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

In over 1000 cancer patients treated with intravenous hyperalimentation (IVH), tumor growth has not been identified and catheter-related sepsis has been minimal. Studies in rats demonstrated that the host benefits more than the tumor during nutritional repletion, and any stimulation of tumor growth in the rat-tumor model could be manipulated with DNA specific drugs to benefit the host. A study of 65 malnourished cancer patients undergoing oncologic therapy and treated with IVH indicated that much of the immune suppression in these patients was the result of malnutrition coincident with or secondary to oncologic treatment. Conclusions reached in this study were that nutritional repletion resulted in a return of skin test reactivity, proper wound healing in the surgical patient, and possibly an increase in response to chemotherapy. Certainly, the use of IVH allowed specific oncologic therapy to be administered to a group of malnourished patients who otherwise might not have been acceptable candidates for intensive antineoplastic therapy.
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PMID:Nutrition, cancer, and intravenous hyperalimentation. 10 87

Streptozotocin-induced diabetes in the rat alters intestinal function, causes hyperphagia and arrests body growth, but stimulates intestinal growth, particularly in the mucosa. Therefore we measured several indices of epithelial cell proliferation to gain insight on possible factors responsible for the increased mucosal cell mass in the small intestine. We examined epithelial cell proliferation in upper jejunum and terminal ileum of weight-matched control and diabetic rats pair fed or eating ad libitum. Cell proliferation was measured two ways: (1) isolating whole crypts 1 hr after injection of [3H]thymidine ([3H]TdR) and calculating disintegrations per minute per crypt (dpm per crypt), and (2) autoradiography of mucosal sections to obtain labeled cells per crypt, total cells per crypt-villus column, and cell migration rates. Autoradiography showed diabetes: (1) increased cell number of crypt-villus columns and increased labeled cells per crypt section, primarily jejunum, and (2) did not alter cell migration except for an increase in the ileum of diabetics eating ad libitum. Cell proliferation measured as dpm per crypt virtually doubled in diabetics in both segments regarless of dietary regimen. Dpm per crypt is a three-dimensional measurement based on the whole crypt. The increase in cell number and labeled cells per crypt in jejunal sections is also consistent with increased cell division, but shows a much smaller effect. The nature of the histological technique (two-dimensional) limits its usefulness for measuring morphological changes, and this may explain the discrepancy. Hence, the primary effect of diabetes is increased DNA synthesis (dpm per crypt) and this appears to be the main explanation for stimulated mucosal growth.
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PMID:Proliferation rate and transit time of mucosal cells in small intestine of the diabetic rat. 91 75

Mammalian response to injury essentially is that of tissue repair and re-epithelialization. The most important component of repair tissue is collagen, and after injury collagen turnover is greatly increased. Collagen biosynthesis is initiated by nuclear DNA of fibroblasts; the steps in biosynthesis are complex but studies of collagen biosynthesis may eventually have clinical potential. Normally, wound healing lasts for up to 2 years but nutritional and metabolic factors, such as malnutrition, delay healing; hyperalimentation would likely be beneficial under these conditions. Other factors that influence wound healing are the oxygen tension in tissues, the hemodynamic status, and the effects of substances such as cortisone, vitamins A and C, and zinc.
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PMID:Some aspects of wound healing research: a review. 109 Mar 54

Although environmental factors are important triggers of non-insulin-dependent diabetes mellitus (NIDDM), heredity plays a major role in the pathogenesis of the disease. Insulin resistance manifested as impaired activation of glycogen synthase and thereby storage of glucose as glycogen in skeletal muscle is demonstrable early on in NIDDM relatives, suggesting that NIDDM could be an inherited muscle disease. On the other hand, insulin deficiency is almost unequivocally present before manifest diabetes develops. An intensive search for candidate genes for NIDDM has been initiated; so far it has not been possible to ascribe NIDDM to any alterations in the human genome. Given the heterogenous nature of NIDDM, its age-dependent penetrance and strong influence of environmental factors, it may not be fruitful to use NIDDM as an end-point in genetic linkage or association studies. It is more likely that DNA defects result in either insulin resistance or insulin deficiency, which in turn, can both lead to NIDDM. In accordance with the thrifty gene hypothesis, the insulin resistance gene has protected individuals during long periods of starving by storing energy as fat rather than as glycogen in muscle. The abundance of food in Western society has made this once protective gene a deleterious one, suggesting that these individuals are not equipped with the metabolic machinery to handle overeating.
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PMID:The etiology and pathogenesis of non-insulin-dependent diabetes. 148 43

Weight gain in ovariectomized Syrian hamsters occurs without increased food intake, which suggests that metabolic efficiency may be enhanced through a reduction in energy expenditure. We examined the effect of ovariectomy on metabolic activity in brown adipose tissue and liver. Four groups of hamsters (n = 13, each) were killed 0, 2, 4, or 16 weeks following ovariectomy. Ovariectomized hamsters rapidly gained weight without overeating. Body weights stabilized after 8 weeks and remained 12-17% above sham-operated control weights for the duration of the experiment. Weight gain in the hamsters ovariectomized for 16 weeks was characterized by significant increases in retroperitoneal white adipose tissue weight and carcass lipid content. Similar trends were seen in 2-week and 4-week ovariectomized animals. There were no differences in interscapular brown adipose tissue weight, protein content, DNA content, or norepinephrine (NE) content among sham-operated and 2-, 4-, or 16-week ovariectomized hamsters, indicating that ovariectomy had no effect on brown adipose tissue growth. Similarly, there was no difference in either sympathetic nervous system activity (estimated by the rate of NE turnover) or mitochondrial GDP binding among the four groups of hamsters. In contrast, hepatic cytochrome P-450 activity was significantly reduced 2, 4, and 16 weeks after ovariectomy. These results suggest that reduced thermogenic activity in liver, but not in brown adipose tissue, could contribute to the weight gain in Syrian hamsters after ovariectomy.
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PMID:Effects of ovariectomy on thermogenesis in brown adipose tissue and liver in Syrian hamsters. 194 29

Quantitative cytophotometry and ocular filar micrometry were used to monitor T-2 toxin induced alterations in chromatin and neuronal nuclear volume in supraoptic-magnocellular neurons of rat hypo-thalami. Thirty male Sprague-Dawley rats (200-220g) were given a single i.p. injection of T-2 toxin (0.5, 0.75, 1.0 and 1.5 X LD50), a trichothecene mycotoxin; rats were decapitated 8 hours post-dosing. After stoichiometric Feulgen-DNA staining of brain sections, scanning-integrating microdensitometry was used to quantify changes in the susceptibility of chromatin to Feulgen acid hydrolysis. Changes in neuronal nuclear volumes were also determined histometrically. Within the magnocellular neurons of the supraoptic nuclei, significant reductions in F-DNA reactivity were observed in the 0.5, 0.75, and 1.0 X LD50 groups (i.e. 3.7%, 4.4% and 2.5%, respectively); however, rats receiving 1.5 X LD50 T-2 toxin showed no difference in F-DNA reactivity compared to controls. In addition, ocular filar micrometry demonstrated increased neuronal nuclear volumes in all groups receiving T-2 toxin, and following an inverse trend to that seen with F-DNA stainability. Additional observations included pronounced polydipsia, polyphagia and horripilation in the experimental groups, independent of the dosages employed; these changes were evident within 1 hour post-injection. It is postulated that the T-2 toxin induced reduction in the susceptibility of chromatin to Feulgen acid hydrolysis and concomitant increases in neuronal nuclear volumes represent an early indication of impaired metabolic activity. Since these neurons are important sites of vasopressin (antidiuretic hormone) synthesis, these data suggest an impaired osmoregulatory ability. The pronounced polydipsia which occurred shortly after intoxication is further evidence of this impairment. Although these findings do not provide insight relating to the mechanism of osmoregulatory disruption, it is evident that an impaired ability to osmoregulate is among the earliest indications of acute T-2 toxin mycotoxicosis.
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PMID:Cytophotometric analysis of T-2 toxin induced alterations in chromatin condensation and neuronal nuclear volume of rat supraoptic-magnocellular neurons. 247 68

1. The effects of starvation post partum (24 h) and tumour growth pre partum on the initiation of lactation in the rat were studied. 2. Tumour growth decreased food intake at 24 h, but not at 2 days post partum. 3. Pup growth rate increased with hyperphagia; starvation and tumour burden decreased pup growth, and starvation decreased maternal body weight. 4. Starvation decreased gastrointestinal-tract mass; tumour growth decreased gastrointestinal-tract and mammary-gland mass. 5. Mammary-gland DNA-synthesis rate was high immediately post partum, but decreased by day 3 of lactation; starvation and tumour burden decreased this rate, and also decreased gastrointestinal-tract DNA-synthesis rate. 6. Arteriovenous differences for glucose and lactate across the mammary gland did not change with time, nor were they affected by the tumour. Starvation decreased arterial glucose and lactate, and the gland extracted less glucose but produced lactate. 7. Mammary-gland lipogenesis was sensitive to starvation and to tumour growth. 8. In contrast with the gradual development of mammary-gland lipogenic enzyme activities, lipoprotein lipase activity was high in the gland by 2 days post partum; starvation or tumour burden decreased the activity. 9. The mammary gland is sensitive post partum to decreased food intake, and to tumour presence. The effects of the latter are apparently independent of hypophagia.
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PMID:Lipid metabolism during the initiation of lactation in the rat. The effects of starvation and tumour growth. 259 Jan 73

Syrian hamsters (Mesocricetus auratus) were fed a high-fat (HF) diet for up to 16 wk. Sympathetic and thermogenic activities in their brown adipose tissue (BAT) were assessed by measuring norepinephrine content and turnover and mitochondrial GDP binding and cytochrome c oxidase activity. Chronic ingestion of the HF diet resulted in significant increases in carcass lipid and interscapular BAT wet weight by the end of the second week. HF-fed hamsters were slightly hyperphagic during the first 2 wk of HF feeding only. Significant weight gains persisted beyond the period of hyperphagia. Hypertrophy of interscapular BAT after 16 wk on the HF diet was accompanied by increases in protein and DNA content, indicating growth of functional tissue. Norepinephrine turnover and content in BAT were decreased throughout the entire period of HF feeding, regardless of changes in caloric intake or body weight. Mitochondrial cytochrome c oxidase activity and GDP binding were increased after 16 wk on the HF diet, a time when the HF-fed animals were obese but not hyperphagic. These results demonstrate a dissociation of BAT thermogenesis from sympathetic activity in the tissue. It appears that sympathetic nervous system activity in BAT was suppressed by the HF diet, whereas thermogenic activity of the tissue was activated when the hamsters became obese.
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PMID:Dissociation of sympathetic and thermogenic activity in brown fat of Syrian hamsters. 300 19

Two experiments were performed to determine if bilateral parasagittal hypothalamic knife-cuts (KCs), which produce long-term overeating and obesity, after biochemical indices of brown adipose tissue (BAT) reactivity to thermogenic stimuli. In the first study, responses to environmental cold were tested. Four weeks after surgery, KC rats had gained 4-5 times more weight than controls and were obese (increased Lee Obesity Index and weight of gonadal white fat). Before being sacrificed, groups of KC and control rats were exposed to 4 degrees C for 21 hr or remained at 28 degrees C. Interscapular BAT weighed 300% more in KC rats, due largely to increased white fat content. Functional indices of BAT thermogenic capacity (protein content, DNA content, cytochrome oxidase activity and mitochondrial guanosine diphosphate (GDP) binding) were normal at 28 degrees C. Exposure to 4 degrees C produced greatly enhanced responses but these were equivalent for both groups. This suggested an intact capacity for non-shivering thermogenesis in obese KC rats. In the second study, the same BAT responses were examined in other rats fed a palatable "cafeteria" diet (CAFE). One week after surgery, KC and control rats were subdivided into groups that received chow alone or chow plus four different palatable foods daily. Before sacrificing 4-5 weeks later, KC rats had gained 3-4 times more weight than controls and were obese. Interscapular BAT weighed 200-300% more in KC rats. CAFE feeding produced larger increments in all variables for KC vs. control rats. Most importantly, GDP binding was reduced in both KC groups, and significantly more so after CAFE feeding.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Impaired diet-induced thermogenesis in brown adipose tissue from rats made obese with parasagittal hypothalamic knife-cuts. 402 98

The effect of feeding an alpha-amylase inhibitor (BAY e 4609, 700 mg/100 g food) for 20 or 90 days on the enzymes of the exocrine pancreas of the rat was investigated. The amylase inhibitor-fed rats gained significantly less weight despite a higher food intake than control rats on a standard diet. Fecal weight increased threefold. Pancreatic wet weight, pancreatic DNA, protein and insulin concentrations were not influenced. The amylase content of the pancreas was significantly diminished compared with controls. The trypsin level increased and the changes in the amount of lipase were not significant. Also in response to an infusion of 15 or 60 IU CCK/kg/h combined with 0.5 clinical units of secretin/kg/h amylase secretion was significantly diminished after both feeding periods compared with controls, while trypsin output increased as did the output of lipase to a lesser extent. The enzyme pattern of the pancreatic juice reverted to normal when the animals consumed the control diet again. Gut weight and length increased significantly in the experimental animals. It is concluded that the changes in the pancreatic enzymes are induced by altered food intake. The amylase inhibitor prevents the digestion of starch and by this carbohydrate absorption. As a consequence, hyperphagia develops resulting in an increased protein and fat intake. Unlike trypsin a negative feedback regulation does not exist between alpha-amylase concentration in the gut and pancreatic enzyme secretion.
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PMID:Influence of short- and long-term feeding of an alpha-amylase inhibitor (BAY e 4609) on the exocrine pancreas of the rat. 616 90


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