Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0011849 (diabetes)
277,896 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Adrenal growth occurs in experimental diabetes, and evidence exists for increased adrenal function. The concentration of PPRibP has been examined in the rat adrenal gland at various times after induction of diabetes with STZ, in view of the key role it plays in the synthesis of Purs and Pyrs. The PPRibP level was exceptionally high in the adrenal gland and increased faster than the rate of growth during the initial rapid growth phase--the first 7 days after STZ was given; PPRibP synthetase showed a parallel increase. Formation of R5P via the oxidative and nonoxidative segments of the PPP also was measured. The oxidative enzymes, G-6-PD and 6-PGD, increased in parallel with growth during the early phase, but showed a more marked rise during the secondary, slower, growth phase seen 6 wk after STZ was given, when this may be associated with the known sustained rise in plasma corticosteroids. The nonoxidative enzymes of the PPP, an alternate route for the production of R5P, showed smaller changes. The specifically high adrenal concentration of PPRibP may be related to the high Km for PPRibP (250 microM) of the first enzyme of the de novo pathway of Pur synthesis, as such synthesis may be required in the rat to replace the net loss of ATP associated with catecholamine secretion. Factors controlling PPRibP synthetase and their potential relative importance in the adrenal gland have been considered.
Diabetes 1992 Nov
PMID:Phosphoribosyl pyrophosphate formation in the rat adrenal gland in relation to adrenal growth in experimental diabetes. 138 69

The effect of developmental growth on the kidney content of phosphoribosyl pyrophosphate PPRibP was studied in rats at ages between the foetal animal and up to 100 days of age. In addition, the effect of short-term diabetes (up to 14 days) on the renal content of PPRibP was studied in immature rats and in adults aged approx. 60 days. The developmental pattern of PPRibP is such that the PPRibP content is lowest in the young rat and increases as the rate of kidney growth slows. In the adult rat, the early kidney hypertrophy of diabetes is accompanied by a fall in PPRibP content and, again, the PPRibP content returns to normal as the rate of kidney hypertrophy diminishes. Induction of diabetes in the immature rat causes a lesser degree of kidney hypertrophy and also a smaller depression of renal PPRibP content. The activity of PPRibP synthetase (EC 2.7.6.1) is not significantly affected by age or diabetes. The changes in PPRibP content are discussed in relation to the generation of ribose 5-phosphate by the pentose phosphate pathway and the utilization of PPRibP for nucleotide synthesis via the 'de novo' and salvage pathways.
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PMID:Concentration of phosphoribosyl pyrophosphate in the kidney during development and in experimental diabetic hypertrophy. 242 32

Measurements were made of the activity of phosphoribosyl pyrophosphate amidotransferase (PPRibP-At, EC 2.4.2.14) and of adenine (APRT, EC 2.4.2.7) and hypoxanthine (HPRT, EC 2.4.2.8) phosphoribosyltransferases, representing the 'de novo' and salvage pathways respectively. PPRibP-At activity increased within 3 days of diabetes, whereas APRT and HPRT increased later. Incorporation of [14C]formate and of [8-14C]adenine into the nucleic acids of kidney slices showed that formate was incorporated earlier, and to a greater extent, than was adenine. These results indicate that, although the 'de novo' pathway for nucleotide synthesis is the main route in early diabetes, the salvage pathway assumes greater importance at later stages.
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PMID:Renal hypertrophy in experimental diabetes. The activity of the 'de novo' and salvage pathways of purine [corrected] synthesis. 245 5

The lens has a very high content of UDP sugars. These are required for glycoprotein and proteoglycan synthesis, as components of fiber cell membranes and the capsule. In diabetes, changes in these sugar nucleotides are related to pathological changes in the basement membranes of cells from non-insulin-requiring tissues. We have investigated whether this is the case in the lens in diabetes and we report here that UDP-sugar levels are, in contrast to the norm in other non-insulin-requiring tissues, decreased at 2 and 4 weeks of diabetes. This is despite an elevation in the precursors of their formation, both of the pyrimidine (PPRibP) and carbohydrate (glucose, glucose 6-phosphate) components. Also reported here is the observation that lens pyrimidine biosynthesis occurs primarily by the de novo route, and that orotate phosphoribosyltransferase and orotidine-5'-phosphate decarboxylase are unchanged in diabetes. We have measured the energy charge of the adenine and uridine nucleotide pools and report both to be compromised under the diabetic condition. The fall in ATP provision is proposed to be responsible for the fall in UTP and hence leads to the recorded decrease in the UDP sugars. These changes are discussed in relation to the change in capsular and fiber cell composition and the functional significance of this in cataract formation.
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PMID:Changes in uridine nucleotides and uridine nucleotide sugars in diabetic rat lens: implications in membrane glycoprotein formation. 812 94