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)

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.
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PMID:Sugar absorption by the biliary ductular epithelium of the rat: evidence for two transport systems. 158 53

The possibility of alterations in the metabolism of glucose in the small intestine of C57BL/6J (ob/ob) obese-diabetic mice has been investigated. Glucose metabolism was assessed by direct measurement in vitro, and by assaying the activities of glycolytic and pentose phosphate pathway enzymes. The small intestine of 3-week-old obese mice exhibited a reduced glucose metabolism and hexokinase activity in comparison with lean controls. In adult animals there was little evidence for an effect of hyperphagia or hyperinsulinaemia on metabolism of glucose supplied from the lumen, except that the elevated pyruvate kinase activity in the intestinal mucosa of 20-week-old obese mice might have been a consequence of hyperinsulinaemia.
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PMID:Metabolism of glucose in the small intestine of lean and obese (ob/ob) mice. 663 48

We have studied in Macaca mulatta both the gastric emptying of glucose, D-xylose, and fructose and the effects of these sugars on feeding. Glucose and D-xylose empty in the same fashion, i.e., linearly and more slowly with increasing concentration so that the delivery of solute to the small intestine is constant at 0.1 g/min over time and across concentrations. Fructose empties exponentially and more rapidly than the other sugars. When solutions of each of these sugars (37.5 g in 150 ml) preceded the monkey's daily 4-h feeding period there was a similar total reduction in food intake for each. However, fructose inhibited food intake in the first 2 h of feeding less than did the other sugars just as it inhibited gastric emptying less. D-Xylose, although mimicking glucose in both gastric emptying and feeding on the experimental day, produced, as it is poorly metabolized, a caloric deficit replaced by overeating on the subsequent control day. We conclude from the similarities between glucose and xylose that the stomach, while emptying nutrients, influences feeding and can be at least one source of signals for preabsorptive satiety and caloric homeostasis. The results with fructose require that other sites must be active to permit a similar regulation of feeding to occur despite differing gastric emptying characteristics.
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PMID:Distinctions among three sugars in their effects on gastric emptying and satiety. 724 98

Energy supply may be a limiting factor in tissue repair when infants with severe prolonged diarrhoea are fed orally. Xylose tolerance tests were done on 8 female infants who had had severe dehydrating diarrhoea requiring treatment in hospital for 7 days. Seven infants had flat xylose tolerance curves, 5 of these being at very low levels. Very early intervention with hyperalimentation, elemental diets or antibacterial agents and basic anion exchange resins may reduce morbidity.
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PMID:Xylose absorption in infants with severe prolonged diarrhoea. 742 1

ChREBP is the master regulator of carbohydrate dependent glycolytic and lipogenic flux within metabolic tissues. It plays a vital role in hyper-calorific milieu by activating glycolysis, lipogenesis along with pentose phosphate shunt and glycogen synthesis, fostering immediate reduction in the systemic glycemic levels. Liver being the primary organ to sense disproportionate dietary intake and linked physiological stress, stimulates ChREBP to perform the aforementioned processes. Activated ChREBP also inhibits lipolysis and encourages proper disposal of excessive triglycerides into adipocytes from the liver ablating hepatic intracellular lipid trafficking. Chronic overeating or onset of positive energy balance, hyper-activates ChREBP and signals development, intensification of hepato-metabolic disorders, and allied discrepancies in the whole-body metabolic functioning. ChREBP thus gets negatively connotated as the primary regulator of hepatic disorders, owing to its inherent features as the primary glycemic sensor and the only transcription factor that can transduce glucose-dependent glycolytic and lipogenic signals. Through this review, we - try to recapitulate and emphasize on the sanative events coordinated by ChREBP in several pathophysiological states. In totality, we aim to uncouple the disease-causing aspects of ChREBP from its positive attributes evoked during a metabolic crisis, in hepato-metabolic diseases.
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PMID:Causative and Sanative dynamicity of ChREBP in Hepato-Metabolic disorders. 3323 83