Chronic infusion of islet amyloid polypeptide causes anorexia in rats

1996 ◽  
Vol 271 (6) ◽  
pp. R1654-R1659 ◽  
Author(s):  
U. Arnelo ◽  
J. Permert ◽  
T. E. Adrian ◽  
J. Larsson ◽  
P. Westermark ◽  
...  
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Islet Amyloid Polypeptide ◽  
Reduce Food Intake ◽  
Islet Amyloid ◽  
Minimal Effective Dose ◽  
Subcutaneous Infusion ◽  
Pathophysiological Role ◽  
Chronic Infusion ◽  
High Doses

Islet amyloid polypeptide (IAPP) is a hormonal peptide that at high doses has been shown to reduce food intake. In the present study, the dose-response effects of subcutaneous infusion of IAPP (0, 2, 7, and 25 pmol.kg-1.min-1) for 8 days on food intake and meal patterns in rats were investigated. At the end of the experiment, plasma was obtained and levels of IAPP were measured by radioimmunoassay. IAPP dose-dependently and transiently inhibited food intake. The minimal effective dose (2 pmol.kg-1.min-1) caused a small but significant (up to 14%, P < 0.01) inhibition of food intake that lasted 5 days. The highest dose administered (25 pmol.kg-1.min-1) had the greatest effect (up to 44%, P < 0.001), which lasted throughout the 8-day period. Reductions in feeding during light and dark phases occurred through a decrease in number of meals consumed rather than meal size or meal duration. IAPP also decreased body weight gain and water intake dose dependently. IAPP infusion of 2, 7, and 25 pmol.kg-1.min-1 increased plasma IAPP concentrations from a basal level of 10.3 +/- 0.7 pM to 35.1 +/- 5.4, 78.1 +/- 11.2, and 236.6 +/- 23.6 pM, respectively, values that are likely to be close to physiological and within the pathophysiological ranges. Thus IAPP may play an important physiological or pathophysiological role in control of food intake.

Effects of Acute and Chronic Infusion of Islet Amyloid Polypeptide on Food Intake in Rats

1996 ◽  
Vol 31 (1) ◽  
pp. 83-89 ◽  
Author(s):  
U. Arnelo ◽  
J. E. Blevins ◽  
J. Larsson ◽  
J. Permert ◽  
P. Westermark ◽  
...  
Keyword(s):  
Food Intake ◽  
Islet Amyloid Polypeptide ◽  
Islet Amyloid ◽  
Chronic Infusion

scholarly journals Effect of chronic infusion of olanzapine and clozapine on food intake and body weight gain in male and female rats

Life Sciences ◽  
2007 ◽  
Vol 81 (12) ◽  
pp. 1024-1030 ◽  
Author(s):  
SuJean Choi ◽  
Briana DiSilvio ◽  
JayLynn Unangst ◽  
John D. Fernstrom
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Female Rats ◽  
Male And Female ◽  
Male And Female Rats ◽  
Chronic Infusion

scholarly journals Effects of estradiol and progesterone on food intake, body weight, and carcass adiposity in weanling rats

1981 ◽  
Vol 240 (5) ◽  
pp. E499-E503 ◽  
Author(s):  
S. M. Schwartz ◽  
G. N. Wade
Keyword(s):  
Body Weight ◽  
Adipose Tissue ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Estradiol Benzoate ◽  
Female Rats ◽  
Reduce Food Intake ◽  
Reduced Body ◽  
Adipose Tissue Lipoprotein Lipase

The effects of estradiol and progesterone on food intake, body weight, carcass adiposity, and adipose tissue lipoprotein lipase (LPL) activity were investigated in weanling female rats. Treatment with estradiol benzoate (EB) reduced body weight gain in ovariectomized (OVX) weanlings as it does in adults. However, other responses to EB were attenuated or absent in weanlings. EB treatment did not reduce food intake, carcass adiposity, or adipose tissue LPL activity. This impaired responsiveness to EB may be due to decreased levels of cytoplasmic estrogen receptors in liver and adipose tissue (but not hypothalamus) in weanlings. On the other hand, responsiveness to progesterone was adultlike in weanlings. Treatment of OVX, EB-primed weanlings with progesterone increased food intake, body weight gain, and carcass adiposity. This adultlike responsiveness to progesterone was associated with adultlike levels of adipose tissue progestin receptors. However, progesterone treatment did not increase adipose tissue LPL activity in weanlings, indicating that changes in LPL activity are not necessary for progesterone-induced obesity.

Endogenous ACTH, not only α-melanocyte-stimulating hormone, reduces food intake mediated by hypothalamic mechanisms

2010 ◽  
Vol 298 (2) ◽  
pp. E237-E244 ◽  
Author(s):  
Carla Schulz ◽  
Kerstin Paulus ◽  
Ralf Lobmann ◽  
Mary Dallman ◽  
Hendrik Lehnert
Keyword(s):  
Food Intake ◽  
Body Weight Gain ◽  
Reduce Food Intake ◽  
Melanocyte Stimulating Hormone ◽  
Paraventricular Nuclei ◽  
Close Proximity ◽  
Robust Evidence ◽  
Stimulating Hormone

ACTH and α-melanocyte-stimulating hormone (α-MSH) are both consecutively processed from proopiomelanocortin (POMC), which is synthesized in hypothalamic arcuate neurons innervating the paraventricular nuclei (PVN). POMC secretion/synthesis is regulated by energy availability. ACTH and α-MSH bind with equal affinity to melanocortin-4 receptors and elicit similar effects on signal transduction in-vitro. Endogenous α-MSH thus far is believed to be the major physiological agonist and to act in an anorexigenic manner. Until now, it was fully unknown whether endogenous ACTH is also involved in the regulation of appetite and food intake. In this study in rats, we now show that icv ACTH as well as α-MSH possess anorexigenic effects in the PVN or areas in close proximity in vivo and that the effect of ACTH is direct and not mediated via α-MSH. We investigated the roles of endogenous ACTH and α-MSH by PVN application of the respective antibodies under different physiological conditions. In satiated rats with high levels of ACTH and α-MSH in the PVN, antibody administration increased food intake and body weight gain; hungry animals were unaffected. Finally, repeated injections of ACTH antibodies into PVN resulted in persistently increased food intake during the light period. These data now provide robust evidence that endogenous ACTH without further processing acts in the PVN or areas in close proximity to reduce food intake under conditions of feeding-induced satiety.

Commissural nucleus of the solitary tract lesions reduce food intake and body weight gain in rats

1996 ◽  
Vol 740 (1-2) ◽  
pp. 102-108 ◽  
Author(s):  
Jose Vanderlei Menani ◽  
Eduardo Colombari ◽  
William T. Talman ◽  
Alan Kim Johnson
Keyword(s):  
Body Weight ◽  
Weight Gain ◽  
Food Intake ◽  
Body Weight Gain ◽  
Reduce Food Intake ◽  
Solitary Tract

scholarly journals Suppression of Food Intake by Glucagon-Like Peptide-1 Receptor Agonists: Relative Potencies and Role of Dipeptidyl Peptidase-4

Endocrinology ◽  
2012 ◽  
Vol 153 (12) ◽  
pp. 5735-5745 ◽  
Author(s):  
Lene Jessen ◽  
Benedikt A. Aulinger ◽  
Jonathan L. Hassel ◽  
Kyle J. Roy ◽  
Eric P. Smith ◽  
...  
Keyword(s):  
Gastric Bypass ◽  
Food Intake ◽  
Dipeptidyl Peptidase ◽  
Reduce Food Intake ◽  
Wild Type ◽  
Dipeptidyl Peptidase 4 ◽  
Receptor Agonists ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
High Doses

Abstract Administration of the glucagon-like peptide-1 (GLP-1) receptor agonists GLP-1 and exendin-4 (Ex-4) directly into the central nervous system decreases food intake. But although Ex-4 potently suppresses food intake after peripheral administration, the effects of parenteral GLP-1 are variable and not as strong. A plausible explanation for these effects is the rapid inactivation of circulating GLP-1 by dipeptidyl peptidase-4 (DPP-4), an enzyme that does not alter Ex-4 activity. To test this hypothesis, we assessed the relative potency of Ex-4 and GLP-1 under conditions in which DPP-4 activity was reduced. Outbred rats, wild-type mice, and mice with a targeted deletion of DPP-4 (Dpp4−/−) were treated with GLP-1 alone or in combination with the DPP-4 inhibitor vildagliptin, Ex-4, or saline, and food intake was measured. GLP-1 alone, even at high doses, did not affect feeding in wild-type mice or rats but did reduce food intake when combined with vildagliptin or given to Dpp4−/− mice. Despite plasma clearance similar to DPP-4-protected GLP-1, equimolar Ex-4 caused greater anorexia than vildagliptin plus GLP-1. To determine whether supraphysiological levels of endogenous GLP-1 would suppress food intake if protected from DPP-4, rats with Roux-en-Y gastric bypass and significantly elevated postprandial plasma GLP-1 received vildagliptin or saline. Despite 5-fold greater postprandial GLP-1 in these animals, vildagliptin did not affect food intake in Roux-en-Y gastric bypass rats. Thus, in both mice and rats, peripheral GLP-1 reduces food intake significantly less than Ex-4, even when protected from DPP-4. These findings suggest distinct potencies of GLP-1 receptor agonists on food intake that cannot be explained by plasma pharmacokinetics.

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