thus glucocorticoids and insulin are major, antagonistic, long-term regulators of energy balance. The effects of corticosterone and insulin on food intake may be mediated, in part, through regulation of hypothalamic NPY synthesis and secretion.


2003 ◽  
Vol 5 (11) ◽  
pp. 977-983 ◽  
Author(s):  
Jingjing Jiang ◽  
Eiji Yamato ◽  
Jun-ichi Miyazaki

Obesity ◽  
2014 ◽  
Vol 22 (10) ◽  
pp. 2147-2155 ◽  
Author(s):  
Yongbin Yang ◽  
Daniel L. Smith ◽  
Karen D. Keating ◽  
David B. Allison ◽  
Tim R. Nagy

2001 ◽  
Vol 281 (1) ◽  
pp. R76-R90 ◽  
Author(s):  
Gerald A. Lincoln ◽  
Stewart M. Rhind ◽  
Sueli Pompolo ◽  
Iain J. Clarke

This study used a hypothalamo-pituitary disconnected (HPD) sheep model to investigate the central regulation of long-term cycles in voluntary food intake (VFI) and body weight (BW). VFI, BW, and circulating concentrations of metabolic hormones [α-melanocyte-stimulating hormone (α-MSH), insulin-like growth factor-1 (IGF-1), insulin, and leptin] were measured in HPD and control Soay rams exposed to alternating 16 weekly periods of long and short days for 80 wk. In the controls, the physiology was cyclical with a 32-wk periodicity corresponding to the lighting regimen. VFI and BW increased under long days to a maximum early into short days, and there were associated increases in blood concentrations of α-MSH, insulin, and leptin. In the HPD rams, there were no significant photoperiod-induced changes in any of the parameters. VFI increased after surgery for 8 wk and then gradually declined, although BW increased progressively and the HPD rams became obese. Concentrations of α-MSH, insulin, and leptin in peripheral blood were permanently increased (>200%), and levels of IGF-1 decreased (<55%). The HPD lesion effectively destroyed the entire median eminence [no nerve terminals immunostained for tyrosine hydroxylase (TH) and gonadotropin-releasing hormone] and the adjacent arcuate nucleus (no perikarya immunostained for proopiomelanocortin or TH, and no cells expressed neuropeptide Y mRNA). The results support the conclusion that arcuate hypothalamic systems generate long-term rhythms in VFI, BW, and energy balance.


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