Changes in feeding behavior after intracerebral injections in the rat

1963 ◽  
Vol 204 (3) ◽  
pp. 483-487 ◽  
Author(s):  
J. W. Wagner ◽  
J. De Groot
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Globus Pallidus ◽  
Water Intake ◽  
Liquid Food ◽  
Lateral Amygdala ◽  
Lateral Hypothalamic ◽  
Chemical Solutions ◽  
Fasted Rats

Changes in basal liquid food intake in sated or fasted rats were measured after localized intracerebral injections (5 µl) of 17 chemical solutions. Lidocaine, pentobarbital, and epinephrine produced feeding in sated or fasted rats with ventromedial hypothalamic (VMH) cannulas; neostigmine, norepinephrine, pentylenetetrazol, and 1.5% NaCl reduced food intake in fasted rats; acetylcholine, histamine, and dextrose had no effect in either state. In sated rats with lateral hypothalamic (LHA) implants, epinephrine, norepinephrine, and 1.5% NaCl produced feeding; lidocaine and neostigmine reduced, whereas norepinephrine augmented food intake in fasted LHA animals. No effect on consumatory behavior was observed after injections into the lateral amygdala. Lidocaine reduced food intake in fasted rats with globus pallidus implants; epinephrine and norepinephrine initiated feeding. Eight other chemicals had no effect on feeding in limited tests. Neostigmine and acetylcholine produced drinking in sated VMH and LHA animals, respectively. These results suggest that closely adjacent neuronal aggregates (VMH-LHA) may have different metabolic requirements for single compounds, and that the VMH functions in satiety mechanisms for food as well as water intake.

Modulation of feeding by endogenous sugar acids acting as hunger or satiety factors

1984 ◽  
Vol 246 (4) ◽  
pp. R542-R550 ◽  
Author(s):  
N. Shimizu ◽  
Y. Oomura ◽  
T. Sakata
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Food Consumption ◽  
Single Neuron ◽  
Cerebral Ventricle ◽  
Neuron Activity ◽  
Hypothalamic Area ◽  
The Third ◽  
Single Neuron Activity ◽  
Fasted Rats

Endogenous sugar acids, 3,4-dihydroxybutanoic acid (2-deoxytetronic acid, 2-DTA) and 2,4,5-trihydroxypentanoic acid (3-deoxypentonic acid, 3-DPA), have been identified in the serum of fasted rats. Effects of these sugar acids on rat feeding behavior and neuron activity were investigated. Injections of 2-DTA (2.5 mumol) into the third cerebral ventricle of chronic rats suppressed food intake and single-neuron activity in the lateral hypothalamic area (LHA). Food consumption was reduced for 24 h, even in 72-h food-deprived rats. The same amounts of 3-DPA elicited feeding and increased LHA single-neuron activity with latencies of 6-8 min. Electrophoretically applied 2-DTA significantly and specifically suppressed activity of glucose-sensitive neurons in the LHA, whereas 3-DPA facilitated the activity. Nonglucose-sensitive LHA neurons were not affected by these sugar acids. The high correlation between modulation of feeding behavior and changes in LHA neuron activity after injection of these sugar acids suggested that 2-DTA may act as an endogenous satiety substance and 3-DPA as a hunger substance. The effects may be mediated through glucose-sensitive neurons in the LHA.

Glucagon like peptide (GLP)-1-(7–36)-amide suppresses food intake of fasted rats at lateral hypothalamic sites

1992 ◽  
Vol 40 (2) ◽  
pp. 244
Author(s):  
RR Schick ◽  
T Vorm Walde ◽  
JP Zimmermann ◽  
V Schusdziarra ◽  
M Classen
Keyword(s):  
Food Intake ◽  
Lateral Hypothalamic ◽  
Glucagon Like Peptide ◽  
Fasted Rats

Glucagon-like peptide 1-(7–36) amide acts at lateral and medial hypothalamic sites to suppress feeding in rats

2003 ◽  
Vol 284 (6) ◽  
pp. R1427-R1435 ◽  
Author(s):  
Rafael R. Schick ◽  
Jens P. Zimmermann ◽  
Thomas vorm Walde ◽  
Volker Schusdziarra
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Effective Dose ◽  
Ventromedial Hypothalamus ◽  
Brain Regions ◽  
Central Administration ◽  
Minimal Effective Dose ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Fasted Rats

Glucagon-like peptide 1-(7–36) amide (GLP-1) potently inhibits rat feeding behavior after central administration. Because third ventricular injection of GLP-1 appeared to be less effective than lateral ventricular injection, we have reexamined this issue. In addition, we attempted to identify brain regions other than the paraventricular nucleus of the hypothalamus that are sensitive toward GLP-1-induced feeding suppression. Finally, we examined the local role of endogenous GLP-1 by specific GLP-1 receptor blockade. After lateral ventricular injection, GLP-1 significantly inhibited food intake of 24-h-fasted rats in a dose-dependent fashion with a minimal effective dose of 1 μg. After third ventricular injection, GLP-1 (1 μg) was similarly effective in suppressing food intake, which extends previous findings. Intracerebral microinjections of GLP-1 significantly suppressed food intake in the lateral (LH), dorsomedial (DMH), and ventromedial hypothalamus (VMH), but not in the medial nucleus of the amygdala. The minimal effective dose of GLP-1 was 0.3 μg at LH sites and 1 μg at DMH or VMH sites. LH microinjections of exendin-(9–39) amide, a GLP-1 receptor antagonist, at 1 or 2.5 μg did not alter feeding behavior in 24-h-fasted rats. In satiated animals, however, a single LH injection of 1 μg exendin-(9–39) amide significantly augmented food intake, but only during the first 20 min (0.6 vs. 0.1 g). With three repeated injections of 2.5 μg exendin-(9–39) amide every 20 min, 1-h food intake was significantly increased by 300%. These data strongly support and extend the concept of GLP-1 as a physiological regulator of food intake in the hypothalamus.

Separate lateral hypothalamic pathways for extracellular and intracellular thirst

1975 ◽  
Vol 228 (1) ◽  
pp. 295-301 ◽  
Author(s):  
J Kucharczyk ◽  
GJ Mogenson
Keyword(s):  
Hypertonic Saline ◽  
Globus Pallidus ◽  
Water Intake ◽  
Lateral Hypothalamus ◽  
Marked Decrease ◽  
Internal Capsule ◽  
Ventromedial Nucleus ◽  
Neural Pathways ◽  
Lateral Hypothalamic

Small lesions of the midlateral zone of the lateral hypothalamus in rats attentuated water intake elicted by the central microinjection angiotensin or by the peripheral injection of isoproterenol or renin without attenuating drinking to peripherally administered hypertonic saline. Lesions placed further lateral in the hypothalamus, which destroyed the medial aspects of the internal capsule and globus pallidus, produced a marked decrease in water intake induced by hypertonic saline. Abaltion of the ventromedial nucleus of the hypothalamus increased drinking elicited by angiotension, isoproterenol, or renin.These results suggest that extracellular and intracellular thirst stimuli are mediated by separate neural pathways at the level of the lateral hypothalamus.

scholarly journals A reassessment of the role of serotonergic system in the control of feeding behavior

2005 ◽  
Vol 77 (1) ◽  
pp. 103-111 ◽  
Author(s):  
Magda A. Medeiros ◽  
Ricardo H. Costa-e-Sousa ◽  
Emerson L. Olivares ◽  
Wellington S. Côrtes ◽  
Luís C. Reis
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Feeding Behavior ◽  
The Body ◽  
Serotonergic System ◽  
Initial Increase ◽  
Energetic Balance ◽  
Electrolytic Lesions ◽  
Fasted Rats

The role of serotonergic system in the feeding behaviorwas appraised by electrolytic lesions in the dorsal raphe nucleus (DRN) and administration of para-chlorophenylalanine (PCPA, 3 mg/5 mul, icv). Chronic evaluations were accomplished through 120 and 360 days in PCPA-injected and DRN-lesioned rats, respectively. Acute food intake was evaluated in fasted rats and submitted to injection of PCPA and hydroxytryptophan (LHTP, 30 mg/kg, ip). DRN-lesioned rats exhibited 22-80% increase in food intake up to sixth month, whereas the obesity was evident and sustained by whole period. In PCPA-injected rats was observed an initial increase in the food intake followed by hypophagy from 25th to 30th day and a transitory increase of body weight from 5th to 60th day. In the acute study, the LHTP reverted partially the PCPA-induced increase in food intake of fasted rats suggesting a sustained capacity of decarboxylation of precursor by serotonergic neurons. Slow restoration of the levels of food intake in DRN-lesioned rats reveals a neuroplasticity in the systems that regulate feeding behavior. A plateau on the body weight curve in lesioned rats possibly represents the establishment of a new and higher set point of energetic balance.

Effects of neurosecretory protein GL on food intake and fat accumulation under different dietary nutrient compositions in rats

2021 ◽  
Author(s):  
Keisuke Fukumura ◽  
Kenshiro Shikano ◽  
Yuaki Narimatsu ◽  
Eiko Iwakoshi-Ukena ◽  
Megumi Furumitsu ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior ◽  
Body Mass ◽  
Mass Gain ◽  
Chow Diet ◽  
Tissue Mass ◽  
Fat Accumulation ◽  
Intracerebroventricular Infusion ◽  
Body Mass Gain ◽  
Sucrose Diet

Abstract We recently identified a novel hypothalamic small protein, named neurosecretory protein GL (NPGL), which is involved in energy homeostasis in birds and mammals. However, whether the action of NPGL is influenced by nutritional composition remains unknown. Thus, we investigated the effect of chronic intracerebroventricular infusion of NPGL for 13 days on feeding behavior and body mass gain under a normal chow diet (NC), high-fat diet, high-sucrose diet (HSD), and medium-fat/medium-sucrose diet (MFSD) in rats. NPGL stimulated food intake of NC and MFSD, especially during the light period. By contrast, NPGL decreased body mass gain under NC and increased total white adipose tissue mass in HSD- and MFSD-fed rats. These data suggest that the effects of NPGL on feeding behavior, body mass gain, and fat accumulation depend on nutrient type. Among them, sucrose in diets seems to contribute to fat accumulation elicited by NPGL.

scholarly journals Impaired branched chain amino acid metabolism alters feeding behavior and increases orexigenic neuropeptide expression in the hypothalamus

2011 ◽  
Vol 212 (1) ◽  
pp. 85-94 ◽  
Author(s):  
Megan N Purpera ◽  
Li Shen ◽  
Marzieh Taghavi ◽  
Heike Münzberg ◽  
Roy J Martin ◽  
...  
Keyword(s):  
Amino Acid ◽  
Food Intake ◽  
Feeding Behavior ◽  
Control Diet ◽  
Peripheral Tissues ◽  
Protein Status ◽  
Branched Chain Amino Acid ◽  
Branched Chain ◽  
Branched Chain Aminotransferase ◽  
Deficient Mice

Elevation of dietary or brain leucine appears to suppress food intake via a mechanism involving mechanistic target of rapamycin, AMPK, and/or branched chain amino acid (BCAA) metabolism. Mice bearing a deletion of mitochondrial branched chain aminotransferase (BCATm), which is expressed in peripheral tissues (muscle) and brain glia, exhibit marked increases in circulating BCAAs. Here, we test whether this increase alters feeding behavior and brain neuropeptide expression. Circulating and brain levels of BCAAs were increased two- to four-fold in BCATm-deficient mice (KO). KO mice weighed less than controls (25.9 vs 20.4 g,P<0.01), but absolute food intake was relatively unchanged. In contrast to wild-type mice, KO mice preferred a low-BCAA diet to a control diet (P<0.05) but exhibited no change in preference for low- vs high-protein (HP) diets. KO mice also exhibited low leptin levels and increased hypothalamicNpyandAgrpmRNA. Normalization of circulating leptin levels had no effect on either food preference or the increasedNpyandAgrpmRNA expression. If BCAAs act as signals of protein status, one would expect reduced food intake, avoidance of dietary protein, and reduction in neuropeptide expression in BCATm-KO mice. Instead, these mice exhibit an increased expression of orexigenic neuropeptides and an avoidance of BCAAs but not HP. These data thus suggest that either BCAAs do not act as physiological signals of protein status or the loss of BCAA metabolism within brain glia impairs the detection of protein balance.

Participation of alpha-1 and alpha-2 adrenoceptors of the lateral hypothalamic area in water intake, and renal sodium, potassium and urinary volume excretion induced by central administration of angiotensin II

2000 ◽  
Vol 52 (6) ◽  
pp. 491-497 ◽  
Author(s):  
Wilson Abrão Saad ◽  
Ismael Francisco Motta Siqueira Guarda ◽  
Ana Cristini Ferreira ◽  
Luis Antonio de Arruda Camargo ◽  
Abrão Fadlala Saad Neto ◽  
...  
Keyword(s):  
Angiotensin Ii ◽  
Water Intake ◽  
Lateral Hypothalamic Area ◽  
Central Administration ◽  
Urinary Volume ◽  
Hypothalamic Area ◽  
Sodium Potassium ◽  
Lateral Hypothalamic

scholarly journals GLP-2 receptor in POMC neurons suppresses feeding behavior and gastric motility

2012 ◽  
Vol 303 (7) ◽  
pp. E853-E864 ◽  
Author(s):  
Xinfu Guan ◽  
Xuemei Shi ◽  
Xiaojie Li ◽  
Benny Chang ◽  
Yi Wang ◽  
...  
Keyword(s):  
Gastric Emptying ◽  
Food Intake ◽  
Feeding Behavior ◽  
Gastric Motility ◽  
Late Onset ◽  
Physiological Role ◽  
Immune Defense ◽  
Melanocortin Receptor ◽  
Melanocortin System ◽  
Dorsomedial Nucleus

Glucagon-like peptides (GLP-1/2) are cosecreted from endocrine L cells in the gut and preproglucagonergic neurons in the brain. Peripheral GLP-2 action is essential for maintaining intestinal homeostasis, improving absorption efficiency and blood flow, promoting immune defense, and producing efficacy in treatment of gastrointestinal diseases. However, it is unknown if CNS GLP-2 plays a physiological role in the control of energy homeostasis. Since GLP-1/2 are cotranslated from preproglucagongene and coproduced by prohormone convertase-1, it is challenging to knockout GLP-2 only. Instead, our laboratory has generated a Glp2r-floxed mouse line to dissect cell-specific GLP-2 receptor GLP-2R) action in the regulation of energy balance. Our objective was to determine if GLP-2R in the hypothalamus modulates feeding behavior and gastric emptying. We show that Glp2r mRNA and protein are highly expressed in the arcuate nucleus and dorsomedial nucleus of the mouse hypothalamus. Using the Cre-LoxP system, we generated mice that lack Glp2r expression in POMC neurons (KO; mainly in the hypothalamus). The KO mice showed hyperphagic behavior (such as increases in food intake and meal frequency), accelerated gastric emptying (assessed by [13C]octanoic acid breath test), and late-onset obesity, yet there was no decrease in basal metabolic rate. Infusion of GLP-2 (2.5 nmol into the 4th ventricle) suppressed food intake and gastric emptying, while GLP-2-mediated effects were abolished in the melanocortin receptor-4 (MC4R) KO mice. We conclude that Glp2r deletion in POMC neurons enhances feeding behavior and gastric motility, whereas icv GLP-2R activation suppresses food intake and gastric emptying through the MC4R signaling pathway. This study indicates that CNS GLP-2R plays a physiological role in the control of feeding behavior and gastric emptying and that this is mediated probably through the melanocortin system.

Brain regulation of feeding behavior and food intake in fish

2000 ◽  
Vol 126 (4) ◽  
pp. 415-434 ◽  
Author(s):  
Xinwei Lin ◽  
Hélène Volkoff ◽  
Yuwaraj Narnaware ◽  
Nicholas J Bernier ◽  
Pierre Peyon ◽  
...  
Keyword(s):  
Food Intake ◽  
Feeding Behavior
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