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

Surgical removal of the olfactory bulbs (OB) was performed in mature male red-winged blackbirds, maintained under a short-day light regime. Bulbectomy caused hyperphagia, which was not accompanied by obesity. Bulbectomized (OBX) birds had incresaed thyroid follicular activity and had greater developed testes than sham-operated controls. In the adenohypophyses of the OB-removed birds there was an increase in the populations of 4 types of chromophils: alcianophils, PAS-positive basophils, orangeophils and PAS-positive acidophils. The possibility that the OB are involved in the photoperiodic regulation of the activity of the gonads and thyroids is discussed.
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PMID:The involvement of the olfactory bulbs in the regulation of gonadal and thyroidal activities of male red-winged blackbirds, exposed to short-day light regime. 48 90

Surgical removal of the olfactory bulbs (OB) in the chicken indicated an increase in thyrotropic activity followed by a compensatory increase in food intake, as shown earlier. Basomedial hypothalamic (BMH) lesions in these birds caused changes in certain parameters which strongly infer hypoactivity of the thyrotropic axis. The lesions also caused development of typical hypothalamic obesity demonstrating both dynamic and static phases. Removal of the OB in BMH lesioned birds in their static phase of obesity, caused no demonstrable physiological changes. While removal of the OB caused an increase in somatotropic activity, the opposite was found in BMH lesioned birds. Those animals in which OB were removed and BMH was destroyed, demonstrated a decrease in somatotropic activity. It is suggested that the syndrome caused by BMH lesions dominates that caused by removal of the OB. The possibility of involvement of the OB in the control of thyrotropic and somatotropic activities mediated by the basomedial hypothalamus, is discussed.
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PMID:The interrelationship between the olfactory bulbs and the basomedical hypothalamus in controlling food intake, obesity and endocrine functions in the chicken. 60 42

Neuropeptide Y (NPY) is a potent orexigenic agent capable of producing hyperphagia and obesity. NPY-containing neurons project from the hypothalmic arcuate nucleus to the paraventricular nucleus, an area known to be sensitive to the orexigenic effects of NPY. In this study we investigated the possibility that preproNPY messenger RNA (mRNA) content may be altered in obese Zucker rats compared to that of their lean littermates. Total RNA was isolated from hypothalamic dissections from male and female, obese and lean Zucker rats. RNA was also isolated from dissections of: olfactory bulb, entorhinal cortex, hippocampus, and striatum of female obese and lean rats. PreproNPY mRNA content was determined by solution hybridization-RNase protection analysis. The results revealed a 2- to 3-fold increase in preproNPY mRNA levels in the hypothalamus of obese animals compared to lean. The increase was observed in both sexes and was specific to the hypothalamus. In situ hybridization localized this increase to the arcuate nucleus. An additional RNase protection study was pursued to investigate the effects of 72 h food deprivation on hypothalamic preproNPY mRNA levels in lean and obese animals. Lean animals displayed an approximate 2-fold increase in preproNPY mRNA content, whereas obese animals showed no significant increase after food deprivation. These data are consistent with the hypothesis that NPY projections within the hypothalamus are involved in regulating feeding behavior and weight gain, and that disturbed regulation of hypothalamic NPY expression may play a role in the etiology of obesity in the genetically obese Zucker rat.
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PMID:Increased hypothalamic content of preproneuropeptide Y messenger ribonucleic acid in genetically obese Zucker rats and its regulation by food deprivation. 237 52

Bilateral basomedial hypothalamic (BMH) electrolytic lesions in White Leghorn cockerels produced six main physiological categories characterized by typical sets of symptoms: 1) functional castration (FC); hyperphagia, obesity, occasional diabetes insipidus, involuted adenohypophysis, dwarfism, atrophied comb and testes, reduced hematocrit, reduced plasma testosterone and thyroid activity, involuted thymus and adrenal cortex and elevated liver fat and plasma triglycerides and free fatty acids. The FC birds demonstrated defective immune response for the first 12 to 16 wk post-surgery. 2) functional castration with large comb (FCLC); hyperphagia, obesity, transient diabetes insipidus, slight diminution of adenohypophy-seal weight with marked reduction in basophilic cell population, fully atrophied testes but only slight reduction in comb size and hematocrit, plasma testosterone levels between those found in the first category and the control. 3) obese with normal testes (ONT); hyperphagia, obesity, high level of plasma lipids, normal histological organization of the adenohypophysis, normal testes, semen production and comb size. The next three categories exhibited physiological syndromes identical to the former three categories except for food intake, which operationally could be defined as normal. A marked difference among the BMH-lesioned birds was found in sexual behavior when the FC birds completely lost their libido. None of the replacement therapy regimens caused complete rehabilitation from adiposity or restoration of reproductive traits. Lipoprotein lipase activity increased at an early stage postlesioning and preceeded the development of hyperphagia. Placement of BMH lesions in newly hatched chicks resulted in marked dwarfism and obesity without hyperphagia. The BMH-lesioned heavy breed White Rock cockerels exhibited a lesser degree of adiposity than the light White Leghorn birds. Removal of the olfactory bulbs and destruction of the septal area resulted in increased thyroid activity, with secondary hyperphagia without obesity. In a short-term study, administration of sodium pentobarbital to the BMH area resulted in increased feeding. Conversely, glucose administration to the same area suppressed feeding in satiated but not in food-deprived chickens.
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PMID:Role of the basomedial hypothalamus in regulation of adiposity, food intake, and reproductive traits in the domestic fowl. 267 24

The concentration of immunoreactive insulin (IRI) extracted from the olfactory bulb, hypothalamus, hippocampus, cerebral cortex, amygdala, midbrain, and hindbrain was significantly lower in obese (fa/fa) and heterozygous (Fa/fa) Zucker rats in comparison to lean (Fa/Fa) Zucker rats. This deficit in brain IRI content was most severe in the hypothalamus and olfactory bulb and was independent of severe obesity since the marked reduction of brain IRI content was also found in heterozygous rats which possessed only one copy of the fa allele. These results demonstrate that in the 2-3 month-old female Zucker rat, the fa allele is associated with defective regulation of insulin in the brain.
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PMID:Genetically obese Zucker rats have abnormally low brain insulin content. 388 41

Cholecystokinin (CCK) receptor binding levels were compared between groups of genetically obese (fa/fa) and non-obese (Fa/-) Zucker rats of both sexes. The radioligand used was the iodinated octapeptide (CCK-8). Binding was measured in eight brain regions. The relative distribution among different brain regions of specifically bound CCK per mg protein was similar in all groups of animals. High binding levels were present in the olfactory bulb, cortex and caudate nucleus. Moderate levels were seen in hippocampus and hypothalamus, and low levels were observed in hindbrain, midbrain and thalamus. Obese animals of both sexes had significantly higher CCK receptor binding levels in the hippocampus and in the midbrain in comparison to lean controls. The male obese animals also had significantly elevated binding levels in the thalamic sample. These results demonstrate a correlation between genetic obesity and elevated CCK receptor binding levels in specific brain regions.
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PMID:Cholecystokinin receptor binding levels in the genetically obese rat brain. 632 45

In the laboratory situation the preferences of dogs and cats for food seem to be relatively uniform. Cats prefer fish and commercial cat food to rats. Dogs prefer beef, pork and lamb to chicken, liver and horsemeat and strongly prefer meat to cereal diets. They prefer canned meat to fresh meat, ground meat to cubed meat and cooked meat to raw meat. Canned or semimoist preparations are preferred to dry ones. Pet dogs have much more variable preferences according to their owner's subjective evaluation. A variety of factors seem to be related in an as yet unknown way to some flavor preferences of pet dogs, i.e. the dog's sex/reproductive status, weight and relationship to owners and the content of the dog's meals. The complicated interaction between (a) a pet's taste, texture and olfactory sensation, (b) its owner's perception of the pet and its preferences and (c) its physical and social environment deserves further investigation. Obesity can result from endocrinological causes such as those following ovariohysterectomy, but most cases appear to be related to owner-induced variables. In a kennel situation most, but not all, dogs can be allowed free access to palatable food without becoming obese.
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PMID:Taste preferences and their relation to obesity in dogs and cats. 724 79

Natural BD is a nonpurulent acute/subacute encephalitis of horses and sheep with a propensity to involve the olfactory and limbic systems, and the brain stem. The inflammation is concentrated primarily in the gray matter, but subcortical white matter may also be affected. Experimental BD can be produced in a series of animals from birds to primates. The neuropathology after experimental infection is similar to that in natural disease but the inflammatory changes are more diffuse. In the rat and mouse, a persistent/tolerant infection can also be induced, in which inflammatory changes are conspicuously absent. In the course of persistent infection of the rat, an elective, focal degeneration ensues that involves the dentate gyrus, retina, and, less frequently, the magnocellular part of the hippocampus. The cytopathic destruction of the dentate gyrus is the likely anatomical substrate of learning deficiencies and behavioral changes, prominent features of chronic infection. Later in infection, more diffuse and random degeneration of neurons can be found. In all species infected, viral antigens are produced in excess and fill all neuronal processes. Beside neurons, glial cells are infected as well. The agent spreads in the nervous system axonally and transsynaptically (transneuronally). The type of neurotransmitter receptors in the synapse and their interaction with viral proteins may modulate the spread of infection (Gosztonyi et al. 1994). Virus particles have not been visualized in the brain in any phase of the disease. During persistent infection of the rat, production of viral proteins has a phasic character. Some rats survive acute infection and develop an obesity syndrome. The anatomical basis of this syndrome is not fully clarified; inflammatory destruction of the infundibular region, vacuolar degeneration of the paraventricular nucleus of the hypothalamus and severe, progressive involution of the hippocampal formation most probably play an important role in the production of this neuroendocrine syndrome. In the acute disease, inflammatory reaction can severely aggravate virus-induced cytopathology, but cannot be the sole cause of the neurological disease, since infection with high passage virus can lead to a similarly severe disease in the absence of inflammatory changes.
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PMID:Borna disease--neuropathology and pathogenesis. 778 50

The molecular basis of differences among scrapie strains is unknown. The prion theory posits that there are differences in the conformation of the host protease-resistant protein (PrP) molecules and that these differences are responsible for scrapie strains. A corollary of this theory is that the origin of host PrP variation resides in different neuronal cell types. To assess this concept, preparations from three brain regions (cerebrum, cerebellum and olfactory bulb) and from spleen were passaged in C57BL mice by intracerebral injection. After three passages of three scrapie strains in this manner, homogenates of each brain region and spleen were tested for several of the characteristics that distinguish the three strains: (1) the rank order of incubation periods in C57BL mice, (2) induction of obesity in SJL mice and (3) comparative incubation periods in mice with three genotypes for the scrapie incubation period marker. Analysis revealed that virtually all of the criteria that distinguished the three strains prior to passages of the three brain regions and spleen were retained after this series of passages. This finding argues against cellular-based PrP differences providing a basis for strain specificity.
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PMID:Scrapie strains retain their distinctive characteristics following passages of homogenates from different brain regions and spleen. 901 Mar 15

Contiguous gene syndromes are an interesting clinical phenomenon, resulting from interstitial or terminal deletions of several adjacent genes. The phenotype results in a combination of two or more monogenic disorders and relates clinical findings to corresponding genotypes. We present the case of a male patient with Kallmann syndrome (KS), X-linked ichthyosis (XLI) and X-linked mental retardation (MRX). He was referred at the age of 15.4 years for delayed puberty and obesity. He had a previous history of pyloric stenosis, bilateral orchidopexy and surgical correction of a pes equinovarus adductus. On physical examination, generalised ichthyosis and hypoplastic external genitalia were found. KS was evident with hypogonadotropic hypogonadism, hyposmia and a hypoplastic anlage of the olfactory tract in magnetic resonance imaging. Lipoprotein electrophoresis, and lack of steroid sulfatase and arylsulfatase-C activity in leucocytes confirmed XLI. DNA investigation established an interstitial deletion in Xp22.3 involving the Kallmann (KAL) gene, the steroid sulfatase (STS) gene and a putative mental retardation locus (MRX). The novel MRX locus maps to a 1-Mb region between DXS1060 and GS1.
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PMID:Analysis of an interstitial deletion in a patient with Kallmann syndrome, X-linked ichthyosis and mental retardation. 972 39


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