Factors affecting the formation of sugar alcohols in ocular lens

Kinoshita, Jin H.; Futterman, Sidney; Satoh, Kenshi; Merola, L

doi:10.1016/0006-3002(63)91377-5

Cited by 119 publications

(33 citation statements)

References 20 publications

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“…In fair agreement with a prior obser vation [34], the oxidation of £>-[l-l4C]glucose was much higher, being commensurate with the rate of sorbitol formation. For in stance, at 37 °C and in the presence of 15 mM D-glucose, the rate of /)-[l-l4C]glucose oxidation was estimated at about 2.9 nmol/60 min/lens.…”

Section: Metabolism Ofd-glucose At Anomeric Equilibriumsupporting

confidence: 77%

Metabolism of D-Glucose Anomers in Rat Lens

Sterling¹,

Sener²,

Malaisse³

1988

Ophthalmic Res

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In lens homogenates, hexokinase displayed a greater affinity for α-D-glucose but a higher maximal velocity with β-D-glucose. However, in intact lenses incubated at 10 ^¤ C in the presence of 4–7 mM α- or β-D-glucose, no anomeric difference could be found in either the intracellular content in D-glucose and D-glucose 6-phosphate or the utilization of D-[5–³H]glucose and oxidation of D-[1-¹⁴C]glucose. Even the sorbitol content of the lens was not significantly different after 180 min perifusion at 37 °C in the presence of either α- or β-D-glucose. It is proposed that the lack of anomeric specificity in D-glucose metabolism is attributable, at least in part, to the low turnover rate of glucose 6-phosphate in the lens, allowing for the interconversion of glucose 6-phosphate anomers.

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Section: Metabolism Ofd-glucose At Anomeric Equilibriumsupporting

confidence: 77%

Metabolism of D-Glucose Anomers in Rat Lens

Sterling¹,

Sener²,

Malaisse³

1988

Ophthalmic Res

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“…If these sugar alcohols are generated in the brain during hyperglycemia and are unable to leave the central nervous system when the blood glucose is rapidly lowered, they might act as osmotically active particles, attracting water into the brain and leading to cerebral edema (11). During hyperglycemia, the concentration of sorbitol has been shown to increase in aorta (38), peripheral nerve (39,40), ocular lens (41), and in the CSF (11). When the plasma glucose in hyperglycemic dogs is rapidly lowered by intravenous infusion of 0.9% NaCl, the CSF pressure increases concomitant with a further increase in CSF sorbitol (11).…”

Section: Treatment With Peritoneal Dialysismentioning

confidence: 99%

Studies on Mechanisms of Cerebral Edema in Diabetic Comas. EFFECTS OF HYPERGLYCEMIA AND RAPID LOWERING OF PLASMA GLUCOSE IN NORMAL RABBITS

Arieff¹,

Kleeman²

1973

J. Clin. Invest.

182

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A B S T R A C T To investigate the pathophysiology of cerebral edema occurring during treatment of diabetic coma, the effects of hyperglycemia and rapid lowering of plasma glucose were evaluated in normal rabbits. During 2 h of hyperglycemia (plasma glucose = 61 mM), both brain (cerebral cortex) and muscle initially lost about 10% of water content. After 4 h of hyperglycemia, skeletal muscle water content remained low but that of brain was normal. Brain osmolality (Osm) (343 mosmol/kg H20) was similar to that of cerebrospinal fluid (CSF) (340 mosmol/kg), but increases in the concentration of Na+, K+, Cl-, glucose, sorbitol, lactate, urea, myoinositol, and amino acids accounted for only about half of this increase. The unidentified solute was designated "idiogenic osmoles". When plasma glucose was rapidly lowered to normal with insulin, there was gross brain edema, increases in brain content of water, Na+, K+, Cl-and idiogenic osmoles, and a significant osmotic gradient from brain (326 mosmol/ kg H20) to plasma (287 mosmol/kg). By similarly lowering plasma glucose with peritoneal dialysis, increases in brain Na+, K+, Cl-, and water were significantly less, idiogenic osmoles were not present, and brain and plasma Osm were not different. It is concluded that during sustained hyperglycemia, the cerebral cortex adapts to extracellular hyperosmolality This work was presented in part at International Symposium on the

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“…Aldose reductase requires NADPH as a cofactor, which is provided primarily through the activity of the hexosemonophosphate shunt. A nearly stoichiometric relationship between the hexosemonophosphate shunt activity (NADPH production) and sorbitol formation has been demonstrated for lens (1) and nerve (2). Recent studies indicate an important role for the sorbitol pathway in the etiology of diabetic and galactosemic cataract formation (3), neuropathy (4,5), and tubular nephropathy (6).…”

mentioning

confidence: 99%