Influence of experimental diabetes on the kinetic behaviour of renal cortex hexose monophosphate dehydrogenases

Peragón, Juan; Aranda, Fermín; Salguero, Leticia García; Lupiáñez, José A.

doi:10.1016/0020-711x(89)90391-1

Cited by 13 publications

(5 citation statements)

References 36 publications

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“…However, transketolase activity was decreased during the early phase [47]. These alterations have been implicated in development of renal hypertrophy [46]. Also, in studies performed on isolated rat glomeruli, elevation of glucose levels increased G6P, fructose-6-phosphate, total triose phosphates, lactate, lactate/ pyruvate ratio, sorbitol and fructose, but did not affect snglycerol 3-phosphate or pyruvate levels [48].…”

Section: Pentose Phosphate Shuntmentioning

confidence: 96%

“…Kinetics of the renal pentose phosphate shunt enzymes are altered also in animal models of experimental diabetes [46]. In another study of the effect on enzyme activity during different periods of diabetes, the oxidative segment and glucose flux displayed increased activity during the first 7 days after onset of diabetes.…”

Section: Pentose Phosphate Shuntmentioning

confidence: 97%

“…Studies show that chronic metabolic acidosis, such as untreated or suboptimally treated diabetes, activates both G6P dehydrogenase and 6-phosphogluconate dehydrogenase [45,46]. Kinetics of the renal pentose phosphate shunt enzymes are altered also in animal models of experimental diabetes [46].…”

Section: Pentose Phosphate Shuntmentioning

confidence: 99%

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Diabetes-Induced Alterations in Renal Medullary Microcirculation and Metabolism

Nordquist¹,

Palm²

2007

CDR

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Diabetes-induced renal complications, i.e. diabetes nephropathy, are a major cause of morbidity and mortality. The exact mechanisms mediating the negative influence of hyperglycemia on renal function are unclear, although several hypotheses have been postulated. Cellular mechanisms include glucose-induced excessive formation of reactive oxygen species, increased glucose flux through polyol pathway and pentose phosphate shunt, formation of advanced glycation end-products and activation of protein kinase C and NADPH oxidase. However, the renal effects in vivo of each and every one of these mechanisms are less clear, although recent studies have shown several major alterations predominantly in the renal medulla as a result of sustained hyperglycemia. Already during normal conditions, the renal medulla has a remarkably low oxygen tension (PO2) and a high degree of non-oxygen dependent energy metabolism. Alterations in either blood perfusion or oxygen delivery to the medullary region will have significant effects on both regional metabolism and total kidney function. Recently, sustained hyperglycemia has been shown to induce a pronounced reduction in preferentially renal medullary PO2. This review will present the current knowledge of diabetes-induced alterations in renal medullary metabolism and function, but also discuss future targets for prevention of diabetic nephropathy.

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Section: Pentose Phosphate Shuntmentioning

confidence: 96%

Section: Pentose Phosphate Shuntmentioning

confidence: 97%

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Diabetes-Induced Alterations in Renal Medullary Microcirculation and Metabolism

Nordquist¹,

Palm²

2007

CDR

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“…These results clearly indicate that trout liver undergoes protein repression-induction processes under these two contrasting nutritional conditions. rainbow trout; low-fat and high-carbohydrate diet; glucose-6phosphate dehydrogenase; 6-phosphogluconate dehydrogenase; malic enzyme; dimeric banding pattern; immunohistochemistry THE SUPPLY OF REDUCING equivalents in the form of NADPH is one of the most important factors related to cell growth, proliferation, and detoxification (3,23,24). NADPH, one of the principal end products of several metabolic pathways, is also an indispensable substrate of reductive biosynthetic reactions (34).…”

mentioning

confidence: 99%

“…It is also well established that in higher vertebrates the activity of hexose monophosphate dehydrogenases in various tissues changes under different nutritional and hormonal conditions (10,16,23,24,34). Nevertheless, in fish, the adaptive response of these NADPHproduction enzyme systems to such conditions has not been completely characterized (2,4,18,27).…”

mentioning

confidence: 99%

Impact of starvation-refeeding on kinetics and protein expression of trout liver NADPH-production systems

Barroso

Peragón

Contreras‐Jurado³

et al. 1998

American Journal of Physiology-Regulatory, Integrative and Comp

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Herein we report on the kinetic and protein expression of glucose-6-phosphate dehydrogenase (G6PDH), 6-phosphogluconate dehydrogenase, and malic enzyme (ME) in the liver of the trout ( Oncorhynchus mykiss) during a long-term starvation-refeeding cycle. Starvation significantly depressed the activity of these enzymes by almost 60%, without changing the Michaelis constant. The time response to this nutritional stimulus increased with fish weight. The sharp decline in G6PDH and ME activities was due to a specific protein-repression phenomenon, as demonstrated by molecular and immunohistochemical analyses. Also, the dimeric banding pattern of liver G6PDH shifted from the fully reduced and partially oxidized forms, predominant in control, to a fully oxidized form, more sensitive to proteolytic inactivation. Refeeding caused opposite effects in both protein concentration and enzyme activities of about twice the control values in the first stages, later reaching the normal enzyme activity levels. Additionally, the partially oxidized form of G6PDH increased. The kinetics of these enzymes were examined in relation to the various metabolic roles of NADPH. These results clearly indicate that trout liver undergoes protein repression-induction processes under these two contrasting nutritional conditions.

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