scholarly journals Chemogenetic activation of endogenous arginine vasopressin exerts anorexigenic effects via central nesfatin-1/NucB2 pathway

2021 ◽  
Vol 71 (1) ◽  
Author(s):  
Kenya Sanada ◽  
Mitsuhiro Yoshimura ◽  
Naofumi Ikeda ◽  
Kazuhiko Baba ◽  
Haruki Nishimura ◽  
...  
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Adult Male ◽  
Arginine Vasopressin ◽  
Neutralizing Antibody ◽  
Circadian Rhythmicity ◽  
Transgenic Rat ◽  
Transgenic Rats ◽  
Food And Water Intake ◽  
Fos Expression

AbstractWe examined whether the chemogenetic activation of endogenous arginine vasopressin (AVP) affects central nesfatin-1/NucB2 neurons, using a transgenic rat line that was previously generated. Saline (1 mL/kg) or clozapine-N-oxide (CNO, 1 mg/mL/kg), an agonist for hM3Dq, was subcutaneously administered in adult male AVP-hM3Dq-mCherry transgenic rats (300–370 g). Food and water intake were significantly suppressed after subcutaneous (s.c.) injection of CNO, with aberrant circadian rhythmicity. The percentages of Fos expression in nesfatin-1/NucB2-immunoreactive neurons were significantly increased in the hypothalamus and brainstem at 120 min after s.c. injection of CNO. Suppressed food intake that was induced by chemogenetic activation of endogenous AVP was ablated after intracerebroventricularly administered nesfatin-1/NucB2-neutralizing antibody in comparison with vehicle, without any alteration of water intake nor circadian rhythmicity. These results suggest that chemogenetic activation of endogenous AVP affects, at least in part, central nesfatin-1/NucB2 neurons and may exert anorexigenic effects in the transgenic rats.

Effect of Sham Operations in the Hypothalamus on Food and Water Intake of the Rat

1957 ◽  
Vol 191 (2) ◽  
pp. 255-258 ◽  
Author(s):  
Seoras D. Morrison ◽  
Jean Mayer
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Precise Localization ◽  
Stereotaxic Instrument ◽  
Electrolytic Lesions ◽  
Food And Water Intake ◽  
Electrode Insertion

Exploratory electrode insertions using a stereotaxic instrument, without passing current, have been made bilaterally in and around the area in the hypothalamus of the rat where electrolytic lesions produce complete aphagia and adipsia. These ‘sham operations’ produce pronounced hypophagia and hypodipsia for 1–2 days. Effect on food intake is large and fairly uniform with all insertions peripheral to these nuclei but increases abruptly in the immediate neighborhood of the nuclei. It is suggested that electrode insertion without passing current may be useful as a finer tool than electrolytic lesions for precise localization of the centers involved.

Ontogeny of epinephrine-induced anorexia in rats

1986 ◽  
Vol 250 (2) ◽  
pp. R313-R317
Author(s):  
A. M. Rodriguez-Zendejas ◽  
G. Chambert ◽  
M. C. Lora-Vilchis ◽  
A. N. Epstein ◽  
M. Russek
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Neonatal Rats ◽  
Adult Rats ◽  
Weanling Rats ◽  
Adrenergic Control ◽  
Food And Water Intake ◽  
Old Rats ◽  
Enriched Milk ◽  
Reduced Water

Intraperitoneal or intraportal epinephrine elicits a strong inhibition of food intake in adult rats and dogs but has no effect when injected intramuscularly or intrajugularly, in spite of production of larger hyperglycemia and cardiovascular changes. These facts suggest that the effect of epinephrine on feeding is elicited via the liver. Ontogeny of this adrenergic control of food intake was studied in newborn and weanling rats. Anorexic effect of intraperitoneal epinephrine was clearly observed in dam-deprived 3-day-old neonatal rats (youngest in which it was tested), both when they were offered enriched milk through an anterior oral cannula while they were isolated from their dam and when they were allowed to suckle from her. However, anorectic effect was less in neonatal rats (day 3-13) than in adults. Weanling rats, 21-26 days old, were as sensitive to intraperitoneal epinephrine as adults. In 3- to 4-day-old rats it also reduced water intake, but this effect disappeared by day 12 and was not observed in mildly water-deprived adults. Peripheral adrenergic control of intake appears very early in ontogeny of rats. First, it affects food and water intake equally, but by day 12 it affects only food intake. Increase in sensitivity to epinephrine after weaning is probably due to an increase in number of hepatocytic adrenergic receptors and/or increase in enzymes necessary for hepatic effects of epinephrine.

scholarly journals Effects of essential amino acids on food and water intake of rats

1994 ◽  
Vol 72 (8) ◽  
pp. 841-848 ◽  
Author(s):  
G. Harvey Anderson ◽  
Shuqin Luo ◽  
Leonidas Trigazis ◽  
Greta Kubis ◽  
Edmund T. S. Li
Keyword(s):  
Amino Acids ◽  
Amino Acid ◽  
Food Intake ◽  
Water Intake ◽  
Essential Amino Acids ◽  
Time Period ◽  
Food And Water Intake ◽  
Intake Water ◽  
Comparable Magnitude

This study examined the effects of selected groups of essential amino acids (EAAs), given by gavage, on short-term food and water intake. Amino acid groups were selected on the basis of their common physiologic functions in relation to current hypotheses on the role of amino acids in food intake control, and the quantities given were based on the proportions in 1.5 g of the EAA content of albumin. The complete EAA mixture (1.5 g) suppressed food intake by an average of 60 and 37% during the 1st and 2nd h of feeding, respectively, but had no influence on feeding in the subsequent 12 h. Total daily (14 h) intake was decreased by 9%. With the exception of the aromatic amino acid (Phe + Tyr + Trp, 0.34 g) group, all groups significantly decreased food intake by a comparable magnitude (32%) during the 1st h. In this time period, rats given the EAAs, Arg + Met + Val (0.38 g), and Arg + His + Lys (0.44 g) mixtures increased their water intake, whereas intake by rats given the Phe + Tyr + Trp + Thr (0.46 g) and Ile + Leu + Val (0.45 g) mixtures was unchanged. Thus, the food intake suppression caused by EAAs was not accounted for by an equal effect of its component amino acid groups. As well, food intake suppression by amino acid groups was not explained by increased water consumption, nor was it simply related to the quantity of nitrogen provided by the treatment.Key words: food intake, water intake, essential amino acids.

scholarly journals Brain somatostatin receptor 2 mediates the dipsogenic effect of central somatostatin and cortistatin in rats: role in drinking behavior

2014 ◽  
Vol 307 (7) ◽  
pp. R793-R801 ◽  
Author(s):  
Hiroshi Karasawa ◽  
Seiichi Yakabi ◽  
Lixin Wang ◽  
Andreas Stengel ◽  
Jean Rivier ◽  
...  
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Somatostatin Receptor ◽  
Drinking Behavior ◽  
Male Rats ◽  
Receptor Subtype ◽  
Dark Phase ◽  
Intracerebroventricular Injection ◽  
Water Ingestion ◽  
Food And Water Intake

Intracerebroventricular injection of stable somatostatin (SST) agonists stimulates food and water intake in rats. We investigated the receptor subtype(s) involved in the dipsogenic effect of intracerebroventricular injection of SST agonists, mechanisms of action, and role. In nonfasted and non-water-deprived male rats with chronic intracerebroventricular cannula, intake of water without food or food without water was monitored separately to avoid any interactions compared with intracerebroventricular vehicle. SST-14 and cortistatin (CST-14) (1 μg/rat icv) increased water intake by 3.1- and 2.7-fold, respectively, while both peptides did not alter food intake at 1 h postinjection in the light phase. By contrast, the stable pan-somatostatin agonist ODT8-SST (1 μg/rat icv) increased both water and food intake by 4.9- and 3.7-fold, respectively. S-346-011, a selective receptor 2 (sst2) agonist (1 μg/rat icv) induced water ingestion, while sst1 or sst4 agonist, injected under the same conditions, did not. The sst2 antagonist S-406-028 (1 μg/rat icv) prevented the 1-h water intake induced by intracerebroventricular ODT8-SST and CST-14. Losartan (100 μg/rat icv), an angiotensin receptor 1 (AT1) antagonist, completely blocked the water consumption induced by intracerebroventricular ODT8-SST, whereas intracerebroventricular injection of S-406-028 did not modify the intracerebroventricular ANG II-induced dipsogenic response. The sst2 antagonist reduced by 40% the increase of the 3-h water intake in the early dark phase. These data indicate that SST-14 and CST-14 interact with sst2 to exert a potent dipsogenic effect, which is mediated downstream by angiotensin-AT1 signaling. These data also indicate that sst2 activation by brain SST-14 and/or CST-14 may play an important role in the regulation of drinking behavior.

Relationship of food and water intake in aurothioglucose obesity

1962 ◽  
Vol 203 (4) ◽  
pp. 631-633 ◽  
Author(s):  
Gerald Friedman ◽  
Jerome D. Waye ◽  
Henry D. Janowitz
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Regulatory Mechanisms ◽  
Obese Mice ◽  
Food And Water Intake ◽  
And Control ◽  
Relationship Of ◽  
Extensive Damage ◽  
Daily Patterns

After ld50 doses of aurothioglucose (ATG), extensive damage to hypothalamic structures other than those strictly involved in food intake has been demonstrated. The injury to areas previously shown to be concerned with the regulation of water intake prompted an investigation of the daily patterns of food and water intake in mice from the 2nd day after ATG injection for a period of 6 months. During the 1st month after ATG no statistically significant differences were noted in food or water intake or water-to-food ratios among mice destined to become obese, ATG-nonobese mice, or controls. From the 2nd to 6th month statistically significant increases in food and water intake were demonstrated among obese mice compared to ATG-nonobese and control mice. At no time after the injection of ATG was there a demonstrable difference in water-to-food ratios among the three groups. It is concluded that alteration of water intake regulatory mechanisms is not a concomitant of aurothioglucose obesity.

Feeding behavior in monkeys with and without lesions of the hypothalamus

1976 ◽  
Vol 230 (3) ◽  
pp. 818-830 ◽  
Author(s):  
CL Hamilton ◽  
PJ Ciaccia ◽  
DO Lewis
Keyword(s):  
Body Weight ◽  
Food Intake ◽  
Water Intake ◽  
Arcuate Nucleus ◽  
Serum Insulin ◽  
Hormone Release ◽  
Hypothalamic Lesions ◽  
Feeding Efficiency ◽  
Daily Food ◽  
Food And Water Intake

In monkeys (Macaca mulatta) without hypothalamic lesions, food intake was found to increase with increasing age and body weight; however, food intake per kilogram body weight showed a decline over the same period of time. As the animals became older, the amount of food intake converted to body weight decreased dramatically (feeding efficiency). Water intake was shown to be closely coupled to food intake. Both daily food and water-intake data were highly reliable over a period of years. Monkeys with ventromedial hypothalamic lesions exhibited hyperphagia and increased feeding-efficiency ratios and eventual obesity. The obese animals developed symptoms of diabetes mellitus. Animals with lesions restricted primarily to the arcuate nucleus showed no hyperphagia but increased feeding efficiency. These animals exhibited decreased growth hormone release and a transitory elevation of serum insulin.

Food and water intake following lesions or electrical stimulation of the amygdala

1963 ◽  
Vol 205 (4) ◽  
pp. 761-765 ◽  
Author(s):  
Sebastian P. Grossman ◽  
Lore Grossman
Keyword(s):  
Electrical Stimulation ◽  
Food Intake ◽  
Water Intake ◽  
Water Consumption ◽  
Drinking Behavior ◽  
Food And Water Intake ◽  
Bilateral Lesions ◽  
Reduced Water ◽  
Observation Period ◽  
Stimulation Of

In the first experiment, very small bilateral lesions were placed into the posteroventral amygdala of 12 rats. Food and water intake was recorded for 6 weeks prior to the operation and for 12 weeks following it. Water consumption rose sharply immediately after the operation and remained near the maximal level for 12–16 days. Food intake increased gradually, reaching a maximum after 3–4 weeks. Feeding and drinking returned to near-normal within the 12-week observation period. In the second experiment, electrodes were implanted into anterior, medial, and posterior portions of the ventral amygdala. Electrical stimulation of anterior points inhibited food intake but increased water consumption. Stimulation of the medial placements produced no consistent effect. Both feeding and drinking behavior were inhibited during and immediately following the stimulation of posterior points. Lesions in the anterior area increased food intake but reduced water consumption. Medial lesions reduced water intake but had no reliable effect on feeding behavior. Posterior lesions produced hyperphagia and hyperdipsia. The lesion effects appeared to be permanent.

scholarly journals Activation of endogenous arginine vasopressin neurons inhibit food intake: by using a novel transgenic rat line with DREADDs system

2017 ◽  
Vol 7 (1) ◽  
Author(s):  
Mitsuhiro Yoshimura ◽  
Kazuaki Nishimura ◽  
Haruki Nishimura ◽  
Satomi Sonoda ◽  
Hiromichi Ueno ◽  
...  
Keyword(s):  
Food Intake ◽  
Arginine Vasopressin ◽  
Transgenic Rat ◽  
Inhibit Food Intake ◽  
Vasopressin Neurons

Atropine Depression of Food and Water Intake in the Rat

1958 ◽  
Vol 192 (3) ◽  
pp. 543-545 ◽  
Author(s):  
H. Schmidt ◽  
S. J. Moak ◽  
W. G. Van Meter
Keyword(s):  
Food Intake ◽  
Water Intake ◽  
Atropine Sulfate ◽  
Total Effect ◽  
Albino Rat ◽  
Food And Water Intake ◽  
Reduced Drinking ◽  
Limiting Value

The effect of atropine upon food and water intake was investigated in the albino rat. Dosages up to approximately 7 mg/kg of atropine sulfate were used in two experiments upon water intake and an experiment upon food intake. Atropine depressed both food and water intake to some limiting value. Eating was reduced to a greater extent than was drinking relative to the control conditions. The experimental arrangements obviated the possibility that the depression of water intake, by atropine, is contingent upon reduced food intake, while the procedure used for studying food intake did not exclude the possibility of the observed reduction of eating being dependent upon reduced drinking. However, the relatively greater reduction of eating as compared with drinking suggests that such a dependency will not account for the total effect.

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