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

Hepatic-portal infusions of small or large flucose loads in the rabbit had little or no stimulating effect on postinfusion food intake. However, marked differential changes in appetite were observed when small and large glucose loads were infused into the duodenum. The satiating effect of small glucose loads contrasted sharply with an unusually high increase in food intake triggered by the infusions of larger amounts of glucose into the duodenum. The results are interpreted in terms of a possible involvement of the enteroinsular mechanism in the regulation of food intake. This mechanism is bypassed and its influence on food intake eliminated when glucose is infused directly into the portal circulation. The positive relationship between large amounts of alimentary carbohydrates and overeating is seen as a factor that may actively promote the development of obesity and diabetes mellitus.
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PMID:Satiety and hunger induced by small and large duodenal loads of isotonic glucose. 121 47

In form of a survey report the author enters the modern knowledge and opinions concerning the etiopathogenesis of diabetes. Endogenic (hereditary) and exogenic (above all hyperalimentation and malnutrition, deficient muscular conditioning) factors act together. To the functional capacity and functional reserve of the B-cell a central importance is ascribed. The author particularly deals with the possibility of a bihormonal disturbance and with the metabolic syndrome as well as a differentiation into the two most important types of diabetes is performed. As to several problems the results of the Karlsburg team are cited.
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PMID:[Etiopathogenesis of diabetes mellitus today (continuation)]. 122 44

Although characterized as hypothyroid, streptozotocin-diabetic rats have reduced serotonin turnover (5-hydroxyindoleacetic acid/serotonin, 5-HIAA/5-HT) in brain stem, while hypothyroid rats have increased 5-HIAA/5-HT. In the present study the two treatments were combined to determine if they affected 5-HIAA/5-HT through the same mechanism. In addition, an alternative method was used to assess 5-HT activity in thyroidectomized (TX) rats, i.e. measurement of 5-HT disappearance after inhibition of tryptophan hydroxylase with p-chlorophenylalanine (PCPA). Adult male rats were first TX (experiment 1) or given methimazole (METH; experiment 3). Two weeks later, diabetes (DB) was induced with streptozotocin in hypothyroid rats and euthyroid controls. Two weeks later, functional measurements were taken. Rats were then killed, and spinal cord and brain stem serotonin turnover (5-HIAA/5-HT), as well as plasma T3, T4 and corticosterone (CORT) concentrations were measured. TX attenuated diabetic hyperphagia and weight loss. DB alone led to moderate reductions in T3 and T4, but the hormones were barely detectable in plasma of TX and METH rats. CORT was elevated in DB but was not affected by TX. Open field activity was not affected by DB or TX. TX and METH significantly increased 5-HIAA/5-HT in both spinal cord and brain stem. TX also led to enhanced disappearance of 5-HT after PCPA. DB significantly reduced 5-HIAA/5-HT, suggesting independent effects of the treatments. However, DB-TX rats still had significantly higher 5-HIAA/5-HT than control-sham surgery rats, while DB-METH rats had 5-HIAA/5-HT indistinguishable from controls. In both cases, prior induction of primary hypothyroidism interfered with the expected diabetes-induced reduction in 5-HT turnover.
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PMID:Streptozotocin-induced decreases in serotonin turnover are prevented by thyroidectomy. 127 45

The synthesis of the prostaglandins (PG) I2 (measured as 6-oxo-PGF1 alpha), E2, E2 alpha) and thromboxane (TX) A2 (measured as TXB2) by the mucosal and muscular portions of the stomach, duodenum, jejunum, ileum, mesenteric vessels, hepatic portal vein and two arteries (carotid and aorta) was investigated in long term streptozotocin-induced diabetes mellitus (DM; fed ad libitum and pair fed). In all regions of the gastrointestinal tract there were no changes in PG synthesis (per unit weight of tissue) in diabetic rats (pair fed or fed ad libitum) compared to controls. However, there were marked increases in PG synthesis (up to 3 fold) by the mesenteric vasculature and hepatic portal vein in diabetic animals fed ad libitum and in pair fed diabetic rats and decreases in the aorta and carotid artery. These data suggest that increases in PG synthesis by the splanchnic vasculature may constitute a specific adaptive response to DM. The similarity of the responses of pair fed rats to those of rats fed ad libitum indicates that DM and not hyperphagia is the likely determinant of these adaptive changes. Given that increased splanchnic blood flow enhances nutrient uptake (both known to occur in DM), the increase in splanchnic vascular PG synthesis, in particular of vasodilatory PGI2, may contribute to enhanced nutrient uptake.
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PMID:Differential changes of prostanoid synthesis by the gastrointestinal tract, mesenteric vasculature and hepatic portal vein of diabetic rats: comparison between pair and ad libitum feeding. 129 14

Recent developments in laboratory techniques have brought dramatic changes in medical diagnosis, that is, a change from physical diagnosis to laboratory diagnosis. It is imperative that laboratory medicine develop further to meet the continuously growing needs of medical care. Major progress in medical care is classified into two categories, (A) treatment of severe disorders by modern technology and (B) health maintenance to prevent disease and achieve a higher quality of life. In this symposium, category (A) is subdivided in to (A-1) development of new drugs and (A-2) organ transplantation. In (A-1) the field of new drugs, "Recent Trends in Granulocyte Colony Stimulating Factor Therapy and its Relation to Clinical Laboratory Tests" is reviewed as an example of applying recombinant peptides to treatment. In (A-2) transplantation, two papers (A-2a) "Effect of HLA Matching in Renal Transplantation" and (A-2b) "Liver Transplantation and Function of the Graft Liver" are reported. In category (B), health maintenance, (B-1) exercise and (B-2) nutrition are important subjects. (B-1a) "The Role of Clinical Laboratory Examinations During Physical Exercise Therapy for Diabetes Mellitus" and (B-1b) "Exercise Loading Test for Evaluating Cardio-Pulmonary Functions" are given attention. In (B-2) nutrition, artificial feeding, such as intravenous hyperalimentation (IVH) is a current issue. The role of laboratory medicine in modern medical care will be discussed under each of these subjects.
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PMID:[Symposium: the role of laboratory medicine in modern medical care--chairman's remarks]. 130 18

This paper describes four cats with hyperadrenocorticism. Cat 1 showed polydipsia and polyphagia. Diabetes mellitus was initially diagnosed. As the animal appeared to be insulin resistant, pituitary and adrenocortical function tests were performed and the diagnosis of hyperadrenocorticism was made. Resistance to the high-dose dexamethasone suppression test was noticed in this cat. Pathological examination revealed a pituitary chromophobe adenoma. Cat 2 presented with diabetes mellitus, which was treated with insulin. The animal had a pendulous abdomen and its coat was in a poor condition. The low-dose dexamethasone suppression test demonstrated hyperadrenocorticism. Necropsy findings of pituitary tumour and hyperplasia of the adrenal cortex confirmed the diagnosis. Cat 3 showed clinical abnormalities indicative of hyperadrenocorticism, for instance, muscle weakness, alopecia, multiple abscesses. The diagnosis of hyperadrenocorticism was confirmed by the results of the lowe-dose dexamethasone suppression test. Pathological examination revealed an adrenocortical carcinoma. Cat 4 presented with polydipsia. The cause of this symptom was not found initially. One and a half years later additional symptoms, such as nephritis and polyphagia developed. Hyperadrenocorticism was diagnosed because of a palpable mass cranial to the left kidney. The diagnosis was confirmed by the results of the lowe-dose dexamethasone suppression test and the necropsy findings.
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PMID:Hyperadrenocorticism in four cats. 141 43

Contrary to normal rats, diabetic rats are known to develop marked hypercholesterolemia when fed a cholesterol-enriched diet. The triggering factor involved in this hyperresponse has not been identified. With the aim of clarifying the role of the intestinal acyl-CoA:cholesterol acyltransferase (ACAT), we studied the effects of a high fat diet and the changes of intestinal ACAT activity during the early development of streptozotocin-diabetes in rats. Feeding diabetic rats with a diet enriched in cholesterol and saturated fat produced an increase in plasma and in tissue cholesterol as early as 3 days after streptozotocin injection in the absence of hyperphagia. Under these experimental conditions, treatment with insulin or with the ACAT inhibitor CL-277082 significantly reduced the plasma cholesterol to levels measured in nondiabetic rats fed the same high fat diet. An increase in [14C]cholesterol in plasma very low density lipoprotein was observed after oral administration of labeled cholesterol to 3-day diabetic rats. In parallel experiments, the direct measurement of small intestine microsomal ACAT activity revealed an increase, averaging 288% in diabetic rats 3 days after diabetes induction. This change in ACAT activity occurred simultaneously with an increase in plasma glucagon and was normalized by insulin treatment. The induction of intestinal ACAT activity in diabetic rats, its modulation by insulin, and the hypocholesterolemic effects of insulin or CL-277082 treatment clearly indicate that ACAT activity plays a major role in the initiation of diabetes-associated hypercholesterolemia.
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PMID:Role of the intestinal acyl-CoA:cholesterol acyltransferase activity in the hyperresponse of diabetic rats to dietary cholesterol. 143 72

Untreated insulin-deficient diabetes causes hyperphagia and neuroendocrine disturbances that may be partly mediated by increased hypothalamic activity of neuropeptide Y (NPY), a potent central appetite stimulant. The metabolic signal that stimulates hypothalamic NPY is unknown. This study aimed to determine whether insulin deficiency or hyperglycemia was responsible. Regional hypothalamic NPY concentrations were compared in streptozocin-diabetic (STZ-D) rats rendered nearly normoglycemic by either insulin replacement or food restriction. Untreated STZ-D rats were hyperphagic and showed significantly increased (p less than 0.01) hypothalamic NPY concentrations in the arcuate nucleus and lateral hypothalamic area. Once-daily ultralente insulin injections corrected hypoinsulinemia and hyperglycemia, abolished hyperphagia, and normalized NPY concentrations in all hypothalamic regions. By contrast, food restriction effectively lowered glycemia without raising insulin levels. In these underfed diabetic rats, NPY concentrations rose further and were significantly higher than nondiabetic and untreated diabetic levels in most hypothalamic regions. We conclude that insulin deficiency is a major stimulus to hypothalamic NPY in STZ-D, whereas hyperglycemia may exert an inhibitory influence. These findings support the hypothesis that hypothalamic NPY responds to specific metabolic cues and is involved in regulating energy balance and conserving body weight.
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PMID:Insulin deficiency is a specific stimulus to hypothalamic neuropeptide Y: a comparison of the effects of insulin replacement and food restriction in streptozocin-diabetic rats. 143 14

The hypothalamus, in addition to regulating the anterior and posterior pituitary, controls water balance through thirst, regulates food ingestion and body temperature, influences consciousness, sleep, emotion and other behaviors. Much has been learned of these effects in human disease through the clinical manifestations that occur with hypothalamic lesions. This study reviews the clinical pathologic correlations that have been made in recent years showing that regions of the hypothalamus exert functions in humans that are similar to those identified in experimental animals. Clinical pathologic correlations have not always provided precise analysis of hypothalamic function. The hypothalamus is small and often lesions that come to clinical attention achieve considerable size before their recognition, making local anatomic dissections of the effects of the lesions difficult. Nevertheless, the use of modern non-invasive techniques including CT scans and magnetic resonance imaging (MRI) have provided new information not previously available. This paper reviews several cases of hypothalamic disorder recognized recently. (1) A 33-year-old black man with hypothalamic sarcoidosis. Manifestations of hypothalamic dysfunction included panhypopituitarism, aggressive hyperphagia, polydipsia (partially due to hyperglycemia secondary to diabetes mellitus), drowsiness, depression, and irritability. (2) A 37-year-old woman with a large intrahypothalamic tumor (biopsy showed pituitary adenoma), with drowsiness, poikilothermia, lack of satiety, confusion, and memory loss. She becomes depressed when she is transiently more alert (as after hypertonic contrast-dye infusion). (3) A 60-year-old man with hypothalamic compression by a pituitary tumor, associated with syndrome of inappropriate ADH (SIADH), severe anorexia, memory loss, but preserved thirst. After surgical decompression of the tumor his appetite acutely recovered, but he developed severe hypo(poikilo)thermia. (4) A 45-year-old woman with a suprasellar craniopharyngioma presented with severe drowsiness, hyperphagia, depression, and memory loss post-operatively, which responded to antidepressants (except for the memory loss). She had extremely labile blood pressures and serum Na for about 1 week post-operatively.
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PMID:Neurologic manifestations of hypothalamic disease. 148 Jul 55

Obesity occurs in both clinical and animal forms in a variety of specific models which allow study of its underlining endocrine and mechanistic features. Among the neuroendocrine varieties of obesity, polycystic ovaries are probably the most common. The importance of the gonadal feedback system for regulation of food intake and obesity is indicated by the effects of castration in experimental animals which is a widely used mechanism for producing experimental obesity. Cushing syndrome and hypothalamic obesity are rare clinical syndromes. The current evidence suggests that there are two types of hypothalamic obesity from a mechanistic point of view--one associated with hyperphagia as a necessary and sufficient cause and a disturbance of the autonomic nervous system without hyperphagia as a second mechanism. Although genetic factors underlie most types of human obesity, there are several dymorphic forms of obesity including the Prader-Willy syndrome, Cohen's syndrome, Carpenter's syndrome, Ahlstrom's syndrome and the Bardet-Biedel syndrome. The Prader-Willi syndrome is characterized by obesity hypotonia hypogonadism and mental retardation. In animals, a dominant form of inheritance of obesity is seen in the yellow mouse. Current evidence suggests that this syndrome can be explained by reduced acetylation of MSH in the pituitary and/or hypothalamus. Several recessively inherited forms of obesity exist including the obese mouse, the diabetes mouse, fatty rat, the fat mouse, tubby mouse and the corpulent rat. In addition, there are a number of polygenic types of experimental obesity. The final mechanistic classification of obesity are those due to dietary manipulation. For both human beings and animals, a highly fat diet appears to be particularly problematic for the development of obesity.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Genetic, hypothalamic and endocrine features of clinical and experimental obesity. 148 Jul 57


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