Abnormally Increased Glomerular Filtration Rate in Short-term Insulin-treated Diabetic Subjects

Ditzel, Jørn; Schwartz, Michael W.

doi:10.2337/diab.16.4.264

Cited by 134 publications

(45 citation statements)

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“…Several investigators have demonstrated an increase in PG synthesis in glomerular and mesangial cells in experimental diabetes, and some studies have postulated a role for vasodilatory PGs in the glomerular hyperfiltration observed in early diabetes (3,4). A similar trend was observed in our results of hyperglycemia-induced PGE 2 synthesis in HMCs, as shown in Fig.…”

Section: Discussionsupporting

confidence: 79%

“…Glomerular hyperfiltration is a characteristic finding of early diabetes in both humans and animal models of diabetes and may play a major role in the pathogenesis of diabetic nephropathy (3,4). The mechanisms that mediate an increase in glomerular filtration rate are not well identified, but the vascular reactivity of the renal glomerular efferent arterioles has been shown to be controlled, at least in part, by the release of endogenously synthesized prostaglandins (PGs), allowing autoregulation of glomerular capillary pressure (5).…”

mentioning

confidence: 99%

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Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

et al. 2003

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Hyperglycemia increases the production of reactive oxygen species (ROS) from the mitochondrial electron transport chain in bovine endothelial cells. Because several studies have postulated a role for prostaglandins (PGs) in the glomerular hyperfiltration seen in early diabetes, we evaluated the effect of mitochondrial ROS on expression of the inducible isoform of cyclooxygenase (COX-2) in cultured human mesangial cells (HMCs). We first confirmed that incubation of HMC with 30 mmol/l glucose significantly increased COX-2 mRNA but not COX-1 mRNA, compared with 5.6 mmol/l glucose. Similarly, incubation of HMCs with 30 mmol/l glucose significantly increased mitochondrial membrane potential, intracellular ROS production, COX-2 protein expression, and PGE2 synthesis, and these events were completely suppressed by thenoyltrifluoroacetone or carbonyl cyanide m-chlorophenylhydrazone, inhibitors of mitochondrial metabolism, or by overexpression of uncoupling protein-1 or manganese superoxide dismutase. Furthermore, increased expression of COX-2 mRNA and protein was confirmed in glomeruli of streptozotocin-induced diabetic mice. In addition, hyperglycemia induced activation of the COX-2 gene promoter, which was completely abrogated by mutation of two nuclear factor κB (NF-κB) binding sites in the promoter region. Our results suggest that hyperglycemia increases mitochondrial ROS production, resulting in NF-κB activation, COX-2 mRNA induction, COX-2 protein production, and PGE2 synthesis. This chain of events might contribute to the pathogenesis of diabetic nephropathy.

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Section: Discussionsupporting

confidence: 79%

mentioning

confidence: 99%

Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

et al. 2003

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“…These alterations constitute the characteristic features of diabetic microangiopathy [1]. While the morphological thickening of basal laminae has been well documented in various tissues [2][3][4][5][6], the biochemical and functional alterations, which concern the composition of basal lamina material and the loss of the filtration selectivity, accompanied by an increase in capillary permeability, have been well described only for the glomerulus and for a preparation of isolated capillaries [7][8][9][10][11][12]. However, a controversy has been raised concerning the biochemical changes occurring in the diabetic glomerular basal laminae [13].…”

mentioning

confidence: 99%

Alteration in the distribution of type IV collagen in glomerular basal laminae in diabetic rats as revealed by immunocytochemistry and morphometrical approach

Bendayan

1985

Diabetologia

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Summary.The gomerular basal laminae of normoglycaemic and long-term streptozotocin-induced hyperglycaemic rats was studied by morphometrical and immunocytochemical approaches. Using the orthogonal intercept method, we have confirmed that in long-term diabetes, the thickness of the glomerular basal laminae increases significantly. Applying the high resolution protein A-gold immunocytochemical technique, type IV collagen was localized in the glomerular basal laminae. In tissues from normoglycaemic animals the labelling was present over the central lamina densa. However, the labelling obtained over the thickened glomerular basal laminae of the hyperglycaemic animals was restricted to the subendothelial site of the lamina. Thus major alteration in the distribution of type IV collagen occurs during the development of diabetic microangiopathy in hyperglycaemic animals.

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“…First, distinct glomerular lesions develop in patients with diabetes mellitus (1,2). Second, the glomerular filtration rate (GFR)' becomes higher than normal early in the course of juvenile onset diabetes mellitus while renal plasma flow remains normal, resulting in an elevation ofthe filtration fraction; filtration fractions averaging 28-30% have been reported (3)(4)(5). Because diabetes mellitus is a condition in which deficiency of insulin or tissue resistance to insulin exists, insulin may play some role in the regulation of glomerular function and metabolism.…”

Section: Introductionmentioning

confidence: 99%

Binding of 125I-insulin to the isolated glomeruli of rat kidney.

Kurokawa¹,

Silverblatt²,

Klein³

et al. 1979

J. Clin. Invest.

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A B S T R A C T To investigate a possible action of insulin on the glomerulus, the binding 1251-insulin to the isolated glomeruli prepared from rat kidney was examined. When incubated at 22°C, '251-insulin binding proceeded with time and reached a steady state at 45 min at which time nonspecific binding was <25% of total binding. A small fraction of '25I-insulin was degraded during incubation. This binding was specific to insulin in that it was inhibited by unlabeled porcine and beef insulins and to a lesser extent by porcine proinsulin and desalanine-desasparagine insulin, but not by glucagon, parathyroid hormone, vasopressin, calcitonin, and angiotensin II. Increasing concentrations of nonlabeled insulin displaced 1251-insulin binding in a dose-dependent fashion. Scatchard plot of the data was curvilinear consistent with either two classes of receptors with different affinities or a single class of receptors that demonstrate negative cooperativity. The addition of excess nonlabeled insulin to the glomeruli preincubated with 1251-insulin resulted in a rapid dissociation of -70% of bound I251-insulin. Insulin decreased the increments in glomerular cyclic AMP levels by epinephrine and by prostaglandin E2, but not those by histamine. These data showed the presence of specific insulin receptors in the glomeruli, and that insulin action may be, at least in part, through modulation of glomerular cyclic AMP concentrations. Such action of insulin may underlie the alteration in glo-

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Abnormally Increased Glomerular Filtration Rate in Short-term Insulin-treated Diabetic Subjects

Cited by 134 publications

References 1 publication

Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

Reactive Oxygen Species from Mitochondria Induce Cyclooxygenase-2 Gene Expression in Human Mesangial Cells

Alteration in the distribution of type IV collagen in glomerular basal laminae in diabetic rats as revealed by immunocytochemistry and morphometrical approach

Binding of 125I-insulin to the isolated glomeruli of rat kidney.

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