Summary A lower concentration of intracellular myo-inositol has been implicated in the development of diabetic nephropathy. This was based on short-term studies showing that early administration of aldose reductase inhibitors or myo-inositol supplementation reduces increased glomerular filtration rate and partly reduces increased urinary albumin excretion in streptozotocin diabetic rats. We studied the effect of long-term (4 months) administration of 1% myo-inositol supplement to the Cohen diabetic (type 2) rat on the development of nephropathy and renal Na+-K+-ATPase. This treatment reduced the increased renal Na+-K+-ATPase activity but had no effect on blood glucose levels, body weight, increased kidney weight, or creatinine clearance and did not prevent or reduce the development of renal glomerular pathology. There was no correlation between the level of Na+-K § ATPase activity and the degree of nephropathy. It is possible that the renal pathological changes are due to metabolic and humoral factors resulting from hyperglycaemia, other than myo-inositol depletion. The fact that rnyo-inositol treatment had no effect on the development of renal pathological changes but was shown to have a beneficial effect on restoring impaired conduction velocity and on the disruption of structural elements in the nerve indicates that the effect of the biological changes ensuing from hyperglycaemia vary in different tissues depending on local conditions. [Diabetologia (1995) 38: 899-905] Key words Non-insulin-dependent diabetes mellitus (type 2), myo-inositol, glomerulosclerosis, Na+-K +-ATPase, Cohen-diabetic rat.It has been suggested that polyol pathway hyperactivity contributes to the pathogenesis of diabetic renal complications [1][2][3][4]. This was based on the observation that treatment with aldose reductase inhibitors and myo-inositol supplements reduces the increased glomerular filtration rate [5,6] Abbreviations: Pi, Inorganic phosphate; IDDM, insulin-dependent diabetes mellitus; NIDDM, non-insulin-dependent diabetes mellitus; STZ-D, streptozotocin diabetic rats; GS, glomerulosclerosis; PG, prostaglandin.creased urinary albumin excretion [6][7][8] in diabetic animals.Most of these observations have been made in short-term type i streptozotocin diabetic rats (SZT-D). The purpose of the present study was to evaluate the effect of long-term supplementation of myo-inositol in the Cohen diabetic rat (type 2) on the development of pathological changes and Na+-K+-ATPase activity in the kidneys. Materials and methodsAnimals. The Cohen diabetic rat shares essential features with human non-insulin-dependent diabetes such as genetic and environmental disposition [9], an early phase of hyperinsulinaemia, and insulin resistance, followed by hypoinsulinaemia [10], a decreased number and sensitivity of insulin receptors
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