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

The hyperglycemic patient remains persistently at risk for infectious complications. Whether ascribable to diabetes mellitus, to the administration of glucocorticoids, or to the infusion of hyperalimentation fluids, hyperglycemia may impair several mechanisms of humoral host defense, including such varied neutrophil functions as adhesion, chemotaxis, and phagocytosis. In addition, binding of glucose to the biochemically active site of the third component of complement C3 inhibits the attachment of this protein to the microbial surface and thereby impairs opsonization. Last, several pathogens frequently encountered in hyperglycemic patients possess unique mechanisms of virulence that flourish in the hyperglycemic environment. Most notable in this regard is the yeast Candida albicans, which expresses a glucose-inducible protein that is structurally and functionally homologous to a complement receptor on mammalian phagocytes. This protein promotes adhesion in the yeast and subverts phagocytosis by the host. Thus, hyperglycemia serves as a central mechanism in the predisposition of hyperglycemic patients to infection.
Diabetes 1990 Mar
PMID:Handicaps to host defense. Effects of hyperglycemia on C3 and Candida albicans. 240 80

Little definitive data are available concerning the effects of insulin deficiency on the hepatic uptake and biliary excretion of endogenous or xenobiotic substances. To expand our understanding of this area, male Sprague-Dawley rats were pretreated with streptozotocin (45 mg/kg i.v.) to induce uncontrolled diabetes. Four to five weeks later, diabetic rats exhibited elevations in serum glucose (640 +/- 13 mg/dl), biliary glucose (307 +/- 35 mg/dl), urine output (166 +/- 11 ml/24 hr), basal bile flow rate (73 +/- 2 microliter/min/kg), liver weight/body weight ratio and bile acid pool size. Polyphagia and generalized muscle atrophy were also evident. Plasma disappearance and biliary excretion of several organic anions were studied after i.v. administration. There were no differences between control and diabetic rats in the plasma elimination and biliary excretion of eosin, phenol-3,6-dibromphthalein disulfonate and sulfobromophthalein. Although hepatic uptake was unchanged, the biliary excretion of amaranth was decreased 30% in diabetic rats. There were no differences in bile flow rate in control or diabetic rats after administration of these four anions. In contrast, administration of indocyanine green, bromcresol green and rose bengal did not depress bile flow in diabetic rats as was observed in control rats. In addition, the rate of maximal biliary excretion was increased by 390, 240 and 151% for rose bengal, indocyanine green and bromcresol green, respectively. Plasma clearance of rose bengal was 65% higher in diabetic rats. Total body clearance and steady-state volume of distribution values for all other anions were not different after induction of diabetes.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Biliary excretion of organic anions in diabetic rats. 243 94

Myogenic satellite cells were isolated from nondiabetic and streptozotocin-diabetic rats and studied in vitro. Streptozotocin (STZ) administration produced both hyperglycemia and glucosuria in adult rats when compared to controls. (P less than 0.01), with 12.5% mortality in untreated animals. Insulin therapy diminished blood glucose levels to those found in nondiabetic animals. Only STZ-diabetic rats displayed symptoms of Type I diabetes, including polydipsia, polyuria, and hyperphagia. STZ-treated rats possessed less leg muscle mass and less subcutaneous, intermuscular, and intramuscular fat. Conversely, nondiabetic rats had a greater mean body weight (P less than 0.01) at the end of the experiment than did diabetic rats. Primary cultures of diabetic-derived satellite cells displayed decreased overall ability (P less than 0.01) to fuse to form multinucleated myotubes in vitro than controls. In addition, secondary cultures of diabetic-derived satellite cells achieved maximal fusion one day later than secondary cultures of control-derived cells. Collectively, these data provide preliminary evidence to suggest that untreated insulin-dependent diabetes results in altered fusion characteristics of myogenic satellite cells. Additional studies utilizing satellite cells from diabetic animals will provide valuable definition of the satellite cell involvement in skeletal muscle autophagy which is a symptom of type I diabetes.
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PMID:Satellite cells derived from streptozotocin-diabetic rats display altered fusion parameters in vitro. 252 36

The activity of tyrosine hydroxylase (TOH), the rate-limiting enzyme in norepinephrine biosynthesis, was measured in selected sympathetic ganglia to develop a quantitative measure of sympathetic autonomic neuropathy in streptozocin-induced diabetic rats. Surprisingly, TOH activity was elevated twofold in diabetic prevertebral ganglia innervating the alimentary tract (i.e., superior mesenteric, celiac, and inferior mesenteric), which has terminal processes that develop neuroaxonal dystrophy in this model system. TOH activity of paravertebral ganglia (i.e., superior cervical and stellate) with nonalimentary targets was not increased in the same animals. Increased TOH activity in the prevertebral ganglia 1) developed within the 1st wk of diabetes and persisted for 10 mo, 2) did not represent a change in TOH affinity for d-1,6-methyl-5,6,7,8- tetrahydropterine cofactor, 3) was prevented by both nicotinamide pretreatment and early institution of insulin therapy, and 4) did not develop as a result of classical transsynaptic induction. Pair-feeding experiments confirmed that the most likely cause of increased TOH activity in this system was the marked hypertrophy and hyperplasia of the diabetic bowel resulting from compensatory hyperphagia. We conclude that TOH activity does not represent a suitable marker for sympathetic autonomic neuropathy in this experimental system. Rather, the increase appears to be an example of a selective increase in the synthesis of neurotransmitter enzymes, possibly in response to increased trophic support provided by the expanded target, i.e., the hypertrophic gut. The additional synthetic stress imposed on prevertebral neurons by the expansion of the innervation of the alimentary target coupled with the complex diabetic metabolic milieu may contribute to the development and selective distribution of dystrophic axonopathy to the innervation of the alimentary tract.
Diabetes 1989 Aug
PMID:Tyrosine hydroxylase activity in sympathetic nervous system of rats with streptozocin-induced diabetes. 256 57

Numerous studies have demonstrated that poor glycemic control is associated with elevated plasma cholesterol levels in diabetic patients. Experiments have shown that cholesterol synthesis is increased in the small intestine of various diabetic animals. This increase is a generalized phenomenon occurring in all segments of the small intestine. Insulin therapy that normalizes blood glucose levels markedly decreases intestinal cholesterol synthesis in diabetic animals to a level similar to that observed in control animals. Studies have suggested that the hyperphagia that accompanies poorly controlled diabetes is the chief stimulus for the increase in intestinal cholesterol synthesis. However, the direct contact of the intestinal mucosa with nutrients is not the sole trigger for increasing cholesterol synthesis in the small intestine, suggesting that circulating and/or neurological factors play a role. The transport of newly synthesized cholesterol, most of which is in the chylomicron lipoprotein fraction, from the intestines to the circulation is increased in diabetic rats. The sterols associated with these chylomicrons are rapidly cleared from the circulation and delivered to the liver. The increased transport of chylomicrons from the intestine to the circulation in diabetic patients could potentially result in several alterations in lipid metabolism that may increase the risk of atherosclerotic vascular disease.
Diabetes 1989 Feb
PMID:Importance of small intestine in diabetic hypercholesterolemia. 264 36

Diet therapy is an important factor in overall care of most GI patients. Historically, diets have been used unscientifically in many of these patients without positive results. Nutritional care and diet therapy are critical for two reasons. First, malnutrition is an expected sequelae to most, if not all, GI diseases or disorders. Failure to eat, digest, or assimilate nutrients can provoke malnutrition in just a few weeks, although careful assessment of anthropometric, clinical, biochemical, and nutritional history by a trained professional can protect against this. Diet therapy through the elimination of offending foods such as wheat gluten or lactose, or inclusion of specialized products such as medium chain triglycerides or elemental formulas, can sustain nutritional status. Dietary components such as insoluble fiber appear to have physiologic effects, while soluble fibers may have metabolic effects important to diabetes and cardiovascular disease. There is a high potential for malnutrition in Crohn's disease during active and remittent phases. Elemental enteral formulas or TPN are used during the active phase to ensure optimal nutritional status and bowel rest. Hyperalimentation using the GI tract during remittent stage maintains this. Avoiding offending foods by Crohn's patients is an acceptable practice as long as entire categories of foods are not deleted. Avoiding all foods containing gluten from wheat, rye, barley, and oats, however, is a crucial prerequisite to recovery from celiac disease. Gluten is commonly used as a stabilizer, emulsifier, and extender in the food industry and is not always shown on food labels. Careful consultation with a registered dietitian can identify hidden sources of gluten in the diet.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary therapy in gastrointestinal disease. 264 90

Glucose tolerance factor (GTF), the biologically active form of Cr3+, has been ascribed a role in the potentiation of insulin action and glucose homeostasis. The present study investigated the effects of dietary supplementation with GTF-rich brewer's yeast (Saccharomyces cerevisiae) or GTF-deprived Torula yeast (Torulaspora delbrueckii) in genetically diabetic C57BL/KsJ db/db mice. At 15 weeks of age, db/db mice exhibited increased body weight, hyperphagia, hyperglycaemia, hyperinsulinaemia and increased glycosylated haemoglobins compared with control (+/+) mice. During 56 days consumption of diets supplemented with 50g brewer's yeast or Torula yeast per kg, body weights of both groups of db/db mice decreased by 35%, in association with 1.2-1.7 fold increases of food intake, plasma glucose, glycosylated haemoglobins and an 83% decrease of plasma insulin. With the exception of slightly decreased weight loss, addition of brewer's yeast as opposed to Torula yeast did not affect tissue or plasma chromium nor ameliorate any of the parameters monitored including glucose tolerance and insulin sensitivity at 52-54 days. These findings do not support the contention that the glucose intolerance of genetically diabetic C57BL/KsJ db/db mice partly reflects GTF deficiency.
Diabetes Res 1989 Mar
PMID:Failure of glucose tolerance factor-containing Brewer's yeast to ameliorate spontaneous diabetes in C57BL/KsJ DB/DB mice. 268 Feb 28

Hyperglycaemic hyperosmolar non-ketotic syndrome (HHNS) is a life-threatening complication of uncontrolled diabetes mellitus. This syndrome is characterised by severe hyperglycaemia, a marked increase in serum osmolality, and clinical evidence of dehydration without significant accumulation of ketoacids. HHNS is typically observed in elderly patients with non-insulin-dependent diabetes mellitus, although it may rarely be a complication in younger patients with insulin-dependent diabetes, or those without diabetes following severe burns, parenteral hyperalimentation, peritoneal dialysis, or haemodialysis. Patients receiving certain drugs including diuretics, corticosteroids, beta-blockers, phenytoin, and diazoxide are at increased risk of developing this syndrome. Patients usually present with a prolonged phase of osmotic diuresis leading to severe depletion of both the intracellular and extracellular fluid volumes. Losses of water exceed those of sodium, resulting in hypertonic dehydration. Therefore, correction of the syndrome will ultimately require administration of hypotonic fluids. Patients presenting with HHNS also have significant depletion of potassium and other electrolytes that will need to be replaced. The principal goal at the outset of therapy must be restoration of the intravascular volume to assure adequate perfusion of vital organs. It remains controversial whether 0.9% or 0.45% NaCl should be the initial fluid infused intravenously. We prefer to administer 0.9% NaCl until the vital signs have stabilised and then substitute 0.45% NaCl. 10 to 15 units of regular human insulin should be injected as a bolus, followed by a continuous infusion of approximately 0.1 U/kg/h. Once the blood glucose approaches 13.9 to 16.7 mmol/L (250 to 300) mg/dl, 5% dextrose should be added to the intravenous fluids and the rate of insulin infusion reduced. Following recovery many patients presenting with HHNS will not require long term insulin therapy and can be managed effectively with diet or oral agents. Precipitating causes of HHNS must be identified and treated simultaneously with correction of the metabolic abnormalities. Appropriate management of precipitating illnesses will limit the high mortality associated with HHNS. This review discusses the current state of knowledge concerning the pathogenesis of HHNS, the clinical features of the disorder, and a systematic approach to treatment.
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PMID:Treatment of hyperglycaemic hyperosmolar non-ketotic syndrome. 268 Apr 38

Marked weight loss is the major nutritional defect in chronic pancreatitis. Inadequate food intake owing to recurrent or near continuous pain usually accounts for the initial 10 to 20 per cent of loss of body weight, which decreases again with the onset of diabetes and is often precipitous with the development of steatorrhea. Treatment of pain, control of diabetes, and intensive pancreatic replacement therapy for steatorrhea usually causes weight gain, but seldom to ideal weight. It appears that the patient's body weight gets set at a new "weight-stat." Although isolated abnormalities of small bowel function tests can be elicited and deficiencies of fat-soluble vitamins, calcium, zinc, selenium, and so forth may be demonstrated, these rarely lead to clinical syndromes, as with demonstrable low B12 uptake in some 10 to 15 per cent of patients. In the late stage of the disease and particularly in NATP, extreme protein-calorie malnutrition may occur, which may not be correctable even by hyperalimentation. Although the mortality of the disease was reportedly higher in areas of socioeconomic deprivation, it appears from recent studies in Switzerland and other developed countries that mortality during a 12-year period may be in the region of 50 per cent worldwide.
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PMID:Nutritional deficiencies in chronic pancreatitis. 268 Sep 66

The effects of streptozotocin-induced diabetes on weight gain, bone growth and GH secretion have been studied in conscious chronically cannulated male rats. In addition to the classic diabetic symptoms (hyperphagia, polydipsia, polyuria, glycosuria and hyperglycaemia), the slow body weight gain (0.95 +/- 0.5 compared with 2.63 +/- 0.5 g/day in non-diabetic controls) was associated with a reduction in bone growth (from 162 +/- 9 to 48 +/- 4 microns/day) and a reduced pituitary GH content (from 1.5 +/- 0.2 to 0.6 +/- 0.06 mg/gland). Serial blood sampling during the day or overnight showed that the normal male episodic GH secretory pattern was obliterated in the diabetic animals. The constant osmotic stimulation of hyperglycaemia and high fluid turnover was reflected in a significant reduction in pituitary oxytocin and arginine vasopressin (AVP) stores. Intravenous insulin infusions (67-1340 pmol/h for 4 or 7 days) caused a large initial weight gain (greater than 20 g in 2 days) followed by a slower increase, and stimulated tibial bone growth (to 100 +/- 16 and 126 +/- 8 microns/day after 4 or 7 days respectively). Insulin infusion for 7 days also increased pituitary GH content (to 1 +/- 0.15 mg/gland), and the normal episodic GH secretory pattern returned. Intravenous infusions of insulin which reduced, but did not completely normalize, blood glucose levels, allowed the resumption of growth and pulsatile GH secretion. Continuous infusion of recombinant human insulin-like growth factor-I (hIGF-I) at 1110 pmol/h for 54 h also caused a large initial rise in body weight in diabetic rats (17.1 +/- 1.6 compared with 7.5 +/- 2.8 g in saline-infused controls) due primarily to increased fluid retention. This effect of hIGF-I occurred without any significant changes in pituitary GH, AVP, oxytocin, blood glucose or bone growth over this short-term infusion, nor was there any obvious effect on spontaneous GH secretion, monitored over the entire infusion period. We conclude that the diabetic rat is not a good model to study growth stimulation by short-term insulin or IGF-I treatments because the insulin-like effects of these peptides obscure their specific growth-promoting activities in this model.
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PMID:Growth hormone and growth in diabetic rats: effects of insulin and insulin-like growth factor-I infusions. 268


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