[Role of biogenic amines (catecholamines, histamine, serotonin, etc.) in food intake].
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Animals↗
Biomedical subjects
S Tsujii
Publications and source records attributed to S Tsujii.
Food intake of lean and obese Zucker rats following ventricular infusions of adrenergic agonists.
The effect on food intake of adrenergic agonists administered into the third cerebral ventricle was studied in Zucker fatty and lean rats. The alpha 2 agonist, clonidine, produced a larger dose-related increase in food intake in lean rats than in the fatty rats. Dose-response curves show similar sensitivity, but decreased responsiveness in the lean animal. The beta 2 adrenergic agonist, salbutamol, produced similar food effect in obese and lean rats reducing food intake in the lean rats at the highest dose (300 nmol), and in the fatty rats at the two highest doses. The effects were small in both groups. The beta 3 agonist, BRL 37344, ([4-(2-((2-hydroxy-2-(3-chlorophenyl)ethyl)amino)-propyl)-phenoxy acetate]) produced a larger dose-related decrease in food intake in the fatty rat than in the lean rats. Dose-response curves showed that sensitivity of beta-receptors was similar, but the lean animals were less responsive. The beta-adrenergic blocking drug propranolol blocked the anorectic effect of BRL 37344 in the fatty rat. These studies suggest that in the fatty rat, the alpha 2 receptor system is tonically more active and the beta 3 receptor system tonically less active, a relationship that would explain the hyperphagia and development of obesity in these animals.
Adrenergic beta-Agonists↗
Enterostatin suppresses food intake following injection into the third ventricle of rats.
The effect on food intake of an activation peptide from pancreatic pro-colipase, called enterostatin, has been studied after parenteral or third ventricular administration. The activation peptide (enterostatin = Val-Pro-Asp-Pro-Arg = VPDPR) reduced food intake when given intraperitoneally. Low doses of this peptide also reduced food intake when given into the third ventricle, but high doses were ineffective. Enterostatin did not modify the stimulatory effects on food intake of clonidine, an alpha 2-adrenergic agonist, suggesting that its anorectic effects are not mediated via the alpha 2-adrenergic system. These data suggest that enterostatin, an activation peptide from pro-colipase, may play a role in producing satiety.
Analysis of Variance↗
GABA-related feeding control in genetically obese rats.
Feeding in response to glucoprivation induced by 2-deoxy-D-glucose (2-DG) is impaired in genetically obese (Zucker) rats. Muscimol, a GABAA-agonist (0.5 nmol/0.5 microliter in each area) increased food intake in lean rats over 3 h but in fatty rats only at 30 min after infusion into the VMH. Injection of muscimol into the DMH and PVN increased feeding of both phenotypes. Picrotoxin, a non-competitive GABAA-antagonist (0.1 nmol/0.5 microliter) increased food intake after infusion into the LH of both phenotypes and decreased food intake over a 3 h period when infused into the VMH. DMH and PVN of fatty rats. In the lean littermates, picrotoxin was only effective in reducing food intake at 30 min after infusion into the VMH and PVN but not the DMH. The present results suggest that the fatty Zucker rat has a disturbance in the GABA-related regulatory mechanism of feeding behavior in the ventromedial hypothalamus, which may be responsible for the impaired response to glucoprivation found in these rats.
Animals↗
Effects of glucose, 2-deoxyglucose, phlorizin, and insulin on food intake of lean and fatty rats.
Glucose, 2-deoxyglucose, phlorizin, and insulin were injected into the third ventricle of lean and fatty rats, and food intake recorded hourly for the next 6 h. In the lean rats, there was a significant but unimpressive decrease in food intake after the intraventricular injection of glucose, but there was no effect of glucose in the fatty rat. Phlorizin in the lowest dose (10 micrograms) increased the food intake in lean animals at 1 and 2 h, and all three doses increased it significantly at 6 h after intraventricular injection. The fatty rat, in contrast, showed no response to phlorizin. 2-Deoxyglucose showed a dose-related stimulation of food intake in the lean rats at 1, 2, 3, and 6 h after injection. In the fatty rat, there was no significant effect on food intake at any dose. The intraventricular injection of insulin had no effect on food intake in either the lean or fatty rats. These studies indicate that glucose-responding systems in the region of the third ventricle are defective in the fatty rat to signals that normally increase or decrease food intake in lean animals.
Animals↗
Acetylation alters the feeding response to MSH and beta-endorphin.
The effects on food intake of the N-acetylation of MSH and beta-endorphin have been examined following their injection into the third ventricle. Desacetyl-MSH and alpha-MSH were injected into fasted rats, and beta-endorphin and N-acetyl-beta-endorphin into fed rats. Desacetyl-MSH had no effect on food intake following ICV injection into food-deprived rats at any dose between 100 and 2500 pmoles. Alpha-MSH, the N-acetylated form of MSH, on the other hand, showed a highly significant inhibition of food intake in food-deprived rats with doses of 100 and 250 pmoles but no effect with the higher doses. With beta-endorphin, there was a dose-related biphasic effect. One hour after injection of beta-endorphin (2500 pmole) food intake was inhibited whereas the lowest dose, 100 pmole, significantly stimulated it. By 3 hours, the 2 lowest doses of beta-endorphin both significantly stimulated food intake, but the highest dose remained inhibitory. By 6 hours all doses of beta-endorphin stimulated food intake compared to the vehicle-treated animals. In contrast, N-acetylation of beta-endorphin eliminated all effects on food intake following injection into the third ventricle. These data suggest that N-acetylation of products formed by the processing of POMC can markedly alter their biological properties.
Acetylation↗
The effect of DQ-2511, a newly synthesized anti-ulcer drug, on the gastric mucosal hemodynamics and ulceration in rats.
DQ-2511, which is a dopamine derivative, is a newly synthesized anti-ulcer drug. Pretreatment with DW-2511 in the hemorrhagic shock-reperfusion model in rats significantly prevented the decreases of gastric mucosal blood volume, mucosal blood oxygenation index and the ulcer formation. The decrease in gastric mucosal blood oxygenation index in hemorrhagic shock state has a linear correlation with the size of the mucosal ulcers both in DQ-2511 and control groups. The results suggested that DQ-2511 exerts its anti-ulcer activity by improving mucosal hemodynamics in hemorrhagic shock-reperfusion rat model.
Animals↗
Effect of food deprivation on regional brain glucose utilization in lean and fatty Zucker rats.
Regional brain glucose utilization was investigated in lean and fatty Zucker rats when feeding status was changed. Ad-lib-fed fat rats exhibited lower glucose utilization in the central amygdala than ad-lib-fed lean rats. Food deprivation for 72 h enhanced glucose utilization in the ventromedial hypothalamus, lateral hypothalamic area of both phenotypes, hippocampus of fat rats, mammillary body and ventral tegmental area of leans. These results suggest association of the central amygdala with the development of genetic obesity and of the latter 5 areas with hunger-motivated behaviors.
Amygdala↗
Monoamine metabolism and its responses to food deprivation in the brain of Zucker rats.
Monoamines and their metabolites levels were simultaneously measured by high-performance liquid chromatography in brain regions of lean and fatty Zucker rats when fed ad lib and deprived of food for 72 hr to evaluate each monoamine metabolism. Metabolite/monoamine ratios were shown for brevity to represent its metabolism. 3-Methoxy-4-hydroxyphenylethyleneglycol/noradrenaline ratios were not affected by the phenotype factor but increased in the cortex of fatty rats and reduced in the midbrain of both phenotypes after fasting; the interaction between phenotype and feeding factors was observed in the cortex and hippocampus. 3,4-Dihydroxyphenylacetic acid/dopamine ratios were increased in the cortex of deprived fatty rats and in the medulla-pons of ad lib-fed fatties compared with lean counterparts and also increased in the striatum of lean rats after food deprivation; the interaction was observed in the cortex, midbrain and medulla-pons. Homovanillic acid/dopamine ratios were decreased in the striatum of deprived fatty rats and in the midbrain and medulla-pons of fatty rats whether deprived or not, but the ratios were not significantly changed by fasting; the interaction was observed in the striatum. 5-Hydroxyindoleacetic acid/5-hydroxytryptamine ratios were reduced in the cortex, striatum and medulla-pons of fatty rats in both feeding states and in the midbrain of deprived fatties, and after food deprivation increased in the cortex and midbrain of lean rats and in the hippocampus of both phenotypes; the interaction was observed in the midbrain.(ABSTRACT TRUNCATED AT 250 WORDS)
Animals↗
Effects of food deprivation and high fat diet on immunoreactive beta-endorphin levels in brain regions of Zucker rats.
The levels of immunoreactive beta-endorphin (ir-beta-EP) were measured in the brain and pituitary of lean Zucker rats subjected to food deprivation for 72 h and to a high fat diet, and in fatty Zucker rats after food deprivation for 72 h. Ir-beta-EP was increased in the neurointermediate (NI-) pituitary lobe but reduced in the medulla-pons of fatty rats when compared to lean littermates fed ad libitum. Food deprivation decreased ir-beta-EP in the cortex and medulla-pons of lean rats and in the cortex, midbrain and NI-pituitary of fatty rats. In contrast, ir-beta-EP was increased in the anterior pituitary of lean rats and in the striatum of fatty rats after deprivation. The high fat diet produced a decrease in ir-beta-EP in the cortex, midbrain and NI-pituitary with an increase in the striatum and hypothalamus of lean rats. These results suggest that the ir-beta-EP concentration could be differentially affected in different brain regions of Zucker rats by changes in the energy balance.
Animals↗
Effects of food deprivation and high fat diet on opioid receptor binding in rat brain.
The effect of food deprivation for 72 h or a high fat diet on [3H]naloxone binding in the discrete brain regions of male lean Zucker rats was studied. In the midbrain, both treatments increased Bmax for the high-affinity site with no change in Kd. In the cortex, the high fat diet increased Bmax for the high-affinity site. These results suggest that dietary manipulations could produce significant changes in the endogenous opioid system.
Animals↗
Effect of food deprivation on opioid receptor binding in the brain of lean and fatty Zucker rats.
The effect of food deprivation on opioid receptor binding was studied in 6 brain regions of lean and fatty Zucker rats; using [3H]dynorphin A. There was no significant difference between lean and fatty rats fed ad libitum in binding parameters for any regions studied. Food deprivation increased Bmax and/or Kd for cortex, midbrain and striatum of lean rats, and the former two regions of fatty rats. These results suggest that food deprivation may influence opioid receptor binding in lean and fatty Zucker rats.
Animals↗
[Biosynthesis of pituitary hormones. Gene organization and processing--proopiomelanocortin peptides].
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ACTH Syndrome, Ectopic↗
Modulation of luteinizing hormone(LH) release by clonidine and opioid peptides in castrated male rats.
The effect of clonidine, a central alpha-adrenergic agonist, on the suppression of LH release induced by beta-endorphin or FK33-824, an endogenous opioid peptide or its synthetic analog, was investigated in castrated male rats, with or without pretreatment with reserpine. Pulsatile LH secretion was inhibited by intravenous injection of FK33-824 (400 micrograms/kg), or intraventricular injection of beta-endorphin (5 micrograms). Without pretreatment with reserpine, intraperitoneal administration of clonidine (1 mg/kg) failed to reverse the inhibition of LH release induced by these peptides. However, with pretreatment with reserpine (10 mg/kg), clonidine abolished the inhibitory effect on LH secretion induced by these peptides in castrated male rats. These data indicate that, unlike the results in ovariectomized, steroid-primed rats, pretreatment with reserpine allows the alpha-adrenergic system to act more peripherally than the opioid neuronal system in a neuronal network-regulating LH release in castrated male rats.
Animals↗
Serotonin involvement in the inhibition of luteinizing hormone (LH) release during immobilization in castrated male rats.
The involvement of serotonin in mediating the inhibitory effect of immobilization stress on LH secretion in castrated male rats was examined by employing p-chlorophenylalanine (PCPA, 320 mg/kg, ip), an inhibitor of serotonin synthesis, and 5,6-dihydroxytryptamine (5,6-DHT, 50 micrograms, icv), a drug toxic to the indoleaminergic system. Immobilization stress suppressed pulsatile LH release and decreased mean plasma LH levels. Pretreatment with PCPA or 5,6-DHT apparently eliminated the inhibitory effect of immobilization stress on LH release. These results suggest the possible involvement of a serotoninergic mechanism in mediating the suppression of LH release induced by immobilization stress in castrated male rats.
Animals↗
Plasma disappearance of ovine corticotrophin-releasing factor in man.
Disappearance of immunoreactive ovine corticotrophin-releasing factor (IR-oCRF) from plasma after a single intravenous injection of ovine corticotrophin-releasing factor (oCRF) was studied in man in the morning and evening. Synthetic oCRF (80 micrograms) was injected intravenously to four normal male volunteers at 0900 h or at 2200 h. Blood samples were drawn before and 2, 5, 10, 15, 30, 45, 60, 90 and 120 min after the oCRF injection. Plasma IR-oCRF was measured by a specific radioimmunoassay for OCRF. Plasma concentrations of IR-oCRF after oCRF injections in the morning and in the evening did not differ significantly (P greater than 0.05). Disappearance of IR-oCRF was modelled with a two-exponent function by using a non-linear least squares computer program. The metabolic clearance rate, the apparent initial volume of distribution, the plasma half-life for the fast component and that for the slow component calculated from all eight tests in the morning and evening were 1.49 +/- 0.05 ml/min X kg, 44.4 +/- 1.7 ml/kg, 6.8 +/- 0.7 min and 46.2 +/- 2.3 min (mean +/- SEM), respectively. This relatively long half-life may be responsible for the prolonged biological effect of oCRF administered intravenously. There were no significant differences between parameters of IR-oCRF disappearance curves in the morning and those in the evening (P greater than 0.05).
Adult↗
Plasma adrenocorticotropin and cortisol responses to ovine corticotropin-releasing factor in patients with adrenocortical insufficiency due to hypothalamic and pituitary disorders.
Plasma ACTH and cortisol responses to intravenous injection of 100 micrograms synthetic ovine corticotropin-releasing factor (CRF) were studied in 4 patients with hypothalamic hypopituitarism, 2 patients with Sheehan's syndrome, 2 patients with isolated ACTH deficiency and 10 normal subjects. All 4 patients with hypothalamic hypopituitarism had exaggerated plasma ACTH responses to CRF compared to normal subjects and gradual but definite increases in plasma cortisol from low basal levels. Of 2 patients with Sheehan's syndrome, one had slight ACTH and cortisol increases after CRF injection, whereas the other had no increase in either. In 2 patients with isolated ACTH deficiency, plasma ACTH and cortisol remained undetectable (ACTH less than 10 pg/ml, cortisol less than 0.6 microgram/dl) after CRF injection. These results suggest that the CRF test is a useful tool in evaluating patients with secondary adrenocortical deficiency.
Adolescent↗
Evidence for noradrenergic involvement in naloxone-induced stimulation of luteinizing hormone release in prepubertal female rats.
The effects of phenoxybenzamine an alpha-adrenergic blocker, propranolol a beta-adrenergic blocker, and diethyldithiocarbamate a noradrenaline synthesis inhibitor, on the LH increase induced by naloxone an opiate antagonist, was investigated in 25 day old female rats. Pretreatment with phenoxybenzamine or diethyldithiocarbamate suppressed the LH increase induced by naloxone, whereas pretreatment with propranolol had no significant effects on the naloxone-induced LH release. These results suggest that naloxone-induced increase in LH release is mediated via a noradrenergic mechanism.
Animals↗