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)

Overt diabetes (NIDDM) was induced by overeating in neonatally streptozocin (60 mg/kg.BW) treated impaired glucose tolerant mice. We imposed a food restriction and a high fiber diet to evaluate the effects of dietary treatment in this NIDDM model mouse. Furthermore, insulin secretion after the dietary treatment was studied using the perfused pancreas technique. One group of IGT mice (SZ) was maintained on ordinary mouse chow during 6 to 14 weeks of age. The others received a cookie and chocolate mashed diet (C.C. diet) to induce overt diabetes during 6 to 10 weeks of age. Thereafter, the mice with induced overt diabetes were divided according to their diet treatment. The C.C. diet was continued in one group (SZC) for 4 weeks, and the others were divided into a food restriction group (SZR: 4 g/mouse/day of ordinary mouse chow, for 4 weeks) and a high fiber diet group (SZF: 20% W/W of cellulose in ordinary mouse chow, for 8 weeks). The mean caloric intake/mouse/day in SZC, SZR and SZF were 140, 80 and 98% of that in SZ, respectively. Amelioration of hyperglycemia and impaired glucose tolerance was noted in SZR and SZF. A better glycemic control was obtained in SZF with keeping a normal growth rate. On the pancreas perfusion, the insulin secretion to 30 mM glucose was improved in SZR and SZF. Furthermore, the incremental first phase peak insulin release to 30 mM glucose in SZF was significantly greater than that in SZC (SZF, 10.5 +/- 1.0 vs. SZC, 4.5 +/- 1.9 microU/min).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Dietary treatment ameliorates overt diabetes and decreased insulin secretion to glucose, induced by overeating in impaired glucose tolerant mice. 217 33

Neuropeptide Y (NPY), a major brain neurotransmitter, is expressed in neurons of the hypothalamic arcuate nucleus (ARC) that project mainly to the paraventricular nucleus (PVN), an important site of NPY release. NPY synthesis in the ARC is thought to be regulated by several factors, notably insulin, which may exert an inhibitory action. The effects of NPY injected into the PVN and other sites include hyperphagia, reduced energy expenditure and enhanced weight gain, insulin secretion, and stimulation of corticotropin and corticosterone release. The ARC-PVN projection appears to be overactive in insulin-deficient diabetic rats, and could contribute to the compensatory hyperphagia and reduced energy expenditure, and pituitary dysfunction found in these animals; overactivity of these NPY neurons may be due to reduction of insulin's normal inhibitory effect. The ARC-PVN projection is also stimulated in rat models of obesity +/- non-insulin diabetes, possibly because the hypothalamus is resistant to inhibition by insulin; in these animals, enhanced activity of ARC NPY neurons could cause hyperphagia, reduced energy expenditure, and obesity, and perhaps contribute to hyperinsulinemia and altered pituitary secretion. Overall, these findings suggest that NPY released in the hypothalamuss, especially from the ARC-PVN projection, plays a key role in the hypothalamic regulation of energy balance and metabolism. NPY is also found in the human hypothalamus. Its roles (if any) in human homeostasis and glucoregulation remain enigmatic, but the animal studies have identified it as a potential target for new drugs to treat obesity and perhaps NIDDM.
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PMID:Neuropeptide Y, the hypothalamus, and diabetes: insights into the central control of metabolism. 747 13

Characteristics are hypotonia, problems with feeding and thriving in the neonate and infant, later hyperphagia and severe obesity. Other findings are dysmorphic traits, hypogonadism, short stature, developmental delay, mental retardation and behavioural problems. Diabetes mellitus (NIDDM) is frequent in adults. Treatment is symptomatic. Prognosis is determined by obesity. PWS occurs almost always sporadically and is found in all ethnic groups and in both sexes. The epidemiology of PWS in Denmark is unknown. In 95% of cases with PWS cytogenetic and molecular genetic investigations show either deletion of the paternal chromosome 15q11q13 or uniparental maternal disomy of chromosome 15. Since 1992 150 bloodsamples of patients suspected for PWS have been investigated by cytogenetic and molecular genetic techniques at the John F. Kennedy Institute, DK-2600 Glostrup; deletion of the paternal chromosome 15 was found in 15 and uniparental maternal disomy of chromosome 15 in eight cases.
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PMID:[Prader-Willi syndrome--clinical picture and genetics]. 772 49

Insulin receptor substrate (IRS)-1 and IRS-2, which mediate phosphatidylinositol (PI) 3-kinase activation, play essential roles in insulin-induced translocation of GLUT4 and in glycogen synthesis. In this study, we investigated the process of PI 3-kinase activation via binding with IRS-1 and -2 in liver, muscle, and fat of high-fat-fed rats, a model of insulin-resistant diabetes. In the liver of high-fat-fed rats, insulin increased the PI 3-kinase regulatory subunit p85alpha and the PI 3-kinase activities associated with IRS-1 3.6- and 2.4-fold, and with IRS-2, 4.7- and 3.0-fold, respectively, compared with those in control rats. The tyrosine phosphorylation levels of IRS-1 and IRS-2 were not significantly altered, however. In contrast with the liver, tyrosine phosphorylation levels and associated PI 3-kinase proteins and activities were decreased in the muscle and adipose tissue of high-fat-fed rats. Thus, high-fat feeding appears to cause insulin resistance in the liver by a mechanism different from the impaired PI 3-kinase activation observed in muscle and adipose tissue. Taking into consideration that hepatic PI 3-kinase activation is severely impaired in obese diabetic models such as Zucker fatty rats, it is possible that the mechanism by which a high-fat diet causes insulin resistance is quite different from that associated with obesity and overeating due to abnormality in the leptin system. This is the first report to show increased PI 3-kinase activation by insulin in an insulin-resistant diabetic animal model. These findings may be important for understanding the mechanism of insulin resistance in human NIDDM, since a high-fat diet is considered to be one of the major factors exacerbating insulin insensitivity in humans.
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PMID:Enhanced insulin-stimulated activation of phosphatidylinositol 3-kinase in the liver of high-fat-fed rats. 989 38

To understand latent autoimmune diabetes mellitus in adults (LADA), we compared the clinical characteristics, fasting plasma glucose and C-peptide level, genetic frequency of HLA-DQA1, -DQB1 chain in 25 patients with LADA, 57 patients with insulin-dependent diabetes mellitus (IDDM, 21 patients with children-onset IDDM, 36 patients with adult-onset IDDM with ketosis), 38 patients with NIDDM (mild and moderate 30 patients and severe 8) and 42 normal persons. The onset of age was 20-48 years old associated with obvious polyphagia, and weight loss. Body mass index (BMI) was < or = 25 and fasting plasma glucose was > or = 16.5 mmol/L (297 mg/dl). Fasting and 1, 2 hour post prandial C-peptide level showed low and flatter curve (0.4, 0.8 and 0.8 nmol/L respectively). Glutamate decarboxylase (GAD) antibody was positive. HLA-DQ beta chain substitution of aspartate molecule was at position 57 (susceptic gene). LADA could be diagnosed if a patient has the first point and any point of the second to the fourth point. Patients with LADA should take diet, exercises, especially insulin as early as possible in order to control fasting and post prandial plasma glucose, and prevent from further destroy of residue islet B cells and reduce diabetic complications of eye, kidney and nerve.
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PMID:[Clinical characteristics and main diagnostic points of latent autoimmune diabetes mellitus in adults]. 1037 7