Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0020505 (hyperphagia)
 6,116 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Five callitrichids (three common marmosets -Callithrix jacchus -, a black tufted-eared marmoset -C. penicillata-, and a saddle-back tamarin -Saguinus fuscicollis) were diagnosed with islet hyperplasia by histopathology and immunohistochemistry. All were privately-owned, unrelated callitrichids ranging from 2- to 4-year-old. Relevant findings were anorexia (3/5), vomiting (2/5), ptyalism (1/5), polyuria/polydipsia (1/5), respiratory distress (1/5), hyperglycemia (2/3) and glycosuria (1/1); hyperglycemia and glycosuria were associated with pregnancy in a common marmoset and resolved after reducing simple carbohydrates in diet. All five animals died, three of them after few premonitory signs; in two cases, other concurrent diseases unrelated to islet hyperplasia were considered the cause of death. Additional animals from two facilities had high weight (4), physical obesity (3), polyuria/polydipsia/polyphagia/uriposia (1), hyperglycemia (1), and/or glycosuria (2). Pathologic findings in the deceased callitrichids were: islet hyperplasia (5/5); hemosiderosis (5/5); lipomatosis (4/5) of several tissues (atria, 3/5; pancreas, gall bladder, intestine, esophagus, and thyroid, 2/5; liver, 1/5); pancreatic necrosis or steatonecrosis, and/or acute pancreatitis (3/5); and vacuolation of hepatocytes and renal tubular cells most likely consistent with hepatorenal lipidosis (2/5). The islets of Langerhans were more numerous and larger than in a control, and morphologically normal in all cases, except in a common marmoset that had a few cells with a foamy cytoplasm and shrunken hyperchromatic or picknotic nucleus. Insulin (5/5), glucagon (3/5), and somatostatin (3/5) immunohistochemistry revealed that most cells stained positively for insulin diffusely in their cytoplasm (5/5) (staining restricted to the vascular pole of b-cells in the control). These findings suggest that obesity, insulin resistance and/or type II diabetes may be implicated and thus a prospective study on these diseases in callitrichids is necessary to determine their etiopathogenesis.
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PMID:Islet hyperplasia in callitrichids. 1214 99

Type 1 diabetic patients depend on insulin replacement therapy. However, chronic hyperglycemia due to failure to maintain proper glycemic control leads to microvascular, macrovascular, and neurological complications. Increased glucose disposal by tissues engineered to overexpress key regulatory genes in glucose transport or phosphorylation can reduce diabetic hyperglycemia. Here we report that differentiated myoblast cells expressing the glucose-phosphorylating enzyme glucokinase (GK) showed a glucose-dependent increase in glucose uptake and utilization in vitro. Transplantation of GK-expressing myotubes into healthy mice did not alter blood glucose levels and recipient mice maintained normoglycemia. After streptozotocin treatment, mice transplanted with GK-expressing myotubes counteracted hyperglycemia, polydipsia, and polyphagia, whereas mice transplanted with control myotubes developed diabetes. Similarly, diabetic mice transplanted with control myotubes remained hyperglycemic. In contrast, transplantation of GK-expressing myotubes into diabetic mice lowered hyperglycemia. These results suggest that the use of genetically engineered muscle cells to express glucokinase may provide a glucose-regulated approach to reduce diabetic hyperglycemia.
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PMID:Glucose-regulated glucose uptake by transplanted muscle cells expressing glucokinase counteracts diabetic hyperglycemia. 1254 44

Maturity-onset diabetes of the young (MODY) is a rare form of juvenile diabetes mellitus, defined by early onset, absence of ketosis, non-insulin-dependent diabetes and autosomal dominant inheritance. Advances in molecular genetic analysis have identified mutations accounting for different MODY subtypes, all of them associated with defects of insulin secretion. We present a case of a nine year-old boy, admitted to our outpatient clinic because of mild and intermittent osmotic symptoms (polyuria, polyphagia and polydipsia) and persistently high values of fasting blood glucose in the last year. He had a family history of diabetes in three consecutive generations compatible with autossomal dominant inheritance. His height was 138.5 cm (90th centile) and his weight was 33.5 Kg (90th centile). General examination was unremarkable, in a prepubertal boy. A standard oral glucose tolerance test was performed. The fasting blood glucose was 118 mg/dl with a two hour value of 160 mg/dl. ICA, IAA and GAD autoantibodies were undetectable. He started on diet therapy, keeping his fasting blood glucose measurements on the upper limits of normal and HbA1c in the normal range. He was diagnosed as having MODY 2 on a clinical basis, as it is not possible to perform molecular analysis of this pathology in Portugal. As MODY is recently thought to account for 2-5% of all cases of type 2 Diabetes Mellitus it is important to consider it as a possible diagnosis in children who present with incidental hyperglycaemia. Molecular genetic testing is very important as it enables us to make a firm diagnosis of MODY, to define a follow up plan and to reassure patients families, once the prognosis is significantly different among the different sub-types of MODY. We emphathize the need of creating national and international reference centres where such testing can be done.
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PMID:[Mature onset diabetes of the young (MODY)]. 1268 Feb 90

Hyperadrenocorticism is a common endocrinopathy which results from the excessive production of cortisol by the adrenal cortex. In the majority of cases, this increased secretion of cortisol results from stimulation of the adrenal cortex by adrenocorticotrophic hormone secreted from the pituitary gland. In a smaller number of cases adrenal tumours are present. Clinical signs are variable but commonly include polydipsia and polyuria, polyphagia, obesity, a pendulous abdomen, hepatomegaly, alopecia, lethargy, weakness and anoestrus. Haematology, serum chemistry analysis and urinalysis should be performed on a dog with suspected hyperadrenocorticism. Finding a significant number of changes that are consistent with hyperadrenocorticism often allows a presumptive diagnosis to be made. Other tests can then be used to confirm the diagnosis and to help localise the cause, including liver biopsy, radiology, ultrasonography, gamma camera imaging, computed tomography, and measurement of blood and urine hormone levels. The ACTH stimulation test, low dose dexamethasone suppression test and measurement of the urine cortisol:creatinine ratio are used to assess whether hyperadrenocorticism is present. The high dose dexamethasone suppression test, measurement of plasma ACTH, corticotropin-releasing hormone stimulation test, and a modification of the urinary cortisol:creatinine ratio test are then implemented to determine the aetiology. The treatment of choice for adrenal neoplasia is surgical removal of the affected adrenal. On the other hand, pituitary hyperplasia or neoplasia may be treated either surgically, by bilateral adrenalectomy or hypophysectomy, or medically. The drug which is chosen most commonly for medical management is 1,1-dichloro-2(O-chlorophenyl)-2-(P-chlorophenyl) ethane (op'-DDD), which can be used to suppress adrenal function or to completely destroy the adrenal cortex. The antifungal agent ketoconazole also suppresses adrenal steroid synthesis and provides an alternative form of medical treatment for hyperadrenocorticoid dogs.
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PMID:Canine hyperadrenocorticism. 1603 96

Whipple disease is a relapsing systemic illness caused by Tropheryma whippelii. Central nervous system involvement occurs in 5%-40% of all patients. Hypothalamic manifestations occur in 31% of Whipple encephalopathy, including polydipsia, hyperphagia, change in libido and insomnia. We report a case of a 48-year-old man with severe insomnia, depression, dementia, dysarthria, myoclonic movements of the limbs and ophthalmoplegia. The diagnosis of Whipple encephalopathy was confirmed by PCR analysis of blood and faeces. He received a full dose of antibiotic treatment. Despite clinical improvement, resolution of the lesions detected in MRI scan of the brain and negative results of the PCR in blood, faeces and cerebrospinal fluid six months later, insomnia persisted and finally subsided after the administration of carbamazepine (600 mg/day). Our case supports the finding that carbamazepine might be useful in the treatment of insomnia associated with Whipple encephalopathy.
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PMID:An unusual case of insomnia associated with Whipple encephalopathy: first case reported from Greece. 1608 32

Stem bark extracts of Terminalia superba Engl. and Diels and Canarium schweinfurthii Engl. are used in Africa for the treatment of various ailments, including diabetes mellitus. The anti-diabetic effects of the methanol/methylene chloride extracts of the stem barks on streptozotocin (STZ)-induced diabetes were evaluated on male rats. Through the subcutaneous route, diabetes was induced using 60 mg/mL of streptozotocin. After 2 days, the rats received, by gavage, 150 mg/kg and 300 mg/kg of extract daily for 14 days. At 300 mg/kg, the two extracts (Terminalia superba and Canarium schweinfurthii), significantly showed at least 67.1% and 69.9% reduction in blood glucose level, respectively, while insulin (three units) given subcutaneously and once daily, had 76.8% reduction compared to diabetic untreated control rats. Similarly, the weight gains were 6.6% and 4.9%, respectively, and were comparable to the normal rats, whereas, diabetic untreated rats lost 14.1% body weight. Still with the same dose, there was 68.5% and 58.5% (p < 0.001) significant decrease in food consumption and 79.7% and 64.0% (p < 0.001) in fluid intake by diabetic rats treated with the respective plant extracts. The insulin-treated rats showed 56.4% and 75.8% decrease in food and fluid intake compared to an augmentation for diabetic control rats, 43.0% and 383.8%, respectively, at the end of the second week of experimentation. These results showed that the plant extracts can reverse hyperglycemia, polyphagia and polydipsia provoked by streptozotocin, and thus, they have anti-diabetic properties.
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PMID:Anti-diabetic activity of methanol/methylene chloride stem bark extracts of Terminalia superba and Canarium schweinfurthii on streptozotocin-induced diabetic rats. 1627 36

Hummingbirds and other nectar-feeding, migratory birds possess unusual adaptive traits that offer important lessons concerning obesity, diabetes and the metabolic syndrome. Hummingbirds consume a high sugar diet and have fasting glucose levels that would be severely hyperglycemic in humans, yet these nectar-fed birds recover most glucose that is filtered into the urine. Hummingbirds accumulate over 40% body fat shortly before migrations in the spring and autumn. Despite hyperglycemia and seasonally elevated body fat, the birds are not known to become diabetic in the sense of developing polyuria (glucosuria), polydipsia and polyphagia. The tiny (3-4 g) Ruby-throated hummingbird has among the highest mass-specific metabolic rates known, and loses most of its stored fat in 20 h by flying up to 600 miles across the Gulf of Mexico. During the breeding season, it becomes lean and maintains an extremely accurate energy balance. In addition, hummingbirds can quickly enter torpor and reduce resting metabolic rates by 10-fold. Thus, hummingbirds are wonderful examples of the adaptive nature of fat tissue, and may offer lessons concerning prevention of metabolic syndrome in humans.
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PMID:Adipose energy stores, physical work, and the metabolic syndrome: lessons from hummingbirds. 1635 26

Aberrant energy metabolism is one characteristic of diabetes mellitus (DM). Two types of DM have been identified, type 1 and type 2. Most of type 2 DM patients eventually become insulin dependent because insulin secretion by the islets of Langerhans becomes exhausted. In the present study, we show that resveratrol (3,5,4'-trihydroxylstilbene) possesses hypoglycemic and hypolipidemic effects in streptozotocin-induced DM (STZ-DM) rats. In resveratrol-treated STZ-DM rats, the plasma glucose concentration on day 14 was reduced by 25.3 +/- 4.2%, and the triglyceride concentration was reduced by 50.2 +/- 3.2% compared with the vehicle-treated rats. In STZ-nicotinamide DM rats, the plasma glucose concentration on day 14 was reduced by 20.3 +/- 4.2%, and the triglyceride concentration was reduced by 33.3 +/- 2.2% compared with the vehicle-treated rats. Resveratrol administration ameliorates common DM symptoms, such as body weight loss, polyphagia, and polydipsia. In STZ-nicotinamide DM rats, resveratrol administration significantly decreased insulin secretion and delayed the onset of insulin resistance. Further studies showed that glucose uptake by hepatocytes, adipocytes, and skeletal muscle and hepatic glycogen synthesis were all stimulated by resveratrol treatment. Because the stimulation of glucose uptake was not attenuated in the presence of an optimal amount of insulin in insulin-responsive cells, the antihyperglycemic effect of resveratrol appeared to act through a mechanism(s) different from that of insulin.
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PMID:Resveratrol, a red wine antioxidant, possesses an insulin-like effect in streptozotocin-induced diabetic rats. 1643 53

A 10-year-old uncastrated male Dalmatian dog was referred for gait abnormalities consisting of chronic progressive stiffness and rigidity. Other symptoms were polyphagia associated with weight gain, polyuria and polydipsia, excessive panting, and an inspiratory stridor. The owner had noticed progressive thickening of the skin and enlargement of the tongue over the last 3 years. Physical examination revealed thickening of the skin, redundant skin folds, and enlargement of the tongue. The only remarkable abnormalities found on routine laboratory examination were mild anaemia and an increased serum fructosamine concentration. Circulating concentrations of total thyroxine, free thyroxine, and cTSH, and the results of an ACTH stimulation test were all within reference ranges. The basal serum growth hormone (GH) concentration was markedly elevated (23microg/l) and did not decrease during a glucose tolerance test or after somatostatin administration. The serum insulin-like growth factor-1 concentration was also markedly elevated (1254microg/l). Basal serum insulin concentration was high (95mU/l) and insulin concentrations increased considerably after glucose loading, consistent with insulin resistance. Abdominal ultrasonography showed no abnormalities. Survey radiographs of the vertebral column showed severe spondylosis deformans extending from the cervical to the lumbosacral spine. CT scanning of the skull showed an enlarged pituitary gland with normal enhancement pattern. On post-mortem examination, the entire vertebral column appeared as a single and inflexible structure due to the presence of multiple fused osteophytes. The pituitary gland contained an acidophilic adenoma that immunostained positively for GH (and negatively for ACTH and alpha-MSH). In conclusion, this Dalmatian dog with acromegaly and insulin resistance represents the first case of GH hypersecretion proven to be due to a somatotroph adenoma.
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PMID:Acromegaly due to a somatroph adenoma in a dog. 1647 61

This study aimed to examine the function of the tuberomammillary complex in water and food intake of Wistar rats. The results show that lesions restricted to tuberomammillary subnuclei: caudal ventral tuberomammillary nucleus (E1), rostral ventral tuberomammillary nucleus (E2), medial ventral tuberomammillary nucleus (E3) or medial dorsal tuberomammillary nucleus (E4), induce a strong and persistent polydipsia with specific characteristics for each nucleus. Interestingly, the distribution of tuberomammillary hyperdipsia throughout the day was similar to that in non-lesioned animals, in contrast to the lack of rhythmicity observed in rats with anodic lesion to median eminence. This polydipsia appears to be independent of food intake, as food deprivation for 22 h did not significantly reduce the water intake. Finally, lesions in ventral tuberomammillary nuclei E1 and E2 induce hyperphagia, confirming a possible role for the tuberomammillary complex in food intake. This increase in food intake is not observed after lesions in medial subnuclei E3 and E4. These results are interpreted in terms of the hypothalamic systems involved in the consumption of both food and water.
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PMID:Lesions of tuberomammillary nuclei induce differential polydipsic and hyperphagic effects. 1655 93


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