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)

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

Adult female rats were allowed to self-select their diet from separate sources of fat, protein, and carbohydrate (starch). Other rats were fed a composite diet that matched the nutrient composition chosen by the self-selecting rats (50% fat, 28% protein, 22% carbohydrate) or a low-fat, high-carbohydrate chow diet. Half of the rats in each diet condition were given access to a 32% sucrose solution for 30 days. Sucrose availability increased total caloric intake (approximately 20%) and body weight gain in all three groups compared to control groups not fed the sucrose solution. The selection animals compensated for their sucrose intake by reducing their fat intake, and to a lesser degree, their starch intake; protein intake was the least affected by sucrose availability. The selection rats consumed less sucrose than the chow-fed rats and displayed a smaller increase in weight, relative to controls, than the chow-fed rats. These differences were attributed to the high-fat intake of the selection animals since similar results were obtained with the rats fed the composite diet. In particular, both the selection and composite diets produced mild obesity in the absence of sucrose. The results demonstrate that sucrose-induced overeating and overweight is not an artifact of restraining the diet choices of rats to a pure sugar and a nutritionally complete diet.
 ...
PMID:Sucrose-induced hyperphagia and obesity in rats fed a macronutrient self-selection diet. 323 24

Adult male Sprague-Dawley rats were divided into three groups and fed diets containing either 10, 20, or 40% protein for 56 days. Half of the rats in each dietary condition were given a 32% sucrose solution plus the standard diet and water. Sucrose intake varied directly as a function of dietary protein levels. Rats fed either the 10 or 20% protein diet and sucrose had higher caloric intakes, gained more weight, were more efficient at using calories for weight gain, and had more adipose tissue than rats given the same diet without sucrose. Rats fed the 40% protein diet and sucrose did not exhibit overeating, excess weight gain, or increased feed efficiency relative to animals fed the 40% diet alone. Animals given sucrose had more interscapular brown adipose tissue (IBAT) and a greater metabolic potential for thermogenesis in IBAT as determined by GDP binding in mitochondria than rats not fed sucrose. These results demonstrate that dietary protein is important in the development of sucrose-induced obesity and that increases in IBAT mass and activity can occur concomitant with increased feed efficiency.
 ...
PMID:Sucrose-induced obesity: effect of diet on obesity and brown adipose tissue. 360 81

During cold-induced nonshivering thermogenesis, interscapular brown adipose tissue (BAT) lipoprotein lipase (LPL) activity and lipogenesis are elevated. Because of the many similarities between cold- and diet-induced thermogenesis, we examined the effect of ad libitum access to a 32% sucrose solution on caloric intake, adiposity, and BAT enzyme activities in male rats. Daily caloric intakes of sucrose-fed animals were elevated by 20%-25%, and 8 wk of sucrose feeding doubled carcass fat content. This sucrose-feeding induced obesity was associated with increases in circulating triglyceride and insulin levels as well as increased retroperitoneal white adipose tissue LPL activity. However, the increased carcass lipid content accounted for less than half of the excess calories ingested by the sucrose-fed rats. Sucrose feeding stimulated in vivo lipogenesis in BAT and elevated BAT fatty acid synthetase and acetyl-CoA carboxylase activities but not LPL activity. These findings suggest that overeating enhances endogenous lipogenesis but not uptake of circulating triglyceride in BAT. Thus, both cold- and diet-induced thermogenesis increase BAT lipogenesis, while only cold-induced thermogenesis is associated with elevated LPL activity in BAT.
 ...
PMID:Effect of sucrose overfeeding on brown adipose tissue lipogenesis and lipoprotein lipase activity in rats. 682 91

Four groups of adult rats, housed on a 12-12, light-dark cycle, were allowed access to a nutritionally complete diet and water. Three of these groups were also offered a 32% solution of sucrose. The sucrose was available for either the 24-hour period, the 12 hours of light or the 12 hours of dark. Access to sucrose led to overeating and excessive weight gain. These effects were more pronounced when the sucrose was available for the 24-hour period or during the dark. Limited access to sucrose produced a reversal of the rat's usual circadian pattern of feeding when the sucrose was available during the light and increased the rat's nocturnal hyperphagia when it was available during the dark. Sucrose intake and the proportion of calories taken from sucrose were higher in the 24-hour access group and the dark access group than the light access group. Access to sucrose did not induce a pattern of dietary selection that compromised growth or health. It appears that access to a palatable carbohydrate solution can lead to overeating and major changes in the circadian organization of feeding behavior. These data emphasize the potent role that external factors can play in the control of ingestive behavior.
 ...
PMID:Effect of limited access to sucrose on overeating and patterns of feeding. 712 19

While opioid agonists administered into the hypothalamic paraventricular nucleus increase food intake in rats, naloxone reduces deprivation-induced intake. Ventricular administration of either mu (beta-funaltrexamine) or kappa (nor-binaltorphamine) opioid antagonists reduces spontaneous, deprivation, glucoprivic and palatable intake. The present study assessed whether microinjections of either general, mu or kappa opioid antagonists into the paraventricular nucleus altered either deprivation (24 h) intake, 2-deoxy-D-glucose hyperphagia or sucrose intake in rats. Deprivation intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 30-33%), beta-funaltrexamine (5 micrograms, 100 nmol, 26-29%) or naltrexone (10 micrograms, 260 nmol, 26%) in the paraventricular nucleus. 2-Deoxy-D-glucose hyperphagia was significantly reduced only after 2 h by naltrexone (10 micrograms, 260 nmol, 69%), norbinaltorphamine (20 micrograms, 272 nmol, 69%) or beta-funaltrexamine (20 micrograms, 400 nmol, 83%) in the paraventricular nucleus. Sucrose intake was significantly reduced by nor-binaltorphamine (5 micrograms, 68 nmol, 27-36%), naltrexone (5-10 micrograms, 130-260 nmol, 18-31%) and beta-funaltrexamine (5 micrograms, 100 nmol, 20%) in the paraventricular nucleus. These data indicate that general, mu and kappa opioid antagonists administered into the hypothalamic paraventricular nucleus produce similar patterns of effects upon different forms of food intake as did ventricular administration, implicating this nucleus as part of the circuitry underlying opioid mediation of ingestion.
 ...
PMID:Alterations in deprivation, glucoprivic and sucrose intake following general, mu and kappa opioid antagonists in the hypothalamic paraventricular nucleus of rats. 765 22

Ventricular microinjection studies found that whereas mu (beta-funaltrexamine, B-FNA), mu1 (naloxonazine) and kappa (nor-binaltorphamine, Nor-BNI) opioid receptor antagonists, but not delta antagonists, reduce deprivation-induced intake, kappa and mu, but not mu1 or delta antagonists reduce both 2-deoxy-D-glucose (2DG) hyperphagia and sucrose intake. Since opioid agonists stimulate spontaneous food intake in the accumbens, the present study examined whether administration of either naltrexone, B-FNA or Nor-BNI in the accumbens altered intake under deprivation (24 h), glucoprivic (2DG: 500 mg/kg, i.p.) or palatable sucrose (10%) conditions. Naloxonazine's effects in the accumbens were also evaluated for deprivation-induced intake. Deprivation-induced intake was significantly decreased over 4 h by naltrexone (5-20 micrograms, 44%), B-FNA (1-4 micrograms, 55%) and Nor-BNI (4 micrograms, 31%) but not naloxonazine (10 micrograms) in the accumbens. 2DG hyperphagia was significantly decreased by naltrexone (10-20 microgram, 79%), B-FNA (1-4 micrograms, 100%) and NOR-BNI (104 micrograms, 75%) in the accumbens. Sucrose intake was significantly decreased by naltrexone (50 micrograms, 27%) and B-FNA (1-4 micrograms, 37%), but not NOR-BNI in the accumbens. These data suggest that mu receptors, and particularly the mu2 binding site in the accumbens are responsible for the opioid modulation of these forms of intake in this nucleus, and that this control may be acting upon the amount of intake per se.
 ...
PMID:General, mu and kappa opioid antagonists in the nucleus accumbens alter food intake under deprivation, glucoprivic and palatable conditions. 862 11

Opioid receptor subtype antagonists differentially alter food intake under deprivation (24 h), glucoprivic (2-deoxy-D-glucose, 500 mg/kg, i.p.) or palatable (10% sucrose) conditions with mu (beta-funaltrexamine) and kappa (nor-binaltorphamine), but not delta1 ([D-Ala2,Leu5,Cys6]enkephalin) opioid antagonists reducing each form of intake following ventricular microinjection. Both mu and kappa opioid antagonists microinjected into either the hypothalamic paraventricular nucleus or the nucleus accumbens reduce intake under deprivation and glucoprivic conditions. Palatable intake is reduced by both antagonists in the paraventricular nucleus, but only mu antagonists are active in the accumbens. Food intake is stimulated by mu and delta, but not kappa, opioid agonists microinjected into the ventral tegmental area. The present study examined whether food intake under either deprivation, glucoprivic or palatable conditions was altered by bilateral administration of general (naltrexone), mu, kappa, delta1 or delta2 (naltrindole isothiocyanate) opioid antagonists into the ventral tegmental area. Deprivation (24 h)-induced feeding was significantly reduced by high (50 microg), but not lower (10-20 microg) doses of naltrexone (21%), and by delta2 (4 microg, 19%) antagonism in the ventral tegmental area. 2-Deoxy-D-glucose (500 mg/kg, i.p.)-induced hyperphagia was significantly reduced by high (50 microg), but not lower (20 microg) doses of naltrexone (64%), and by delta2 (4 microg, 27%) antagonism in the ventral tegmental area. Sucrose (10%) intake was significantly reduced by naltrexone (20-50 microg, 25-39%) and delta2 (4 microg, 25%) antagonism in the ventral tegmental area. Neither mu, kappa nor delta1 antagonists were effective in reducing any form of intake following microinjection into the ventral tegmental area. These data indicate that the ventral tegmental area plays a relatively minor role in the elicitation of these forms of food intake, and that delta2, rather than mu, kappa or delta1 opioid receptors appear responsible for mediation of these forms of intake by this nucleus.
 ...
PMID:Evaluation of opioid receptor subtype antagonist effects in the ventral tegmental area upon food intake under deprivation, glucoprivic and palatable conditions. 936 10

The neurosteroid allopregnanolone may increase feeding by altering food palatability; however, it may also increase feeding by reducing anxiety (neophobia). Moreover, it is unclear whether this induced hyperphagia is selective to safe, palatable foods only. Male rats were injected with allopregnanolone 20 min prior to behavioral testing. The taste reactivity test was used to examine possible shifts in the palatability of a 0.3 M sucrose solution. A lickometer was used to monitor intake and licking of either a sucrose or sucrose-quinine solution. Sucrose palatability was not enhanced; however, allopregnanolone significantly increased sucrose intake and licking on Test Day 1 when the solution was novel, but not on Test Day 2 when the solution was familiar. Sucrose-quinine intake was not enhanced. Allopregnanolone-induced hyperphagia is not a result of altered sucrose palatability, but rather reflects a reduction in the neophobia elicited by a novel solution; an effect that further seems to be selective to safe, palatable foods.
 ...
PMID:Allopregnanolone produces hyperphagia by reducing neophobia without altering food palatability. 1624 29

In view of an effect of high intake of sugar on brain serotonin (5-hydroxytryptamine, 5-HT) and a role of serotonin in the regulation of appetite, the present study concerns pre and postsynaptic responses to a selective 5-HT-1A receptor agonist 8-hydroxy-2-(di-n-propylamino) tetralin (8-OH-DPAT) following long term consumption of sugar as part of meal in rats. Sugar diet was prepared by mixing standard rodent diet and table sugar in ratio of 3:1 (w/w) and rats were fed freely on this diet for five weeks. Control rats were fed freely on standard rodent diet. After five weeks 8-OH-DPAT at a dose of 0.5mg/kg/ml was injected to both the groups to compare effectiveness of the drug to elicit hyperphagia (presynaptic response) and elicited hyperactivity syndrome (postsynaptic response). Results showed that 8-OH-DPAT-induced forepaw treading and flatbody posture were smaller in sugar than normal diet treated rats. Conversely 8-OH-DPAT-induced hyperlocomotion was greater in sugar than normal diet treated rats. 4h Food consumption was greater in sugar than normal diet treated rats while 8-OH-DPAT-induced hyperphagia significant in normal diet treated rats was not observed in sugar diet treated rats. The results show a decrease in the effectiveness of pre as well as postsynaptic 5-HT-1A receptor dependent responses following long term consumption of sugar diet. Role of serotonin receptor responsiveness on mood and impaired adaptation to stress is discussed.
 ...
PMID:Effects of long term consumption of sugar as part of meal on serotonin 1-a receptor dependent responses. 1675 Nov 17


1 2 Next >>