Glycosylation of glomerular basement membrane in type 1 (insulin-dependent) diabetic children

Schober, Edith; Pollak, Arnold; Coradello, H; Lubec, Gert

doi:10.1007/bf00254295

Cited by 27 publications

(13 citation statements)

References 12 publications

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“…Cohen et al [6] reported that increased glycosylation of G B M collagen from rats with STZ-induced diabetes may alter structure-function relation ships o f the capillary filtration barrier [6]. Schober et al [18] reported marked glycosylation o f G B M in insulindependent diabetic children. Recently, Nishimura et al [19] and Dobashi [20] reported high levels of lipid perox ide in retina, kidneys and plasma in STZ-induced dia betic rats.…”

Section: Discussionmentioning

confidence: 99%

Glomerular Nonenzymatic Glycosylation and Lipid Peroxide Are Increased in the Early Phase of Streptozotocin-Induced Diabetic Rats Prior to Major Histopathologic Alterations

Tomino

Wang²,

Fukui³

et al. 1991

Nephron

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Levels of glomerular nonenzymatic glycosylation and lipid peroxide in streptozotocin (STZ)-induced diabetic rats were examined. Isolation of glomeruli was performed using a sieving technique. The levels of nonenzymatic glycosylation in the glomeruli of these rats were measured by the thiobarbituric acid (TBA) method. Measurement of lipid peroxide, i.e., malondialdehyde (MDA), levels in the renal cortex, medulla and isolated glomeruli was performed by the TBA test. Light-microscopic and immunofluorescent examinations were also performed. An increase in nonenzymatic glycosylation in the glomeruli was observed in the early phase, i.e. after 4 and 12 weeks, in STZ-induced diabetic rats. The levels of MDA in the renal cortex of 12-week-old STZ-induced diabetic rats were also significantly increased compared with those of control rats at the same age. Levels of MDA in the glomeruli of 12-week-old STZ-induced diabetic rats were slightly increased compared with those of control rats, but there was no statistical significance. In immunofluorescence, IgG or IgM was deposited in the glomerular mesangial areas and capillary walls in 12-week-old diabetic rats. However, there was no significant change in renal tissues after 4 and 12 weeks in STZ-induced diabetic rats. It was concluded that glomerular nonenzymatic glycosylation and lipid peroxide were already increased in the early phase of STZ-induced diabetic rats prior to the appearance of marked histologic alterations.

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Section: Discussionmentioning

confidence: 99%

Glomerular Nonenzymatic Glycosylation and Lipid Peroxide Are Increased in the Early Phase of Streptozotocin-Induced Diabetic Rats Prior to Major Histopathologic Alterations

Tomino

Wang²,

Fukui³

et al. 1991

Nephron

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“…Studies to date have not dissociated the effects of glomerular hypertension and hyperperfusion from those of chronic hyperglycemia per se (20)(21)(22). In the present study, glomerular hemodynamic function was deliberately varied in rats with streptozotocin (STZ)-induced diabetes while stable moderate hyperglycemia was maintained by daily exogenous insulin.…”

Section: Introductionmentioning

confidence: 94%

“…Glomerular morphologic changes resembling those seen in diabetes have been associated with increases in capillary pressures and flows in other experimental forms of renal disease, including ablation ofrenal mass (11-13), high-protein diet (14), and some models of hypertension (15, 16). Furthermore, the extent of glomerular lesions in diabetic rats can be enhanced by maneuvers known to increase glomerular capillary pressures and flows, such as contralateral renal arterial clipping (17), ablation of the contralateral kidney (18), or high-protein feeding (19).Studies to date have not dissociated the effects of glomerular hypertension and hyperperfusion from those of chronic hyperglycemia per se (20)(21)(22). In the present study, glomerular hemodynamic function was deliberately varied in rats with streptozotocin (STZ)-induced diabetes while stable moderate hyperglycemia was maintained by daily exogenous insulin.…”

mentioning

confidence: 99%

Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.

Zatz¹,

Meyer²,

Rennke³

et al. 1985

Proc. Natl. Acad. Sci. U.S.A.

491

277

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Six groups of Munich-Wistar rats underwent micropuncture study 2-10 weeks and morphologic studies 11-13 months after induction of streptozotocin diabetes or after sham treatment. Diabetic rats received diets containing 6% (group D6), 12% (D12), or 50% protein (D50) and were maintained under similar conditions of moderate hyperglycemia by daily injections of ultralente insulin. Age-and weightmatched normal control rats were also given 6% (Group N6), 12% (N12), or 50% protein (N50 (9,10) to result from an augmentation of both glomerular plasma flow rate (QA) and local transcapillary hydraulic pressure difference (AlP). Glomerular morphologic changes resembling those seen in diabetes have been associated with increases in capillary pressures and flows in other experimental forms of renal disease, including ablation ofrenal mass (11-13), high-protein diet (14), and some models of hypertension (15, 16). Furthermore, the extent of glomerular lesions in diabetic rats can be enhanced by maneuvers known to increase glomerular capillary pressures and flows, such as contralateral renal arterial clipping (17), ablation of the contralateral kidney (18), or high-protein feeding (19).Studies to date have not dissociated the effects of glomerular hypertension and hyperperfusion from those of chronic hyperglycemia per se (20)(21)(22). In the present study, glomerular hemodynamic function was deliberately varied in rats with streptozotocin (STZ)-induced diabetes while stable moderate hyperglycemia was maintained by daily exogenous insulin. This approach made it possible to relate the early alterations in glomerular pressures and flows in experimental diabetes to the subsequent development of glomerular injury. METHODSNinety-three adult male Munich-Wistar rats (220-260 g each) were studied. Forty-three rats were made diabetic by a single intravenous injection of STZ (60 mg/kg). Morning blood glucose concentration was determined biweekly. Rats received daily evening injections of ultralente insulin (NOVO Industries, Copenhagen) (23) in doses to maintain blood glucose concentration (BG) between 200 and 400 mg/dl. Diabetic rats were maintained on diets containing 50% (group D50, n = 15), 12% (D12, n = 15), or 6% casein (D6, n = 13). Normal control rats matched for initial body weight received the same diets containing 50% (group N50, n = 18), 12% (N12, n = 16), or 6% casein (N6, n = 16). The composition of the diets was 82% (wt/wt) casein plus carbohydrate, 5% lipid, 1% phosphate, 1% calcium, and 11% other components.Twenty-five diabetic rats and 24 control rats underwent micropuncture study 2-10 weeks (mean 4.2) after STZ injection. Rats were anesthetized with Inactin (100 mg/kg) and prepared for mnicropuncture in standard fashion (24). Euvolemia was maintained by iso-oncotic plasma replacement (25). Inulin (10 g/dl in isotonic saline solution) was also infused at a rate of 1.2 ml/hr. Tubule fluid was collected from superficial proximal tubules for determinations of flow rate and inulin concentration (26). Blood samples fro...

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“…Schober et al [3] reported marked glycosylation of GBM in type I (in sulin-dependent) diabetic children. We reported an in crease of glycosylated proteins in renal tissues obtained from patients with non-insulin-dependent diabetes melli tus (NIDDM) with nephropathy [4], However, the patho genesis of renal involvement in patients with diabetes has not yet been clarified.…”

Section: Introductionmentioning

confidence: 99%

Detection of Glomerular Sialic Acids in Patients with Diabetic Nephropathy

Tomino

Inoue²,

Watanabe³

et al. 1988

Am J Nephrol

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A study on immunofluorescence of sialic acids in glomeruli from patients with diabetic nephropathy is described. Measurement of sialic acid in sera from 25 patients with diabetes mellitus was also performed. Renal biopsy specimens from 12 patients with diabetic nephropathy were stained with FITC-labeled antihuman IgG antiserum and rhodamine-labeled Triticum vulgaris (WGA) or Limulus polyphemus (LPA). These specimens were also stained with such reagents after treatment with neuraminidase, trypsin or citrate buffer. Both deposition of IgG and binding of WGA in the glomerular capillary walls were observed in all patients with diabetic nephropaty. The binding of WGA in the glomerular capillary walls in diabetic nephropathy was significantly increased compared with that in four normal renal tissues. However, the binding of LPA was hardly observed in the glomerular capillary walls of patients with diabetic nephropathy. The binding of WGA in the glomeruli was markedly decreased after treatment with neuraminidase although it was hardly decreased after treatment with trypsin or citrate buffer. The levels of sialic acid in sera from patients with diabetic nephropathy were markedly increased. It is suggested that accumulated substances in the glomerular capillary walls with an affinity for WGA are mainly composed of N-acetyl glucosamine and/or N-acetyl neuraminic acid in patients with diabetic nephropathy.

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Glycosylation of glomerular basement membrane in type 1 (insulin-dependent) diabetic children

Cited by 27 publications

References 12 publications

Glomerular Nonenzymatic Glycosylation and Lipid Peroxide Are Increased in the Early Phase of Streptozotocin-Induced Diabetic Rats Prior to Major Histopathologic Alterations

Glomerular Nonenzymatic Glycosylation and Lipid Peroxide Are Increased in the Early Phase of Streptozotocin-Induced Diabetic Rats Prior to Major Histopathologic Alterations

Predominance of hemodynamic rather than metabolic factors in the pathogenesis of diabetic glomerulopathy.

Detection of Glomerular Sialic Acids in Patients with Diabetic Nephropathy

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