Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of bilateral lesions of the hypothalamic paraventricular nuclei (PVN), of rats with a mean weight of 260 g body, on eating habits and body weight, as well as on sympathetic nervous system (SNS) activity in interscapular brown adipose tissue (IBAT) were investigated. In 59 of 131 Sprague-Dawley female rats, PVN lesions resulted in hyperphagia and obesity. Although lesions were considered successful when more than 50% of the PVN was destroyed histologically, such lesions were observed in 35.9% (47/131) of all lesioned rats and all of these 47 rats were obese. Therefore, in this study, these 47 rats which were confirmed histologically, were designated as "PVN-lesioned rats". Plasma insulin levels in these 47 PVN-lesioned ats were more than double those of the controls. However, no significant differences were observed between plasma glucose levels in PVN-lesioned and control groups. Norepinephrine turnover, a reliable indicator of SNS activity, in IBAT, heart and pancreas was similar in PVN-lesioned and sham-operated control animals, even under contrasting conditions of feeding (ad libitum and fasting) and temperature (22 degrees C and 4 degrees C). It is concluded that PVN lesions produce hyperphagia, obesity and hyperinsulinemia in rats with an average body weight of 260g without affecting the SNS activity in IBAT, heart or pancreas.
 ...
PMID:Lesions of the hypothalamic paraventricular nucleus and norepinephrine turnover in rats. 277 98

Destruction of the ventromedial hypothalamus produces hyperphagia, hyperinsulinemia and hypertriglyceridemia. These changes appear to be partly the result of increased firing rate of the vagus nerve and reduced firing rate of the sympathetic nerves. These reciprocal changes in the function of the autonomic nervous system appear to provide an adequate explanation for the hyperinsulinemia in this syndrome, and for the reduced heat expenditure. Destruction of the lateral hypothalamus, has effects opposite to those of the ventromedial hypothalamus with a reduction in food intake, a decrease in body fat, and an increase in the activity of the sympathetic nervous system. These reciprocal functions of the hypothalamus are associated with different adrenergic receptors. A medial hypothalamic alpha-adrenergic system mediates the epinephrine stimulation of feeding, and a beta-adrenergic system mediates the lateral hypothalamic inhibition of eating. Peptides from the endorphin family can stimulate food intake, but most other peptides are inhibitory. Growth hormone and thyroid hormone stimulate food intake under appropriate conditions. Insulin and adrenal steroids appear to play the most important role of all the hormones in regulating food intake. Deficiency of adrenal glucocorticoids is associated with decreased food intake and a wasting of body flesh. Increased levels of glucocorticoids, on the other hand, produce a variety of truncal obesity. In animals with ventromedial hypothalamic lesions and obesity, adrenalectomy will reverse the obesity. In genetically obese rats and mice, adrenalectomy will attenuate the progression of the syndrome. These effects appear to be through a reduction of food intake, and an increase in energy expenditure. Injections of insulin will stimulate food intake and may lead to obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Autonomic and endocrine factors in the regulation of food intake. 286 66

Young and mature, genetically obese and non-obese, spontaneously hypertensive rats (SHR) were injected with saline (controls) or naloxone for 12 weeks. Naloxone stilled the hyperphagia to a normal intake in the obese SHR (Obese/SHR) so that young Obese/SHR did not develop their usual massive obesity and mature Obese/SHR that had become massively obese were reduced to leanness. The naloxone-treated young, obese and non-obese SHR (controls) exhibited marked reduction of the weight of their pituitary and adrenal glands, whereas the pituitary and adrenal glands of naloxone-treated mature, obese and non-obese/SHR were greatly increased in weight. The elevated systolic blood pressure of the obese and non-obese rats was reduced after chronic treatment with naloxone. Naloxone treatment caused reduction of blood ACTH, corticosterone, and beta endorphin levels but elevated growth hormone levels. The characteristic hyperinsulinemia, hyperlipidemia, hyperglycemia, elevated BUN levels, and the Cushingoid spectrum of degenerative changes found in Obese/SHR did not appear in naloxone-treated rats.
 ...
PMID:Anti-opiate (naloxone) suppression of Cushingoid degenerative changes in obese/SHR. 299 79

Pancreatic polypeptide (PP) may function as a regulator of satiety. Its secretion is impaired in certain animal models of obesity and the administration of PP may improve the hyperphagia and hyperinsulinism seen in these animals. In obese humans, decreased, normal or increased, basal and stimulated concentrations of PP in plasma have been reported. However the advent of diabetes confounds the picture since PP levels in diabetes are generally raised. We have therefore examined the PP responses to intravenous secretin, a known PP secretagogue, in 23 obese subjects, 12 with normal and 11 with abnormal glucose tolerance, and compared the results with those in 23 age and sex-matched healthy controls. The mean maximum PP level in obese subjects with normal glucose tolerance (98 +/- 13 pg/ml) was significantly less than that in normal subjects (218 +/- 23 pg/ml) but in obese subjects with abnormal glucose tolerance, it was significantly greater (578 +/- 115 pg/ml). Within each of the 3 study groups taken separately, PP response to secretin was not correlated with glucose or insulin levels, or with the degree of obesity. Thus, obesity per se appears to be associated with impaired PP responses, which may be masked by abnormalities in glucose tolerance.
 ...
PMID:Pancreatic polypeptide response to secretin in obesity: effects of glucose intolerance. 304 79

Results of a number of studies have suggested that hyperinsulinemia and resultant hypoglycemia are part of a sequence of responses that can lead to hunger and to sugar-induced hyperphagia. However, it is argued in the present paper that neither hyperinsulinemia, hypoglycemia, nor any other factor per se is solely responsible for the hyperphagic effect of sugar or any other feeding effect. Also, the present paper emphasizes the need for caution in attempting to evaluate the role of a given factor in sugar-induced hyperphagia, or any other feeding effect, by eliminating the factor of interest. I have reviewed evidence indicating that the elimination of preabsorptive insulin, which may mediate sugar-induced hyperphagia, actually potentiates other factors that may mediate the same effect.
 ...
PMID:Sugar-induced hyperphagia: is hyperinsulinemia, hypoglycemia, or any other factor a "necessary" condition? 305 64

Lesions of the paraventricular nucleus of the hypothalamus (PVN) produce obesity and hyperphagia. However, the underlying mechanism is unknown. The connections of the PVN with brainstem centers for autonomic control suggest that a change in autonomic function could mediate the PVN obesity syndrome. We examined this hypothesis in a series of 3 experiments, searching specifically for changes in insulin secretion. Rats with PVN lesions were hyperphagic and hyperinsulinemic, when obese. However, hyperinsulinemia could not be detected prior to the onset of obesity or following weight reduction. Subdiaphragmatic vagotomy reversed the PVN obesity and lowered insulin levels below those of sham-vagotomized rats. Since noradrenergic innervation of the hypothalamus is implicated in feeding, hypothalamic norepinephrine (NE) was depleted by injection of 6-hydroxydopamine into the central tegmental tract, posterior to the hypothalamus. The effects of NE depletion was compared with those of PVN lesions. Loss of hypothalamic NE resulted in hyperphagia with no increase in body weight and no change in insulin. Histological analyses indicated that the posterior PVN was the most effective lesion focus for producing disturbances in body weight and food intake. Although the results of these experiments implicate the autonomic nervous system in PVN obesity, basal hyperinsulinemia does not appear to be a primary feature of the syndrome.
 ...
PMID:Effect of paraventricular nucleus lesions on body weight, food intake and insulin levels. 309 59

We investigated the anatomical basis of paraventricular (PVN) and ventromedial (VMH) hypothalamic hyperphagia. Asymmetrical electrolytic lesions, damaging the VMH and PVN contralaterally, produced significant hyperphagia and weight gains (mean = 257.2 g) almost three times those of controls (89.8 g) during 56 postsurgical days. Weight gain in these rats was not significantly different from that in rats with bilateral lesions of the VMH (277.2 g) or PVN (188.2 g). Combined bilateral destruction of the PVN and VMH produced weight gain (272.8 g) almost identical to that seen after bilateral VMH lesions alone. The lack of additivity of these combined lesions and the effectiveness of the asymmetrical lesions are consistent with the hypothesis that lesions of either of these two regions damage a longitudinally running system to produce elevated food intake and body weight. Cell bodies of this system may lie within the PVN and send efferent projections through the VMH. Hyperinsulinemia developed only in rats with bilateral damage in the VMH. Thus, hypothalamic hyperphagia and hyperinsulinemia appear to be dissociable, reflecting damage to separate neural systems.
 ...
PMID:Ventromedial hypothalamic and paraventricular nucleus lesions damage a common system to produce hyperphagia. 329 12

Rats with bilateral electrolytic lesions in the general region of the ventromedial hypothalamic (VMH) nucleus develop hyperinsulinemia, excessive food intake and obesity. Monosodium glutamate (MSG) destroys neurons of the arcuate hypothalamic (AH) nucleus and produces hyperinsulinemic but hypophagic obesity. Bipiperidyl mustard (BPM) primarily destroys VMH neurons, but has produced only a slight obesity even when rats were maintained on high-fat diets. In the present study, rats treated with MSG (AH lesion) were hyperinsulinemic, moderately obese and hypophagic; BPM rats (primarily VMH lesion) were not different from controls when fed standard chow diets. However, MSG/BPM rats (AH + VMH lesion) were hyperinsulinemic, massively obese and hyperphagic. Thus, two components of the electrolytic lesion syndrome previously attributed to VMH damage (hyperinsulinemia and obesity) were reproduced simply by MSG treatment alone. The third component (hyperphagia) occurred only when both AH and VMH were lesioned, suggesting that neurons in both nuclei may perform a satiety function and may be able to substitute for one another in this respect. Since MSG treatment is required for all components of both obesity syndromes described here, this underscores the importance of MSG-sensitive neurons in mechanisms of obesity. The combined treatment approach also represents the first rat model of hyperinsulinemic, hyperphagic obesity that can be entirely produced by systemic administration of neurotoxins.
 ...
PMID:Components of hypothalamic obesity: bipiperidyl-mustard lesions add hyperphagia to monosodium glutamate-induced hyperinsulinemia. 345 67

Feeding 0.001% estrone in a diet to C57BL/KsJ mice homozygous for the recessive obesity gene "diabetes" (db) permitted dissociation of the primary consequences of obesity gene expression from the secondary consequences of diabetes effected through interaction between the db gene and other diabetogenic genes in the inbred background. Estrone-treated db/db mice were similar to untreated mutants in exhibiting hyperphagia and marked obesity. However, estrone-treated mutants did not develop the hyperinsulinemia, hyperglycemia, and islet atrophy characteristic of untreated db/db mice. Thus, expression of the primary defect could be studied in the absence of the myriad secondary sequelae elicited by chronic hyperinsulinemia and hyperglycemia. Reduced numbers of hepatocyte plasma membrane insulin receptors (50% of normal) persisted in the estrone-treated mice in the absence of hyperinsulinemia, indicating that this deficiency was a consequence of the primary genetic defect and not merely a downregulation phenomenon secondary to hyperinsulinemia. Comparison of insulin secretion from comparably sized +/+ islets versus islets from estrone-treated db/db mice showed no intrinsic defects in beta-cell sensitivity to glucose. In conclusion, db-induced obesity can be dissociated from hyperinsulinemia, hyperglycemia, beta-cell dysfunction, and hyperphagia but is associated with a generalized membrane defect reflected in part by the persistent deficiency of plasma membrane insulin receptors.
 ...
PMID:Estrone treatment dissociates primary versus secondary consequences of "diabetes" (db) gene expression in mice. 351 26

Adrenalectomy normalizes many abnormalities of the obese (ob/ob) mouse. The high corticosterone concentration in blood may account in part for development of obesity and other abnormalities in the ob/ob mouse. Our objective was to determine dose-response relationships for the effect of corticosterone on the obesity. Lean and ob/ob mice were adrenalectomized or sham-operated at 4.5 wk of age. Adrenalectomized mice received 100 mg implants of cholesterol containing corticosterone (0, 2, 5, 20, or 50 mg) at 8.5 wk of age and were killed at 10.5 wk of age. In ob/ob mice, but not in lean mice, low physiological levels of serum corticosterone (up to 10 micrograms/dl) markedly increased body weight gain, food intake, and serum insulin. They also increased white and brown adipose tissue weights and decreased brown adipose tissue mitochondrial GDP binding. Higher levels of corticosterone (12-22 micrograms/dl) increased body weight gain, white and brown adipose tissue weights, and serum insulin and suppressed brown adipose tissue mitochondrial GDP binding in lean mice also, although in most cases to a lesser extent than in ob/ob mice, but were still without effect on food intake. Only very high levels of corticosterone (approximately 30 micrograms/dl) increased food intake in lean mice. Hyperglycemia was induced in ob/ob, but not lean, mice only at concentrations of corticosterone greater than 17 micrograms/dl. Thermoregulation was unaffected by serum corticosterone at levels from 0 to 30 micrograms/dl in both ob/ob and lean mice. Thus the ob/ob mouse is excessively sensitive and responsive to an effect of physiological levels of corticosterone that results in hyperphagia, hyperinsulinemia, and increased weight gain.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Increased sensitivity of the genetically obese mouse to corticosterone. 354 20


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>