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)

Altered tissue levels of trace metals have been reported in streptozotocin-diabetic (STZ) rats. To determine whether increased hepatic and renal levels of Cu and Zn were associated with enhanced intestinal absorption, trace metal absorption was studied in control (C) and STZ rats using dietary balance and in situ ligated-loop techniques. The apparent daily absorption of dietary Zn and Cu per 100 g body wt was threefold higher in STZ than C rats. In comparison, dietary Fe absorption per day was not altered. Increased Zn absorption was closely correlated with diabetes-associated polyphagia. The initial rate of injected 65Zn excretion was more rapid in STZ rats, although the rate of excretion beyond day 7 was similar from C and STZ animals. The quantity of Zn, Fe, and Cu absorbed per 20 cm duodenal loop was similar for C and STZ rats. Zn, Fe, and Cu absorption per gram dry mucosa were reduced 45-53% in STZ rats due to the 50% increase in mucosal mass. Moreover, the quantity of radioisotopes accumulated per gram dry mucosa and the concentration of metallothionein per gram mucosal cytosol protein were similar in C and STZ animals. Together, these data demonstrate that increased absorption of dietary Zn and Cu is in part responsible for accumulation of these elements in STZ tissues and suggest altered metal transport at the luminal (brush border) surface of the intestinal epithelium.
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PMID:Zinc, iron, and copper absorption in the streptozotocin-diabetic rat. 682 72

Transport of leucine by the small intestine of obese (ob/ob) mice has been compared with that by intestine of lean controls at various stages in the development of the syndrome. At 10 weeks of age, when hyperphagia and hyperinsulinaemia are at their peak, transport (expressed per gram dry weight) of a physiological concentration of leucine (5 mM) by luminally perfused whole small intestine of obese mice was significantly lower both in vitro (-45%) and in vivo (-27%). Experiments involving fasting and long-term partial dietary restriction of obese mice suggested that the reduction in leucine transport was probably not a consequence of hyperphagia. The absence of any difference between lean and obese mice in the kinetics of unidirectional influx of leucine across the brush border contrasted with the findings from the luminal perfusion experiments. This discrepancy could indicate that the effect of the (ob/ob) genotype on leucine transport was at a stage in the process of transepithelial transport distal to the brush border, perhaps that of movement across the basolateral membrane.
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PMID:Transport of leucine by the small intestine of lean and genetically obese (ob/ob) mice. 682 45

The effects of 1 day of streptozotocin-induced diabetes in rats on glucose transport across the brush border membrane (BBM) and basolateral membrane (BLM) prepared from jejunal enterocytes has been studied. The effects on glucose transport of treatment of diabetic animals with insulin to reduce to normal the elevated blood glucose levels has also been assessed. The maximum capacity (Vmax) for SGLT1-mediated glucose uptake by BBM vesicles was unaffected by diabetes or insulin treatment of diabetic rats. In contrast, Vmax for BLM glucose uptake was increased by 206% in diabetes, a response that could not be reversed by treatment with insulin. Western blotting of BBM for SGLT1 protein revealed a single band with a molecular weight of 73 kDa and the intensity of this band was unaffected by diabetes. However, an increased level of GLUT2 was noted in diabetic BLM and this was not a consequence of changes in glycaemic or insulin status. Diabetes hyperpolarised the BBM, implying an increased driving force for Na(+)-sugar co-transport but insulin treatment only partially reversed this enhanced potential difference. Benzamil (2 microns), an epithelial Na+ channel blocker, hyperpolarised the BBM of control but not diabetic enterocytes, implying that a reduced Na+ permeability was responsible for the diabetic hyperpolarisation. It was concluded that in early diabetes, before the onset of hyperphagia, a greater driving force for Na(+)-dependent BBM sugar transport together with increased GLUT2 activity at the BLM promotes sugar movement across the enterocyte. Possible triggers for the transport responses are discussed.
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PMID:Early diabetes-induced changes in rat jejunal glucose transport and the response to insulin. 924 34