scholarly journals Intraventricular GLP-1 reduces short- but not long-term food intake or body weight in lean and obese rats

1998 ◽  
Vol 779 (1-2) ◽  
pp. 75-83 ◽  
Author(s):  
Jamie C.K Donahey ◽  
Gertjan van Dijk ◽  
Stephen C Woods ◽  
Randy J Seeley
Keyword(s):  
Peptides ◽  
1998 ◽  
Vol 19 (2) ◽  
pp. 291-299 ◽  
Author(s):  
Kerstin Meereis-Schwanke ◽  
Hanne Klonowski-Stumpe ◽  
Lieselotte Herberg ◽  
Claus Niederau

1990 ◽  
Vol 258 (1) ◽  
pp. R269-R273 ◽  
Author(s):  
D. C. Chen ◽  
J. S. Stern ◽  
R. L. Atkinson

This study evaluated the effects of ileal transposition (IT) surgery on food intake, body weight, and dietary preferences in Zucker obese rats. Eight rats had a 10-cm segment of terminal ileum transposed to the upper jejunum. Eight rats underwent sham IT (SIT) and six rats had no surgery (CON). During weeks 1-10 and 21-24, rats were fed a selection diet of protein (casein), carbohydrate (corn starch), and fat (lard) in three separate dishes. Rat chow was fed from weeks 11 to 20. IT rats had a lower weight and a lower change in weight from base line throughout most of the study. Energy intake was less in IT vs. SIT rats during the selection periods (weeks 1-10 and 21-24), but did not differ on the chow diet (weeks 11-20). Digestible energy, measured at weeks 10, 20, and 24, was lower in IT rats only at week 10. IT rats had no malabsorption by fecal calorie measurements. IT rats ate fewer fat calories at both selection periods. We conclude that IT causes long-term reduction in body weight, no malabsorption or long-term changes in digestible energy, and a persistent decrease in preference for dietary fat. Further studies are needed to determine whether increased energy expenditure is a mechanism for the long-term difference in body weight after IT.


1982 ◽  
Vol 35 (2) ◽  
pp. 284-293 ◽  
Author(s):  
H S Koopmans ◽  
A Sclafani ◽  
C Fichtner ◽  
P F Aravich

1981 ◽  
Vol 240 (1) ◽  
pp. E72-E78 ◽  
Author(s):  
M. R. Greenwood ◽  
M. P. Cleary ◽  
R. Gruen ◽  
D. Blase ◽  
J. S. Stern ◽  
...  

Young Zucker lean (Fa/-) and obese (fa/fa) female rats were fed the fatty acid synthesis inhibitor (-)-hydroxy-citrate as a dietary admixture for 39 days. In the lean rats, (-)-hydroxycitrate treatment decreased body weight, food intake, percent of body fat, and fat cell size. In the obese rat, food intake and body weight were reduced but the percent of body fat remained unchanged. Throughout the treatment period, obese rats maintained a fat cell size equivalent to their obese controls. Although a reduction in fat cell number in the obese rats occurred during the treatment period, marked hyperplasia was observed during the posttreatment period. The results of this study indicate that the obese rat, despite a substantial reduction in body weight produced by (-)-hydroxycitrate, still defends its obese body composition.


2007 ◽  
Vol 293 (5) ◽  
pp. R1798-R1808 ◽  
Author(s):  
Prasanth K. Chelikani ◽  
Alvin C. Haver ◽  
Roger D. Reidelberger

Chronic administration of anorexigenic substances to experimental animals by injections or continuous infusion typically produces no effect or a transient reduction in daily food intake and body weight. Our aim was to identify an intermittent dosing strategy for intraperitoneal infusion of salmon calcitonin (sCT), a homolog of amylin that produces a sustained 25–35% reduction in daily food intake and adiposity in diet-induced obese rats. Rats (649 ± 10 g body wt, 27 ± 1% body fat), with intraperitoneal catheters tethered to infusion swivels, had free access to a 45% fat diet. Food intake, body weight, and adiposity during the 7-wk test period were relatively stable in the vehicle-treated rats ( n = 16). None of 10 sCT dosing regimens administered in succession to a second group of rats ( n = 18) produced a sustained 25–35% reduction in daily food intake for >5 days, although body weight and adiposity were reduced by 9% (587 ± 12 vs. 651 ± 14 g) and 22% (20.6 ± 1.2 vs. 26.5 ± 1.1%), respectively, across the 7-wk period. The declining inhibitory effect of sCT on daily food intake with the 6-h interinfusion interval appeared to be due in part to an increase in food intake between infusions. The declining inhibitory effect of sCT on daily food intake with the 2- to 3-h interinfusion interval suggested possible receptor downregulation and tolerance to frequent sCT administration; however, food intake increased dramatically when sCT was discontinued for 1 day after apparent loss of treatment efficacy. Together, these results demonstrate the activation of a potent homeostatic response to increase food intake when sCT reduces food intake and energy reserves in diet-induced obese rats.


2012 ◽  
Vol 23 (1) ◽  
pp. 71-79 ◽  
Author(s):  
Shiying Li ◽  
Roland Maude-Griffin ◽  
Yan Sun ◽  
Warren Starkebaum ◽  
Jiande D. Z. Chen

2007 ◽  
Vol 293 (1) ◽  
pp. R39-R46 ◽  
Author(s):  
Prasanth K. Chelikani ◽  
Alvin C. Haver ◽  
Roger D. Reidelberger

Peptide YY(3-36) [PYY(3-36)] is a gut-brain peptide that decreases food intake when administered by intravenous infusion to lean and obese humans and rats. However, chronic administration of PYY(3-36) by osmotic minipump to lean and obese rodents produces only a transient reduction in daily food intake and weight gain. It has recently been shown that 1-h intravenous infusions of PYY(3-36) every other hour for 10 days produced a sustained reduction in daily food intake, body weight, and adiposity in lean rats. Here, we determined whether intermittent delivery of PYY(3-36) can produce a similar response in diet-induced obese rats. During a 21-day period, obese rats (body fat >25%) received twice daily intraperitoneal infusion of vehicle ( n = 18) or PYY(3-36) ( n = 24) during hours 1–3 and 7–9 of the dark period. Rats had free access to both a 45% fat solid diet and a 29% fat liquid diet; intakes were determined from continuous computer recording of changes in food container weights. To sustain a 15–25% reduction in daily caloric intake, the initial PYY(3-36) dose of 30 pmol·kg−1·min−1 was reduced to 10 pmol·kg−1·min−1 on day 10 and then increased to 17 pmol·kg−1·min−1 on day 13. This dosing strategy produced a sustained reduction in daily caloric intake of 11–32% and prevented body weight gain (8 ± 6 vs. 51 ± 11 g) and fat deposition (4.4 ± 7.6 vs. 41.0 ± 12.8 g). These results indicate that intermittent intraperitoneal infusion of PYY(3-36) can produce a sustained reduction in food intake and adiposity in diet-induced obese rodents consuming palatable high-fat foods.


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

2006 ◽  
Vol 290 (3) ◽  
pp. E591-E597 ◽  
Author(s):  
Nadine Simler ◽  
Alexandra Grosfeld ◽  
André Peinnequin ◽  
Michèle Guerre-Millo ◽  
André-Xavier Bigard

Exposure to hypoxia induces anorexia in humans and rodents, but the role of leptin remains under discussion and that of orexigenic and anorexigenic hypothalamic neuropeptides remains unknown. The present study was designed to address this issue by using obese (Leprfa/Leprfa) Zucker rats, a rat model of genetic leptin receptor deficiency. Homozygous lean (LeprFA/LeprFA) and obese (Leprfa/Leprfa) rats were randomly assigned to two groups, either kept at ambient pressure or exposed to hypobaric hypoxia for 1, 2, or 4 days (barometric pressure, 505 hPa). Food intake and body weight were recorded throughout the experiment. The expression of leptin and vascular endothelial growth factor (VEGF) genes was studied in adipose tissue with real-time quantitative PCR and that of selected orexigenic and anorexigenic neuropeptides was measured in the hypothalamus. Lean and obese rats exhibited a similar hypophagia (38 and 67% of initial values at day 1, respectively, P < 0.01) and initial decrease in body weight during hypoxia exposure. Hypoxia led to increased plasma leptin levels only in obese rats. This resulted from increased leptin gene expression in adipose tissue in response to hypoxia, in association with enhanced VEGF gene expression. Increased hypothalamic neuropeptide Y levels in lean rats 2 days after hypoxia exposure contributed to accounting for the enhanced food consumption. No significant changes occurred in the expression of other hypothalamic neuropeptides involved in the control of food intake. This study demonstrates unequivocally that altitude-induced anorexia cannot be ascribed to anorectic signals triggered by enhanced leptin production or alterations of hypothalamic neuropeptides involved in anabolic or catabolic pathways.


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