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Query: UMLS:C0028754 (obesity)
 124,988 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The basic assumption of brain research utilizing lesions is that any observed changes in behavior or physiological responses must be the result of tissue destruction. Reynolds suggested 25 years ago that in the case of electrolytic ventromedial hypothalamic lesions, the observed hyperphagia and obesity were due instead to metallic ion deposits from the electrode tip irritating adjacent tissue. His "irritative hypothesis" was largely ignored after others reported obesity in rats given nonirritative (i.e., no deposits) VMH lesions. However, recent studies have shown that the experimental observations by both Reynolds and his critics were correct and that the early discrepancies were largely due to the sex of the animals used in the experiments. Obesity can be produced with nonirritative VMH lesions, but the weight gain is only about 60% of that observed with irritative VMH lesions and the animals do not display the characteristic lesion-induced elevations in basal insulin levels. A new combination ablation-irritative hypothesis is proposed in which electrolytic VMH lesion obesity is attributed in part to tissue ablation and in part to metallic ion deposits stimulating (rather than disinhibiting) vagally mediated insulin responses.
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PMID:Ventromedial hypothalamic obesity: a reexamination of the irritative hypothesis. 195 3

Neuropeptide Y (NPY), acting through various medial hypothalamic nuclei, is found to have potent effects on a variety of endocrine, physiological and behavioral systems that modulate energy balance. This peptide affects the release of various hormones, such as corticosterone, insulin, aldosterone and vasopressin, which modulate energy metabolism, as well as food intake. It also has direct impact on energy metabolism through an effect on substrate utilization and lipogenesis. Finally, NPY has a remarkably potent stimulatory effect on feeding behavior, which is characterized by a selective increase in carbohydrate ingestion that is strongest at the beginning of the active feeding cycle and is dependent upon circulating levels of corticosterone. This evidence has led to the proposal that NPY exerts anabolic effects to restore energy balance at specific times of energy depletion. Increased NPY activity may occur at the beginning of the active cycle or after a period of food deprivation. Further evidence, that chronic NPY stimulation produces profound hyperphagia and obesity and that endogenous NPY concentration is increased in genetically obese animals, strongly suggests that hypothalamic NPY may contribute to the development of eating disorders and obesity.
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PMID:Brain neuropeptide Y: an integrator of endocrine, metabolic and behavioral processes. 195 27

Diabetes (db) is an autosomal recessive mutation located in the midportion of mouse chromosome 4 that results in profound obesity with hyperphagia, increased metabolic efficiency, and insulin resistance. To clone this gene and generate a molecular map of the region around this mutation, two genetic crosses were established: an intraspecific backcross between C57BL/6J db/db females and C57BL/6J db/db x DBA/2J +/+ F1 (B6D2 db/+ F1) male mice and an interspecific intercross between B6D2 db/+ F1 males and C57BL/6J db/db x Mus spretus F1 (B6spretus db/+ F1) females. The progeny of both crosses were characterized for genotype at the db locus to map a series of restriction fragment length polymorphisms relative to the db locus. Measurements of body weight, body length, and plasma concentrations of glucose and insulin in the animals allowed the assignment of genotype (db/db vs. db/+ or +/+). A total of 132 progeny of the intraspecific cross and 48 db/db progeny of the interspecific cross were typed for individual restriction fragment length polymorphisms to generate a gene order of: centromere-brown (Mt4)-P lambda Mm3(2)-Ifa (Inta)-Cjun-db-D4Rp1-Glut1-Mtv-13-Lck. Several of the genes that are linked to db [Cjun, glucose transporter (Glut1) and Lck] map to human chromosome 1p, suggesting that db may be part of a syntenic group between human 1p and the distal portion of mouse chromosome 4. In addition, phenotyping of the progeny of these crosses revealed a wide range in plasma concentrations of glucose and insulin among the obese progeny, with some animals developing overt diabetes and other remaining euglycemic. Distributions of age-controlled plasma [glucose] and [insulin] among the intraspecific-cross obese progeny were not bimodal, suggesting a role for polygenic differences between the progenitor strains (C57BL/6J and DBA/2J) in the development of overt diabetes.
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PMID:Molecular mapping of the mouse db mutation. 197 28

Genetically obese Zucker rats are hyperphagic, hyperinsulinemic and hyperlipemic. In order to investigate pathophysiological mechanisms underlying hyperphagia in these animals, monoamine metabolism and turnover were studied in discrete hypothalamic nuclei known to participate in the control of feeding behavior. Neurochemical studies in genetically obese Zucker rats and in their lean littermate controls were complemented by investigating feeding behavioral responses to the acute administration of clonidine (15 and 30 micrograms/kg i.p.), an alpha 2-adrenoceptor agonist, and to trifluoromethylphenylpiperazine (TFMPP; 1, 2 and 5 mg/kg s.c.), a putative serotonergic 5-hydroxytryptamine-1B receptor agonist. Obese Zucker rats had significantly lower concentrations of 5-hydroxyindoleacetic acid, the main deaminated metabolite of 5-hydroxytryptamine, in the nucleus paraventricularis (PVN) and in the nucleus ventromedialis (VMN), when compared to their lean littermate controls. The rate of accumulation of 5-hydroxytryptophan after decarboxylase inhibition was reduced in the PVN, nucleus supraopticus, nucleus periventricularis and nucleus suprachiasmaticus of the obese rats. No differences were observed in basal concentrations of norepinephrine, dopamine or 3,4-dihydroxyphenylacetic acid between obese and lean Zucker rats in the brain areas studied. However, the rate of accumulation of 3,4-dihydroxyphenylalanine was lower in the VMN and in the median eminence of the obese rats. The feeding behavioral tests showed significantly augmented hyperphagic responses to clonidine in obese Zucker rats. The anorexic effect of TFMPP was similar in both phenotypes. It is concluded that serotonergic activity is reduced in obese Zucker rats, particularly in the PVN, which plays a key role in the control of feeding behavior. The reduced serotonergic activity may be associated with enhanced alpha 2-adrenoceptor-mediated feeding responses in obese Zucker rats.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Hypothalamic neurochemistry and feeding behavioral responses to clonidine, an alpha-2-agonist, and to trifluoromethylphenylpiperazine, a putative 5-hydroxytryptamine-1B agonist, in genetically obese Zucker rats. 198 Jul 23

In Syrian hamsters, reproduction is sensitive to the availability of metabolic fuels. Estrous cycles can be interrupted by brief periods of food deprivation, by pharmacological inhibition of glycolysis and fatty acid oxidation, or by increasing energy demands for thermoregulation. We predicted that manipulations that divert an excessive portion of the metabolic fuel supply into storage also should inhibit reproduction. Redirection of metabolic fuels from oxidation to storage was accomplished by treatment with protamine zinc insulin suspension (PZI). Syrian hamsters treated with PZI and fed ad libitum increased their food intake by approximately equal to 40% and body fat stores, but there was no effect on estrous cycles. When PZI-treated hamsters were limited to approximately equal to 110% of their preinjection food intake, they still fattened, and there was a significant inhibition of estrous cyclicity. Thus, in the absence of overeating, PZI-enhanced energy storage may lead to a shortage of oxidizable metabolic fuels with the result that reproduction is inhibited in favor of processes essential for survival (e.g., cellular maintenance, thermoregulation). It is unlikely that insulin-induced anestrus is due to actions of PZI unrelated to metabolic fuel partitioning, because the hormone had no effects on estrous cyclicity in ad libitum-fed hamsters. These findings are inconsistent with the hypothesis that nutritional infertility is due to the failure to maintain a minimum body fat content and raise the possibility that the infertility associated with some types of obesity could be due in part to a disorder of macronutrient partitioning.
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PMID:Insulin-induced anestrus in Syrian hamsters. 199 15

Insulin levels in a 7-year-old boy with hyperphagia and obesity following an episode of meningoencephalitis were studied sequentially during the course of progressive weight gain. High fasting insulin levels (1183 pmol/L) and strikingly high insulin release in response to glucose (7892 pmol/L) were found within weeks of the onset of the illness. The abnormality in insulin secretion occurred prior to the marked weight gain. Hyperinsulinemia was not accompanied by hypoglycemia. Early hyperinsulinemia may be a primary event in the development of hyperphagia and obesity following hypothalamic injury.
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PMID:Hypothalamic or central obesity is associated with an early rise in plasma insulin concentration. 201 20

There are dietary factors besides the total energy value of food that can affect adiposity by disrupting the balance between energy intake and expenditure. The purpose of this paper was to examine how perturbation of these dietary factors that control energy balance affects adiposity. There is a substantial amount of evidence suggesting that obesity is not associated with overeating, but with a high dietary fat-to-carbohydrate intake ratio. Physiological adaptations to energy-reduced dieting facilitate both weight regain and make it more difficult to lose weight during subsequent dieting attempts. Since obesity may be better characterized by diet composition than by energy intake, successful weight-loss programs should include diet compositional changes in their regimes.
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PMID:Diet composition, energy intake, and nutritional status in relation to obesity in men and women. 202 Feb 64

Forty obese subjects with normal glucose tolerance test (NGTT) thirteen diabetic obese subjects and sixteen normal subjects were studied to evaluate the possible interactions between beta-endorphin (B-Ep) and glucose homeostasis. On the basis of baseline B-Ep levels, two subgroups were selected: one group with normal mean values of B-Ep (7.02 +/- 0.59 pmol/l); another group with elevated mean values of B-Ep (18.95 +/- 1.52 pmol/l). No differences between these subgroups were found as regards body mass index (BMI), insulin and glucagon levels. Normal B-Ep values were found in diabetic obese subjects. No significant correlation was found between B-Ep and BMI, insulin or glucagon. Considering that B-Ep is involved in eating behavior and on the basis of our results, we suggest that elevated B-Ep levels can be found only in those obese NGTT subjects whose obesity is probably related to an abnormal modulation of food intake, such as hyperphagia.
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PMID:[Plasma levels of beta-endorphin in obese subjects with normal glucose tolerance test and in diabetics]. 202 70

Causes of obesity include a low resting metabolic rate, environmental factors, family behavior patterns, a poorly developed satiety response and reactive eating due to stress or anxiety. Morbid obesity is characterized by an increased number of adipocytes and a degree of irreversibility. Overeating increases the size of adipocytes; however, once adipocytes achieve their maximal size, proliferation is induced and massive, irreversible obesity may result. A syndrome of restrained eating produced by chronic dieting leads to hunger, frustration and rebound overeating. Treatment may be unsuccessful because of the failure to address specific causes of obesity in individual patients and the use of reducing regimens that are not designed to maintain weight loss. Recognition of the diverse clinical forms of obesity and their different etiologies permits treatment regimens to be more specific, increasing the likelihood of success. Even with this approach, treatment failure is common.
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PMID:Obesity: types and treatments. 172 3

The physiologic and behavioral basis of normal canine and feline feeding is given in detail. Abnormalities of ingestive behavior include obesity and anorexia in both species, flank or blanket sucking in Doberman Pinschers, coprophagia and stone chewing in dogs, and wool chewing in cats. Drinking behavior is discussed briefly, and the abnormalities of hypernatremia (a failure of thirst) and psychogenic polydipsia and polyphagia are reviewed.
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PMID:Feeding and drinking behavior problems. 205 51


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