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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Plasma free fatty acid (FFA) levels were measured in the mallard duck (Anas platyrhynchos) following hypothalamic lesions at various sites. The results indicate that ventromedial lesions produced hyperphagia, increased deposition of fat, and significantly elevated levels of plasma FFA. Anterior bilateral lesions resulted in aphagia, severe loss in body weight and a marked decrease in plasma FFA. Lesions in other regions of the hypothalamus produced various changes depending upon the extent of damage. The neural and neuroendocrine mechanisms which regulate FFA levels in the blood are discussed with respect to the involvement of pituitary hormones.
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PMID:Effects of hypothalamic lesions on levels of plasma free fatty acids in the mallard duck. 5 44

A retractable wire knife was used to transect medial or lateral components of the MFB or its lateral projections to the striatum and amygdaloid complex. All cuts produced significant depletions of NE, DA, and 5-HT from telencephalon and striatum but little or no effect on hypothalamic NE or 5-HT. Two of our cuts resulted in aphagia and adipsia, the third in hyperphagia and obesity. A detailed correlational analysis of the magnitude and direction of the behavioral and biochemical consequences of our cuts indicated that the ingestive behavior of all of our experimental animals (including animals which had been aphagic and adipsic after surgery as well as animals which were hyperphagic and obese) was positively correlated with the concentration of DA in striatum and telencephalon and negatively correlated with telencephalic 5-HT. Less consistent evidence for facilitatory noradrenergic influences on food intake was also obtained. Our results suggest that the regulation of food intake may be the result of an interaction between telencephalic serotonergic mechanisms and dopaminergic pathways which exert opposite effects on ingestive behavior.
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PMID:A correlational analysis of the effects of surgical transections of three components of the MFB on ingestive behavior and hypothalamic, striatal, and telencephalic amine concentrations. 30 Aug 83

Lateral hypothalamic lesions that produce aphagia reduce gastric retention and increase intestinal transit of a 10 ml liquid load in anesthetized rats. Ventromedial hypothalamic lesions which produce hyperphagia and obesity have the opposite effects. These results are apparent within minutes after lesioning as well as after postoperative stabilization of body weight (26--41 days). These data suggest that changes in gastrointestinal motor function(s) may contribute to the changes in food intake which follow hypothalamic damage.
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PMID:Differential effects of lateral and ventromedial hypothalamic lesions on gastrointestinal transit in the rat. 63 Apr 17

After unilateral medial hypothalamic damage, rats become hyperresponsive to touch, odors, and visual stimuli presented on the side contralateral to the damage, while responding to ipsilateral stimuli remains near preoperative levels. These rats would orient their snouts more precisely to stimuli presented on the contralateral side, turn toward touch of more caudal points along that body surface, and pursue moving stimuli more vigorously on that side. Rats with unilateral damage would also viciously bite relatively weak noxious stimuli presented on the contralateral side. After injections of amphetamine, rats turned away from the side of the damage. After bilateral damage, rats showed increased responsiveness to sensory stimuli arising on either side. The rats with unilateral damage began eating more food from a container located in the contralateral sensory field than they had preoperatively. In addition, they began to attack mice more frequently and with shorter latencies when the mouse was on the side contralateral to the lesion. Just as the sensory loss after lateral hypothalamic damage contributes to the aphagia and decreased aggressive behavior of such rats, it seems that increased responsiveness to sensory stimuli plays a role in the syndrome of hyperphagia, finickiness, and increased aggressiveness seen after medial hypothalamic damage.
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PMID:Increased orientation to sensory stimuli following medial hypothalamic damage in rats. 116 4

Experiment and clinical evidence of hypothalamic influence on autonomic function has accumulated since the early part of this century. Localization of hypothalamic lesions is difficult, and damage must be bilateral to produce symptoms. Caloric balance may be altered, with ventromedial lesions causing hyperphagia, and lateral hypothalamic lesions producing a syndrome of aphagia and weight loss in experimental animals. Gastric ulcerations are associated with brainstem lesions, including the diencephalon. Anterior hypothalamic lesions cause hyperthermia, while posterior lesions result in hypothermia, often accompanied by disturbance of sweating mechanisms. Disorders of sleep and wakefulness are seen clinically in encephalitis lethargica and Wernicke's syndrome, both associated with hypothalamic damage. The hypothalamus is the regulator and co-ordinator of central autonomic activity.
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PMID:Vegetative dysfunctions of the hypothalamus. 399 47

Two types of bilateral amygdalar lesions were performed successively. The first operation, involving the dorsomedial part, produced aphagia and subsequent hypophagia, vomiting and apathy. Consequently the body weight was reduced. After a few weeks partial recovery occurred. The second operation, involving the lateral part of the amygdaloid complex, produced hyperphagia, increase of body weight and restoration of general arousal. These results indicate the existence of two antagonistic systems: excitatory in the dorsomedial amygdala and inhibitory in the lateral amygdala. Damage of the inhibitory system reverses almost completely the syndrome produced by an initial lesion of the excitatory system.
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PMID:The normalizing effect of lateral amygdalar lesions upon the dorsomedial amygdalar syndrome in dogs. 451 16

The amygdaloid complex plays an important role in various defensive, sexual and metabolic functions of the organism. Our previous experiments on the defensive functions demonstrated that the amygdala may be divided into dorsomedial excitatory and basolateral inhibitory parts. Our recent experiments showed that this division is true also for alimentary mechanisms. The dorsomedial part of the amygdala acts as a facilitatory "center" and the lateral part as an inhibitory alimentary "center". These functions of the amygdala are parallel to those of the hypothalamic feeding centers. Bilateral damage to either the dorsomedial amygdala or to the lateral hypothalamus produced aphagia with adipsia, decrease of body weight and impairment of both classical and instrumental reactions. These changes were accompanied by low general arousal, atonia, catatonic like positions, negavitism and loss of positive emotional reactions. Damage to the lateral amygdala, on the other hand, produces a syndrome similar to damage to the ventromedial hypothalamus, i.e. hyperphagia and an increase of body weight. Slight increase of both classical and instrumental reactions and disinhibition of responses during intertrial intervals were found in both cases. Combined damage of the dorsomedial amygdala and lateral hypothalamus enhanced the symptoms attributable to each and prolonged the period of aphagia. Damage to the lateral amygdala subsequent to lesions of the dorsomedial amygdala and/or the lateral hypothalamus produced restoration of food intake, instrumental reactions and general arousal.
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PMID:Amygdala functions within the alimentary system. 485 May 5

An unusual case of congenital lower oesophageal diaphragm (web) associated with achalasia is described. An 18-year-old nulliparous girl presented with severe cachexia and aphagia following progressive dysphagia. A barium swallow demonstrated the achalasia, and the oesophageal diaphragm with a central pinhole opening was seen at endoscopy. Parenteral hyperalimentation was required for ten weeks prior to surgery. Circumferential excision of the oesophageal diaphragm in conjunction with Y-V advancement oesophagoplasty gave a good result.
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PMID:Lower oesophageal diaphragm and achalasia in an adult. An unusual association. 652 77

From the pathophysiological viewpoint, feeding responses to various stimuli were examined in Zucker fatty rats and their lean littermates. Intraventricular administration of norepinephrine (NE, 10 micrograms/rat) stimulated food intake in both rats. Intraventricular administration of 2-deoxy-D-glucose (2DG, 3.8 mg/rat) induced hyperphagia and concomitant hyperglycemia in lean rats. However, in fatty rats, the blood glucose was elevated but food intake was unaltered after 2DG administration. Subcutaneous administration of insulin (2 or 8 U/kg) stimulated food intake of both rats. Streptozotocin (STZ)-induced hypoinsulinemia produced transient reduction of food intake followed by sustained diabetic hyperphagia in lean rats. In fatty rats, the experimental hypoinsulinemia caused transient aphagia but not sustained diabetic hyperphagia. Daily injection of insulin (5 U/rat) restored energy assimilation in both diabetic rats. An increase in food intake due to insulin injection was remarkable only in diabetic fatty rats. From these findings, the regulatory system of food intake in fatty rats appears to be sensitive to changes in the circulating insulin level but insensitive to either glucoprivation or changes in body storage of energy.
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PMID:Feeding responses of Zucker fatty rat to 2-deoxy-D-glucose, norepinephrine, and insulin. 700 24

Dopamine (DA)-depleting brain lesions of various sizes were produced in rats either by intracerebroventricular injections of 6-hydroxydopamine (6-HDA) or by electrolytic lesions of the lateral hypothalamic (LH) area. Among 30 animals that became aphagic and adipsic for at least four days after large LH or 6-HDA-induced brain lesions, only three developed hyperphagia after electrolytic lesions of the ventromedial hypothalamus (VMH) or daily injections of long-acting protamine-zinc insulin (PZI). In 20 rats with smaller LH or 6-HDA-induced lesions, which had not shown marked initial behavioral dysfunctions, only three gained as much weight after VMH lesions as the control animals. Similarly, 6 of 10 rats with smaller LH lesions could not tolerate a 15-day series of PZI treatments, although 14 of 17 rats with smaller 6-HDA-induced lesions increased their food intake and gained weight during the PZI treatments as did control animals. These results indicate that hypothalamic hyperphagia can be blocked by DA-depleting brain lesions that neither produce an initial period of aphagia and adipsia nor involve hypothalamic tissue. They further indicate that even small LH lesions may prevent the development of hyperphagia elicited by PZI, whereas only very large 6-HDA-induced lesions consistently have this effect.
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PMID:Effects of dopamine-depleting brain lesions on experimental hyperphagia in rats. 707 39


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