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

Thirteen cats with diabetes mellitus were evaluated. Clinical signs included polydipsia, polyuria, polyphagia, lethargy, and weight loss. Results of physical examination included obesity, hepatomegaly, mild seborrhea sicca, muscle wasting, and dehydration. One cat walked plantigrade and was suspected of having a diabetic neuropathy. Persistent hyperglycemia, glucosuria, high liver enzyme activities, hypercholesterolemia, hyperproteinemia, and low electrolyte concentrations were the common laboratory findings. In 3 cats diabetes mellitus developed after megestrol acetate therapy; 2 of these cats required only temporary insulin treatment. In a 3rd cat, which had no history of receiving diabetogenic drug therapy, remission of diabetes mellitus also was observed. Serum insulin and plasma glucose concentrations were determined in 6 cats after administration of an intermediate-acting insulin (isophane insulin) and in 3 cats after administration of a long-acting insulin (protamine zinc insulin). The insulin concentration peaked 2 to 6 hours after the injection of intermediate-acting insulin and 6 to 12 hours after the injection of long-acting insulin. The lowest glucose concentration was recorded 4 to 8 hours after injection of intermediate-acting insulin, and 6 to 12 hours after injection of long-acting insulin. It was concluded that, although insulin therapy must be adjusted to the individual, the diabetic cat usually requires twice-daily administration of isophane insulin; however, the protamine zinc insulin can be given once daily for satisfactory control.
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PMID:Insulin therapy in cats with diabetes mellitus. 629 64

The immediate onset of hypermetabolism after a major burn dictates that nitrogen and calories be supplied as early as possible to such patients to prevent the well-documented catabolic state. However, intravenous hyperalimentation is not always possible, and enteral feeding is not usually attempted in the early resuscitative period. Twelve patients with major burns (40% to 70%) were fed nasoduodenally in the early postburn period with a new solution (3.5% Aminosyn, 25% Polycose, and appropriate additions of electrolytes and vitamins). All patients reached positive nitrogen balance in 9.8 +/- 2.3 days, tolerated the feeding extremely well, and had no distention or diarrhea. Metabolic assessment showed remarkable stability. The characteristic signs of hypermetabolism, such as hyperglycemia and hypoinsulinemia or hyperinsulinemia, were absent. Furthermore, there was no persistent neutrophilia or leukocytosis and there was a significant (p less than .01) decrease in the percentage of juvenile neutrophils and a significant (p less than 0.001) increase in absolute lymphocytes between days 0 and 14 of the study. These data indicate that early enteral feeding of Polycose-Aminosyn is safe and well tolerated, and that the small intestine absorbs nutrients readily in the early postburn period, leading to positive nitrogen balance, preventing loss of serum protein, assisting in the maintenance of normal carbohydrate metabolism, and restoring granulocytes and lymphocytes to normal ratios.
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PMID:Early enteral feeding of patients with major burns: prevention of catabolism. 644 Apr 66

Goodson and Hunt showed that wound healing is impaired in streptozotocin (Sz) diabetic rats; we speculated that this impairment results from defective early inflammatory responses to wounding. Because we had shown that supplemental vitamin A stimulates the early inflammatory response to wounding in nondiabetic rats, we studied the effect of supplemental vitamin A on wound healing in rats with Sz-induced diabetes. Male Sprague-Dawley rats were fed a commercial rat chow containing twice the amount of vitamin A recommended by the NRC for healthy rats. The rats ate and drank (tap water) ad libitum. Two-thirds of the rats were injected (intravenously) with Sz 60 mg/kg body weight. All of these rats became diabetic (hyperglycemia greater than 350 mg/dl, hyperphagic, polydipsic, polyuric, glycosuric greater than 2%). Seven days later, half of the Sz-injected rats were continued on the chow (Group 2) while the other half (Group 3) were switched to the chow supplemented with 150,000 units of vitamin A/kg chow. The next day, all were wounded (7 cm skin incisions and s.c. polyvinyl alcohol sponge implants). Similarly wounded saline injected nondiabetic rats ingesting the unsupplemented chow served as controls (Group 1). The wounds of Group 2 rats healed poorly compared to Group 1 (breaking strength of skin incisions, 308 +/- 19 g vs 584 +/- 23 g, p less than 0.001; hydroxyproline of the sponge reparative tissue, 0.87 mg vs 2.40 mg/100 mg sponge p less than 0.001). Supplemental vitamin A (Group 3) did not affect the hyperglycemia, hyperphagia, polydipsia or glycosuria, but increased the breaking strengths of the incisions of the diabetic rats (468 +/- 40 g, p less than 0.001), and the sponge hydroxyproline (2.38 mg/100 mg sponge, p less than 0.001). In another experiment, in which the wounding and start of supplemental vitamin A were delayed until 28 days after streptozotocin administration (50 mg/kg body weight), similar results were obtained. Streptozotocin diabetes also caused a decrease in the cross-linking of reparative collagen as judged by the ratio of breaking strengths of skin incisions before and after formalin fixation. Supplemental vitamin A did not influence this defect. Sz also caused peripheral lymphocytopenia, adrenal hypertrophy and thymic involution which responded to the supplemental vitamin A. Based upon experimental data and theoretical considerations we conclude Sz diabetes causes two defects in wound healing: a) quantitatively (reduction in reparative collagen accumulation) and b) qualitative reduction in the degree of cross-linking of reparative wound collagen. The action of supplemental vitamin A in correcting the impaired wound healing, adrenal enlargement, thymic involution and lymphocytopenia of Sz-diabetic rats is independent of an effect on their disturbed carbohydrate metabolism.
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PMID:Impaired wound healing in streptozotocin diabetes. Prevention by supplemental vitamin A. 645 99

5-Thio-D-glucose (200 and 500 mg/kg) produced hyperglycemia and significantly retarded emptying of the pregastric pouch of hamsters. 2-Deoxy-D-glucose did not affect stomach-emptying at either of the doses used (500 and 1000 mg/kg), but did cause hyperglycemia at the higher dose. These results are discussed in relation to the failure of these glucose analogs to produce hyperphagia in the golden hamster.
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PMID:Effects of 5-thio-D-glucose and 2-deoxy-D-glucose upon stomach-emptying in the golden hamster. 654 8

The genetically diabetic mouse (db/db) exhibits hyperphagia, progressive weight gain, hyperglycemia, and hyperinsulinemia during the first few months of life during which time characteristic pathologic changes occur in several organ systems including the kidney. The extent to which long chain fatty acid oxidation (LCFAO) contributes to excessive gluconeogenesis and hyperglycemia in these animals in unknown. Therefore, the synthetic fatty acid analogue 2-tetradeclyglycidate (TDHA), a potent inhibitor of LCFAO, was given orally to db/db mice to evaluate its capacity to control the blood glucose and prevent their diabetic nephropathy. Five groups of diabetic mice (N = 6) were assigned to receive TDGA in a dose of 5, 10, and 25 mg/kg/day, vehicle (tragacanth), or nothing (control). TDGA had no observable effects on food intake or growth patterns. Drug-treated animals had significant lowering of fasting glucose at 0 and 4 h after dosing during the midportion of the study (2-6 wk). In the latter part of the study (wk 8-11), blood glucose 4 h after dosing was lowered in mice given 10 and 25 free fatty acids. Animals receiving TDGA 25 mg/kg/day exhibited significant inhibition of immunopathologic changes in the kidney. Heart weight was significantly increased in mice receiving TDGA 25 mg/kg/day, and the total amount of myocardial carnitine content was increased in all three drug-treated groups. Increased tissue deposition of lipid was not apparent on histologic examination of liver in drug-treated animals. Inhibition of long chain fat oxidation in the db/db mouse results in significant lowering of blood glucose, and decreased the renal immunopathologic features of diabetic nephropathy in this animal model.
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PMID:Metabolic control of prevention of nephropathy by 2-tetradecylglycidate in the diabetic mouse (db/db). 675 7

From the pathophysiological viewpoint, feeding responses to various stimuli were examined in Zucker fatty rats and their lean littermates. Intraventricular administration of norepinephrine (NE, 10 micrograms/rat) stimulated food intake in both rats. Intraventricular administration of 2-deoxy-D-glucose (2DG, 3.8 mg/rat) induced hyperphagia and concomitant hyperglycemia in lean rats. However, in fatty rats, the blood glucose was elevated but food intake was unaltered after 2DG administration. Subcutaneous administration of insulin (2 or 8 U/kg) stimulated food intake of both rats. Streptozotocin (STZ)-induced hypoinsulinemia produced transient reduction of food intake followed by sustained diabetic hyperphagia in lean rats. In fatty rats, the experimental hypoinsulinemia caused transient aphagia but not sustained diabetic hyperphagia. Daily injection of insulin (5 U/rat) restored energy assimilation in both diabetic rats. An increase in food intake due to insulin injection was remarkable only in diabetic fatty rats. From these findings, the regulatory system of food intake in fatty rats appears to be sensitive to changes in the circulating insulin level but insensitive to either glucoprivation or changes in body storage of energy.
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PMID:Feeding responses of Zucker fatty rat to 2-deoxy-D-glucose, norepinephrine, and insulin. 700 24

Insulin-induced hyperglycemia was diagnosed in 8 dogs with diabetes mellitus. Owners sought veterinary care because of polydipsia, polyuria, polyphagia, persistent morning glycosuria, or seizures in their dogs. These abnormalities had persisted despite increasing the dosage of insulin. Insulin-induced posthypoglycemic hyperglycemia was diagnosed by determining blood glucose concentrations every 2 hours during a 24-hour period, beginning at 8 A.M. Wide fluctuations in the blood glucose concentration were reduced by decreasing the daily insulin dose. The signs observed by the owners disappeared after the insulin dose was reduced.
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PMID:Insulin-induced hyperglycemia in diabetic dogs. 704 78

Genetically obese mice (obob) and their lean littermates were acclimated to a restricted food-access schedule of six hours and then treated with various doses of amphetamine (0, 3, 5 or 10 mg/kg). Saline-treated obob mice maintained on this schedule retained the primary characteristics of obob mice fed ad lib, i.e., hyperphagia, hyperglycemia, elevated hypothalamic norepinephrine (NE) levels. Both lean and obese mice treated with amphetamine showed a dose-dependent decrease in food intake and hypothalamic NE levels. In obob mice amphetamine treatment reduced food intake and hypothalamic NE levels to values which were not significantly different from those of similarly treated lean mice. When the drug dose was administered on a body weight basis, however, brain amphetamine levels were twice as high in obob as in lean mice. When the amphetamine dose was adjusted to produce approximately equivalent brain levels of amphetamine in obob and lean mice, the obob mice ate significantly more than lean mice. The results indicate that amphetamine is an effective anorectic agent capable of reducing food intake, body weight, and hypothalamic NE levels in obob mice.
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PMID:Amphetamine anorexia and hypothalamic catecholamines in genetically obese mice (obob). 713 37

Several different rodent models are available for metabolic studies on the development of diabetes. Although the abnormalities associated with each diabetes type have many features in common, the documentation of several different genes being involved makes it unlikely that the various syndromes will be reduced to a single disturbance in one metabolic pathway. The severity of the diabetes produced depends on the interaction of the individual mutation with genetic factors in the inbred background of the host. Establishing the nature of these gene-host interactions in rodents should aid us in understanding similar interactions that occur in human diabetes. The development of the syndrome in most models is similar and includes hyperinsulinemia, hyperphagia, and attempts at increasing insulin supply by beta-cell hyperplasia and hypertrophy in the early stages. Hyperglycemia, obesity, and severe diabetes are secondary features that result from a combination of insulin resistance and a failure to sustain the secretion of the large amounts of insulin. Most models utilize ingested food and stored food reserves more efficiently. This increased metabolic efficiency extends to heterozygotes that are normal in all respects having only one dose of the deleterious gene. Establishing this increased metabolic efficiency in heterozygotes lends credence to the thrifty gene hypothesis of diabetes and suggests a mechanism whereby some deleterious diabetes genes may be favored in the human population. The best studied mouse models, and those for which the most complete information is available, are those caused by single genes, e.g., yellow, obese, diabetes, tubby, and fat. In the other models, the mode of inheritance is either polygenic or otherwise unclear, features which interfere with the interpretation of the data. This report briefly summarizes the developing syndrome in each model, points out any differences, and suggests the most appropriate areas where future research should be most productive in the light of contemporary studies.
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PMID:Diabetes-obesity syndromes in mice. 716 May 33

Several different single-gene mutations are known to cause varying degrees of diabetes and obesity in mice. The severity of the diabetes produced depends on both the mutation itself and the interaction of the mutant gene with the inbred background. Establishing the nature of these gene-background interactions should aid us in our understanding of similar interactions that occur in human diabetes. The documentation of several different genes that produce similar, if not identical, diabetes-obesity syndromes suggests that lesions in many pathways can cause diabetes. An understanding of these defects in mice should help us to understand similar defects involved in the human disease. The developmental stages in each mutant are similar. The early symptoms include hyperphagia, hyperinsulinemia, and hypertrophy and hyperplasia of the beta cells of the islets of Langerhans. Hyperglycemia, obesity, and severe diabetes are secondary features that result from insulin resistance and the failure to sustain the secretion of massive amounts of insulin. All models appear to be able to utilize their food in a more efficient manner than normal. Even when restricted to 50% of that amount of food eaten by a normal mouse, mutants are able to maintain their weight and still remain obese. On fasting, the stored fat is utilized more efficiently. One cause of this efficiency in obese and diabetes mice is the ability to convert acetone (the end product of fatty-acid metabolism) to lactate which, in turn, can be converted to glucose, which can sustain continued lipolysis. The occurrence of increased efficiency in obesity and diabetes mutants lends credence to the thrifty-genotype hypothesis regarding the maintenance of the deleterious diabetes genes in human populations.
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PMID:Inherited obesity-diabetes syndromes in the mouse. 724 18


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