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

Female rats fed a cafeteria diet from birth developed obesity at 60 days of age and their stomach, small intestine and caecum were enlarged when compared with controls, i.e. these regions had greater food storage capacity. In spite of the enlargement, these regions had similar or reduced weight and linear density, which is seen as proof of reduced mechanical performances. Cafeteria diet produced increased glucose duodenal absorption in older animals unlike the typical reduction known in controls. Tryptophan absorption was maintained high in adulthood, compensating for the low structural nutritive properties of the cafeteria diet. The results are interpreted as an adaptation to the cafeteria diet effects and properties: the characteristic overeating of foodstuffs with greater energy density, lower mechanical requirements and lower structural nutritive value than pelleted chow.
 ...
PMID:Morphofunctional changes in gastrointestinal tract of rats due to cafeteria diet. 141 Jul 67

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.
 ...
PMID:The etiology and pathogenesis of non-insulin-dependent diabetes. 148 43

Vanadyl sulfate trihydrate was given by gavage to streptozotocin-induced diabetic rats for 21 days at doses of 0, 25, 50, or 75 mg/kg/day. In marked contrast to the reduction in plasma glucose observed in diabetic animals given vanadyl sulfate via drinking water, diabetic rats given vanadyl by gavage were not characterized by normoglycemia. Similarly, in contrast to the normalizing effect of vanadyl in drinking water, vanadyl by gavage had only a minimal influence on diabetes associated hyperphagia and polydipsia. Despite the lack of marked effect of vanadyl by gavage on the above parameters, tissue vanadium accumulation in the gavaged rats was similar to that reported for rats given vanadium by drinking water. The present results (taken together with previous data) show that the administration of vanadium by gavage is not a viable alternative to the use of insulin in diabetes treatment.
 ...
PMID:Administration of vanadyl sulfate by gavage does not normalize blood glucose levels in streptozotocin-induced diabetic rats. 150 5

Neuropeptide Y (NPY) is an important hypothalamic regulator of feeding behavior. In this study we have investigated the regulation of the expression of preproNPY mRNA in male obese and lean Zucker rats by in situ hybridization. These animals represent a model of genetic obesity with hyperphagia, hyperinsulinemia and altered endocrine functions. Obese Zucker rats, treated for 12 days with 0.9% saline, had about 210% higher level of basal preproNPY mRNA expression in the arcuate nucleus when compared to their lean littermate controls. Repeated administrations of 8-hydroxy-dipropylaminotetralin (8-OH-DPAT), a serotonergic 5-HT1A agonist, or mifepristone, a glucocorticoid receptor antagonist, did not modify the basal expression of preproNPY mRNA in the Zucker phenotypes. The 8-OH-DPAT treatment significantly reduced hyperinsulinemia in obese Zucker rats without changing plasma glucose levels. The mifepristone treatment significantly increased plasma corticosterone levels in lean animals, but not in obese animals. The present study demonstrates enhanced expression of preproNPY mRNA in the arcuate nucleus in obese Zucker rats suggesting an involvement of NPY in the pathophysiology of the hyperphagic syndrome and genetically determined obesity in Zucker rats. Neither the antagonism of glucocorticoid receptors by mifepristone, nor repeated treatment with 8-OH-DPAT resulting in reduced insulin levels in obese Zucker rats, modified the basal expression of preproNPY mRNA in the arcuate nucleus.
 ...
PMID:Effects of repeated administration of mifepristone and 8-OH-DPAT on expression of preproneuropeptide Y mRNA in the arcuate nucleus of obese Zucker rats. 165 93

Disturbances in hypothalamic beta-endorphin and dynorphin levels were investigated in non-fasted genetically obese (ob/ob) and homozygous lean mice at 14-15 weeks of age. Eight brain regions were microdissected from fresh, unfixed brain slices, and opioid peptide concentrations were determined in tissue micropunches by radioimmunoassay. A two-fold and five-fold increase in beta-endorphin levels in ob/ob versus lean mice were found in the ventromedial and dorsomedial hypothalamic nuclei respectively. Dynorphin levels were comparable between ob/ob and lean mice in the anterior, lateral, ventromedial and paraventricular hypothalamic areas, but a 5-fold increase in dynorphin concentrations was detected in the dorsomedial hypothalamic nucleus of the ob/ob mouse. These results demonstrate that increased concentrations of beta-endorphin and dynorphin occur in discrete hypothalamic nuclei, which are known to influence food intake and glucose homeostasis. This could signify an important central defect contributing to hyperphagia and glucoregulatory dysfunction in obese mice.
 ...
PMID:Increased beta-endorphin and dynorphin concentrations in discrete hypothalamic regions of genetically obese (ob/ob) mice. 168 94

Sugar absorption by the biliary ductular epithelium under steady-state conditions was examined using isolated perfused rat liver. The test sugar and mannitol (as a putative marker of paracellular entry) were added to the glucose-free recirculating perfusate each at a concentration of 5 mmol/L, and apparent active biliary ductular absorption equated with the change in concentration of the test sugar relative to that of mannitol. A metabolizable hexose (D-glucose), pentose (D-xylose), and three nonmetabolizable hexoses (alpha-methyl-glucoside, 3-o-methyl-glucose, and L-glucose) were used. All five monosaccharides were well absorbed at constant rates for 2 hours with apparent rates of absorption (mumol.kg body weight-1.min-1, mean +/- SE) of D-glucose, 0.24 +/- 0.01; L-glucose, 0.20 +/- 0.02; 3-o-methyl-glucose, 0.19 +/- 0.02; alpha-methyl-glucoside, 0.16 +/- 0.03; and D-xylose, 0.10 +/- 0.04. The addition of phloridzin to the perfusate inhibited D-glucose absorption in part but did not inhibit L-glucose absorption. When perfusate Na+ was replaced by N-methylglucamine, the bile-plasma ratio of mannitol remained unchanged, as did the apparent absorption rate of D-glucose and 3-o-methyl-glucose. In contrast, absorption of L-glucose and alpha-methyl-D-glucoside gradually ceased. The addition of 15 mmol/L glucose to the perfusate caused decreased bile flow and increased taurocholate concentration in bile, suggesting that glucose absorption by the biliary ductules induced water reabsorption. It is concluded that sugars are absorbed by the biliary ductular system by Na(+)-dependent and Na(+)-independent transport systems, the substrate affinities of which differ from those reported for apical membrane hexose transport systems in renal tubular and intestinal epithelia. Ductular absorption of solutes such as glucose that enter bile passively may have biological use, because ductular absorption decreases the concentration of substrates for bacterial growth in gallbladder bile. On the other hand, ductular absorption of solutes induces reabsorption of biliary water, resulting in decreased bile flow; this might contribute to cholestasis during prolonged hyperalimentation with solutions containing glucose.
 ...
PMID:Sugar absorption by the biliary ductular epithelium of the rat: evidence for two transport systems. 158 53

Chronic diabetes enhances intestinal absorption of glucose and induces hyperphagia. We examined the enhanced intestinal absorption of glucose in ad libitum-fed rats with streptozocin-induced diabetes mellitus and compared these results with those obtained from pair-fed diabetic animals. Maximal transport capacity (Vmax) and carrier affinity (K0.5) were determined by measuring jejunal and ileal short circuit current (Isc) responses to varying concentrations of 3-O-methyl-D-glucopyranose and D-glucose. Pair-fed diabetic animals maintained the same body weight as animals fed ad libitum, although ad libitum-fed diabetic rats had an increased oral chow intake. Age-matched control rats maintained a constant jejunal and ileal Vmax and K0.5 throughout the study. Diabetic rats fed ad libitum demonstrated an enhanced Vmax and K0.5 in both jejunum and ileum. Pair feeding diabetic animals further enhanced jejunal Vmax while lowering jejunal K0.5 levels. In contrast, pair feeding diabetic animals delayed and blunted changes in ileal Vmax and prevented changes in ileal K0.5. In conclusion, signals other than those of hyperphagia regulate kinetic changes in glucose absorption during diabetes mellitus. Furthermore, these changes have differing effects on jejunum and ileum.
 ...
PMID:Adaptation of intestinal glucose transport in rats with diabetes mellitus occurs independent of hyperphagia. 178 96

The effect of glucose hyperalimentation on energy metabolism in the cirrhotic rat liver after 70% hepatectomy was studied. After resection, rats received either 30 kcal/kg per day (group I) or 200 kcal/kg per day (group II) of glucose for 48 h. In both groups, hepatic mitochondrial ATP synthesis was accelerated when palmitic acid was used as substrate and suppressed when pyruvate was used. This suggests that the energy substrate of the remnant liver was principally fatty acids rather than glucose. Hepatic energy charge was within normal limits in group I, but decreased significantly in group II after hepatectomy. An abundance of glucose in the early postoperative period, therefore, caused a hepatic energy derangement by suppressing fatty acids utilization; this suppression was corroborated by the findings of lower immunoreactive glucagon and non-esterified fatty-acid concentrations in group II. To determine optimal glucose administration, the predicted value of glucose disposal rate (GDR) was calculated after an intravenous glucose tolerance test. GDR decreased significantly after hepatectomy and did not increase appreciably even with a large dose of insulin administration. These results suggest that glucose administration should be tailored to the GDR values after resection of the cirrhotic liver.
 ...
PMID:Glucose overload and hepatic energy metabolism after resection of the cirrhotic liver in rats. 178 71

Prematurity in Indian births is modeled, based on the hypothesis that reduced protein and glucose and aminoacids and maternal anemia and preeclampsia lead to placental dysfunction which is also affected by metabolic disturbance and fetal circulation related to cellular growth and questions about genetics. There may be an ethnic propensity for early maturation of the fetus which affects the higher stillbirth rates and perinatal mortality. It was observed that among, for instance, black and Indian racial groups there may be meconium release and fetal distress. The significance is that physicians should increase antenatal surveillance before 40 weeks. Maternal nutrition should be advanced and hyperalimentation by cordocentesis. Other interventions such as glucose, oxygen, and aspirin administration are still very experimental. The evidence that velocity of growth is different and low birth weight is due to abnormal growth and shortened gestation is currently being researched among different ethnic groups. The discussion is concerned with reports of ethnic variation among Indian and Malay babies in Singapore and babies of French or African ancestry in France. In these studies findings were that the Indians and Malays in Singapore vs. the Chinese had higher mortality, and black African ancestry in mixed ancestry babies was related to higher infant mortality. Another study on neonatal mortality in India led to the recommendation that 2000 gm be established as the limit for defining low birth weight. In the 1501- 2000 gm birth weight groups, 30-45% are preterm, and the remainder are term or postterm. Low birth weight may transcend generations in India even with emigration. Experimental studies show that intrauterine weight is related to placental volume. Reduced growth and lower fetal insulin/glucose ratio with elevated fetal glycine/valine ratio was found to be related to reduced glucose supply among fetuses with fetal hypertriglyceridemia. Fat seems to be lacking among low birth weight fetuses. Studies of somatomedin and somatostatin in metabolism are helping to provide greater understanding of fetal growth processes.
 ...
PMID:The prematurity paradox of the small Indian baby. 180 Mar 24

The paradigm of long-term sleep deprivation was used as a model of chronic inescapable stress in rats. Several basic metabolic parameters (body weight changes, food and water intake, rectal temperature, serum glucose and creatinine), adrenal and thyroid secretion, norepinephrine and dopamine content and turnover in discrete brain regions, and open field behaviour were examined in the course of the exposure to experimental stress. Sleep deprivation over 7-9 days caused complete physical exhaustion of the animals. It was accompanied by hypothermia and hyperphagia. Adrenal activity was characterized by significant hypercorticism, but also by a relative decrease of the responsiveness to ACTH. A gradual decrease in the thyroid secretion was observed. Sleep deprivation elicited a depletion of norepinephrine in the hypothalamus and decreased its turnover, whereas hippocampal norepinephrine content decreased without considerable turnover alterations. Striatal dopamine content and turnover remained unaffected. Behavioural depression and altered open field activity were also observed in exhausted animals. Long-term sleep deprivation, therefore, seems to reproduce some of the biological correlates of the depressive illness, and may be useful in studying the development of coping failure as a result of chronic stress exposure.
 ...
PMID:Neuroendocrine and neurochemical consequences of long-term sleep deprivation in rats: similarities to some features of depression. 181 84


<< Previous 1 2 3 4 5 6 7 8 9 10 Next >>