Involvement of central nesfatin-1 neurons on oxytocin-induced feeding suppression in rats

To determine whether leptin alone accounts for the satiety activity secreted by native adipose tissue, we prepared culture media conditioned by microdissected adipose tissue from overfed Long-Evans rats, fa/ farats, or db/ dbmice ( media A, B, and C, respectively). Medium A significantly suppressed food intake following intracerebroventricular delivery to Long-Evans rats (2-h chow intake = 68 ± 5% of baseline, P< 0.001). Media B and C significantly suppressed food intake following intraperitoneal delivery to ob/ obmice (24-h chow intake = 56 ± 7% of baseline for medium B, P= 0.001; 4-day chow intake = 78 ± 3% of baseline for medium C, P= 0.004). Using a leptin receptor-based bioassay, we determined that the leptin concentration of medium C was 392 ± 18 ng/ml. This concentration was 20-fold lower than the concentration of recombinant murine leptin required to produce a similar degree of feeding suppression following 5 days of administration to ob/ obmice. Neither medium conditioned by adipose tissue from ob/ obmice nor medium conditioned by adipose tissue from fa/ farats and subsequently immunodepleted of leptin had significant satiety activity. We conclude that leptin is necessary but not sufficient to account for the satiety activity of native adipose tissue, perhaps due to the production by adipocytes of a cofactor that augments the ability of leptin to suppress feeding.

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Analysis of feeding suppression produced by perifornical hypothalamic injection of catecholamines, amphetamines and mazindol

European Journal of Pharmacology ◽

10.1016/0014-2999(78)90269-8 ◽

1978 ◽

Vol 53 (1) ◽

pp. 69-81 ◽

Cited By ~ 60

Author(s):

Sarah F. Leibowitz ◽

C. Rossakis

Keyword(s):

Feeding Suppression

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Paraventricular NUCB2/nesfatin-1 rises in synchrony with feeding suppression during early light phase in rats

Biochemical and Biophysical Research Communications ◽

10.1016/j.bbrc.2013.03.090 ◽

2013 ◽

Vol 434 (3) ◽

pp. 434-438 ◽

Cited By ~ 23

Author(s):

Udval Sedbazar ◽

Yuko Maejima ◽

Masanori Nakata ◽

Masatomo Mori ◽

Toshihiko Yada

Keyword(s):

Light Phase ◽

Feeding Suppression

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Feeding suppression induced by intra-ventricle III infusion of 1,5-anhydroglucitol

Physiology & Behavior ◽

10.1016/0031-9384(83)90072-0 ◽

1983 ◽

Vol 31 (4) ◽

pp. 493-502 ◽

Cited By ~ 10

Author(s):

Koichiro Tsutsui ◽

Toshiie Sakata ◽

Yutaka Oomura ◽

Koichi Arase ◽

Masataka Fukushima ◽

...

Keyword(s):

Feeding Suppression

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Comparison of feeding suppression by the anorexigenic hormones neuromedin U and neuromedin S in rats

Journal of Endocrinology ◽

10.1677/joe-10-0081 ◽

2010 ◽

Vol 207 (2) ◽

pp. 185-193 ◽

Cited By ~ 15

Author(s):

Keiko Nakahara ◽

Tetsuro Katayama ◽

Keisuke Maruyama ◽

Takanori Ida ◽

Kenji Mori ◽

...

Keyword(s):

Food Intake ◽

Time Course ◽

Neuronal Firing ◽

Pcr Analysis ◽

Physiological Conditions ◽

Melanocyte Stimulating Hormone ◽

Feeding Suppression ◽

Neuronal Firing Rate ◽

Dose Dependent Increase ◽

Dose Dependent

We compared the central mechanisms of feeding suppression by the anorexigenic hormones neuromedin U (NMU) and neuromedin S (NMS) in rats. I.c.v. injection of either NMU or NMS dose dependently decreased 3-h food intake during the first quarter of a dark period. Pretreatment involving i.c.v. injection of a specific anti-NMS IgG blocked the suppression of food intake induced by i.c.v.- and i.p.-injected leptin, but anti-NMU IgG elicited no blockade. Quantitative PCR analysis revealed that i.c.v. injection of NMU or NMS caused a dose-dependent increase in CRH and proopiomelanocortin mRNA expression in the paraventricular nucleus (PVN) and arcuate nucleus (Arc) respectively. In tissue cultures of the Arc, secretion of α-melanocyte-stimulating hormone was stimulated by NMU and NMS, with more potent stimulation by NMS. The time-course curves of the increase in neuronal firing rate in Arc slices in response to NMU and NMS showed almost the same pattern, with a peak 10–15 min after treatment, whereas the time-course curves for the PVN slices differed between NMU and NMS. These results suggest that NMS and NMU may share anorexigenic effects, depending on physiological conditions.

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Modulation of glucocorticoid in feeding suppression induced by D-glucose in rats

Neuroscience Research Supplements ◽

10.1016/0921-8696(90)90596-u ◽

1990 ◽

Vol 11 ◽

pp. S48

Author(s):

Mamoru Kurokawa ◽

Koichi Arase ◽

Hironobu Machidori ◽

Tosiie Sakata

Keyword(s):

Feeding Suppression

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Leptin enhances feeding suppression and neural activation produced by systemically administered bombesin

AJP Regulatory Integrative and Comparative Physiology ◽

10.1152/ajpregu.00835.2004 ◽

2005 ◽

Vol 289 (2) ◽

pp. R473-R477 ◽

Cited By ~ 17

Author(s):

Ellen E. Ladenheim ◽

M. Emond ◽

T. H. Moran

Keyword(s):

Food Intake ◽

Fold Increase ◽

Liquid Diet ◽

Individual Response ◽

Neural Activation ◽

Solitary Tract ◽

Significant Suppression ◽

Feeding Inhibition ◽

Feeding Suppression ◽

The Individual

Leptin amplifies feeding inhibition and neural activation produced by either cholecystokinin or intragastric preloads, suggesting that leptin may increase the efficacy of gastrointestinal meal-related signals. To determine whether leptin would similarly potentiate the feeding inhibitory actions of another putative satiety peptide, we evaluated the effects of third ventricular leptin administration on food intake and c-Fos activation in response to systemically administered bombesin (BN). Leptin (3.5 μg) was administered 1 h before either 0.9% saline or BN (0.32 and 1.0 nmol/kg) followed by 30-min access to Ensure liquid diet. Although neither leptin nor 0.32 nmol/kg BN alone suppressed Ensure intake, the combination reduced intake by 28%. The higher BN dose (1.0 nmol/kg) produced a significant suppression by itself but was further enhanced in the presence of leptin. Consistent with the behavioral results, c-Fos activation in the nucleus of the solitary tract was increased by combined dosages of leptin and 0.32 nmol/kg BN beyond the individual response to either peptide. In the presence of leptin, BN produced a 3.4- to 5.2-fold increase in the number of c-Fos-positive cells in the nucleus of the solitary tract compared with when BN was given alone. These data provide further support for the hypothesis that the effect of leptin on food intake may be mediated, in part, by modulating meal-related satiety signals.

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