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  • 1
    Electronic Resource
    Electronic Resource
    Albumin excretion and vascular deaths in NIDDM (1995)
    Springer
    Diabetologia 38 (1995), S. 610-616 
    Details
    ISSN: 1432-0428
    Keywords: Key words Non-insulin-dependent diabetes mellitus ; albumin excretion ; microalbuminuria ; causes of death ; cardiovascular mortality.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Non-insulin-dependent diabetes mellitus (NIDDM) is associated with premature mortality, generally thought to be exaggerated in patients with microalbuminuria. This prospective 8-year follow-up study aimed to determine outcome, mortality and cause of death in NIDDM patients with abnormal urinary albumin excretion compared to those with normal albumin excretion. We recruited 153 NIDDM patients with abnormal urinary albumin excretion and 153 control subjects with albumin excretion within the normal non-diabetic range, matched for age, sex and duration of diabetes, from three University hospital diabetic clinics in Newcastle upon Tyne. The outcome measures were status at follow-up, mortality and cause of death. Subjects with abnormal albumin excretion had a significantly higher 8-year mortality than matched control subjects (Odds Ratio 1.47, p = 0.02; 108 vs 66 per 1000 person years follow-up, p 〈 0.001). This difference was seen at all levels of abnormal albumin excretion, from just outside the normal range (10.6–29.9 μg/min: 104 vs 61 per 1000 person years follow-up, p 〈 0.001) to more conventional definitions of microalbuminuria (≥ 30 μg/min: 111 vs 71 per 1000 person years follow-up, p 〈 0.01). Those with abnormal albumin excretion had an excess of vascular deaths compared to matched control subjects (Odds Ratio 1.70, p = 0.009), again at different levels of albumin excretion (10.6–29.9 μg/min p 〈 0.01, 30–150 μg/min p 〈 0.05). On multivariate analysis, age, initial ischaemic heart disease and initial albumin excretion rates were independent predictors of death from all causes. Even a minor elevation of albumin excretion above the normal non-diabetic range is associated with excess mortality from vascular causes in NIDDM. [Diabetologia (1995) 38: 610–616]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050327
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  • 2
    Electronic Resource
    Electronic Resource
    Renal enlargement and insulin-like growth factor-1 accumulation in the Wistar rat model of experimental diabetes is not prevented by angiotensin converting enzyme inhibition (1996)
    Springer
    Diabetologia 39 (1996), S. 166-171 
    Details
    ISSN: 1432-0428
    Keywords: Renal enlargement ; renal haemodynamics ; angiotensin II ; insulin-like growth factor-1 ; angiotensin converting enzyme inhibition
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Experimental diabetes is associated with renal enlargement and glomerular hyperfiltration. Possible mechanisms for these changes could be the direct effects of growth factors such as insulin-like growth factor-1 and angiotensin II. We investigated whether treatment with trandolapril, an angiotensin converting enzyme inhibitor, prevented renal enlargement in streptozotocin-diabetic rats. Seven groups of male Wistar rats were studied: C (control+placebo); CL (control+low-dose trandolapril, 0.01 mg · kg−1 · day−1); CH (control + high-dose trandolapril, 0.5 mg · kg−1 · day−1); DP (diabetic + placebo); DI (diabetic, insulin-treated); DL (diabetic + low-dose trandolapril); DH (diabetic + high-dose trandolapril) and DI (diabetic + insulin). From day 2 glucose concentrations and body weight were similar in the non-diabetic and diabetic animals treated with insulin. Diabetic animals treated with placebo and low-dose trandolapril weighed significantly less compared to the control group. The diabetic groups, not treated with insulin, showed marked hyperglycaemia throughout the study. Kidney weight was greater in the diabetic, non insulin-treated groups compared with the control and insulin-treated groups. After 24 h of diabetes, kidney insulin-like growth factor-1 content was significantly increased from baseline levels in groups DP, DL and DH but by 48 h these levels had returned to normal. Renal tissue angiotensin converting enzyme activity was similar in groups C and DI but significantly reduced in all trandolapril-treated animals. Despite inhibiting renal angiotensin converting enzyme activity renal enlargement with increased tissue insulin-like growth factor-1 still occurred. This suggests that neither angiotensin II nor glomerular hyperfiltration, with raised intraglomerular pressure, play a role in the initial renal enlargement seen in experimental diabetes. Renal accumulation of insulin-like growth factor-1 appears to be an important factor in early renal hypertrophy and its effects are not modulated by angiotensin converting enzyme or angiotensin II.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00403959
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  • 3
    Electronic Resource
    Electronic Resource
    Examination of two genetic polymorphisms within the renin-angiotensin system: no evidence for an association with nephropathy in IDDM (1996)
    Springer
    Diabetologia 39 (1996), S. 1108-1114 
    Details
    ISSN: 1432-0428
    Keywords: Insulin-dependent diabetes mellitus ; polymerase chain reaction ; diabetic nephropathy ; angiotensinogen ; angiotensin converting enzyme ; gene polymorphism
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Premature cardiovascular disease is common in insulin-dependent diabetic (IDDM) patients who develop diabetic nephropathy. Genetic polymorphism within the renin-angiotensin system has been implicated in the aetiology of a number of cardiovascular disorders; these loci are therefore candidate genes for susceptibility to diabetic renal disease. We have examined the angiotensin converting enzyme insertion/deletion polymorphism and angiotensinogen methionine 235 threonine polymorphism in a large cohort of Caucasian patients with IDDM and diabetic nephropathy. Patients were classified as having nephropathy by the presence of persistent dipstick positive proteinuria (in the absence of other causes), retinopathy and hypertension (n=242). Three groups were examined for comparison: ethnically matched non-diabetic subjects (n=187); a geographically defined cohort of newly diagnosed diabetic patients (n=341); and IDDM patients with long duration of disease (〉15 years) and no evidence of overt nephropathy (n=166). No significant difference was seen in distribution of angiotensin converting enzyme or angiotensinogen genotypes between IDDM patients with nephropathy and recently diagnosed diabetic subjects (p=0.282 and 0.584, respectively), nor the long-duration non-nephropathy diabetic subjects (p=0.701 and 0.190, respectively). We conclude that these genetic loci are unlikely to influence susceptibility to diabetic nephropathy in IDDM in the United Kingdom.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400661
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  • 4
    Electronic Resource
    Electronic Resource
    Renal autoregulation is normal in newly diagnosed, normotensive, NIDDM patients (1998)
    Springer
    Diabetologia 41 (1998), S. 206-211 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Renal autoregulation ; angiotensin converting enzyme inhibitor ; normotension ; nephropathy ; non-insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Abnormalities of renal autoregulation with glomerular hyperfiltration and raised intraglomerular pressure have been suggested as important factors in the initiation and development of diabetic nephropathy. Angiotensin converting enzyme (ACE) inhibition appears to have a specific reno-protective role in diabetic nephropathy, possibly by reducing intraglomerular pressure. The acute effects of ACE inhibition on renal haemodynamics in normotensive, non-insulin-dependent diabetes mellitus (NIDDM) have not been previously reported. We measured simultaneous glomerular filtration rate (GFR) and renal plasma flow (RPF) in 29 (4 female) subjects, mean age 52 years (range 27–70), using 51Cr EDTA and 125I Hippuran. Clearances were corrected to 1.73 m–2. All patients were normotensive (blood pressure 〈 75th centile for age and sex), newly diagnosed ( 〈 30 days), taking no antihypertensive or hypoglycaemic medication. Subjects were randomly allocated (double blind) to receive the ACE inhibitor trandolapril 4 mg day–1 (H) (hypotensive dose), trandolapril 0.5 mg day–1 (L) (non-hypotensive dose) or placebo (P) for 10 days after which renal haemodynamics were remeasured. For all subjects baseline GFR, RPF and filtration fraction (FF) were 97 ± 21 ml min–1 mean ± SD, 439 ± 120 ml min–1 and 22.3 ± 2.9 % respectively. Glomerular hyperfiltration (GFR 〉 120 ml min–1) was only demonstrated in 3 subjects (10.3 %). In group H mean arterial pressure (103 ± 8 vs 93 ± 9 mmHg, p 〈 0.001) and FF (23.8 ± 2.3 vs 20.0 ± 4.0 %, p = 0.03) fell while RPF increased (376 ± 111 vs 426 ± 60 ml min–1, p = 0.02), there was no significant change in GFR. No significant change in mean arterial pressure, GFR, RPF or FF occurred in groups P and L. These studies suggest that in newly diagnosed normotensive NIDDM subjects normal renal autoregulation occurs and glomerular hyperfiltration is uncommon. [Diabetologia (1998) 41: 206–211]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050891
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  • 5
    Electronic Resource
    Electronic Resource
    Adipocyte insulin binding and insulin sensitivity in ‘brittle’ diabetes (1984)
    Springer
    Diabetologia 27 (1984), S. 441-446 
    Details
    ISSN: 1432-0428
    Keywords: Brittle diabetes ; adipocyte ; insulin binding ; insulin action ; intraperitoneal insulin
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Adipocyte insulin binding and insulin sensitivity to stimulation of lipogenesis were assessed in a group of extremely ‘brittle’ diabetic patients who were resistant to subcutaneous insulin therapy and had required frequent and prolonged hospital admission. These patients had significantly lower maximum adipocyte insulin binding (1.78±0.18%) than age-, sex- and weight-matched stable diabetic control subjects (2.57±0.36%; p〈0.05). Scatchard analysis suggested that the decreased binding was secondary to reduced receptor affinity with no change in receptor number. Adipocytes from the brittle subjects displayed resistance to insulin stimulation of lipogenesis compared with those from diabetic or normal control groups (half-maximal stimulation at 34±4, 15±3 and 13±2 pmol/l respectively; p〈0.01 between brittle and stable diabetic groups). In the one subject who was treated with intraperitoneal insulin, the changes in insulin binding and sensitivity were found to have reverted towards normal. The peripheral tissue abnormalities of brittle diabetes may exacerbate the clinical syndrome although the relationship of these changes to the primary cause of the syndrome is uncertain.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00273908
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  • 6
    Electronic Resource
    Electronic Resource
    Circadian variation of blood pressure in patients with diabetic nephropathy (1992)
    Springer
    Diabetologia 35 (1992), S. 1074-1079 
    Details
    ISSN: 1432-0428
    Keywords: Type 1 (insulin-dependent) diabetes mellitus ; diabetic nephropathy ; ambulatory blood pressure ; circadian ; variation
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary The association between diurnal blood pressure variation and diabetic nephropathy was assessed in four groups of Type 1 (insulin-dependent) diabetic patients who underwent 24-h ambulatory blood pressure monitoring using an oscillometrie technique. Patients with nephropathy, who had never been treated for hypertension (group D3,n = 13), were individually matched for age, sex and diabetes duration to a group of microalbuminuric patients (D2,n = 26), to normoalbuminuric patients (D1,n = 26) and to healthy control subjects (C,n = 26). Group D3 was also compared to patients with advanced nephropathy receiving treatment for hypertension, mainly a combination of angiotensin converting enzyme inhibitors, metoprolol and diuretics (D4,n = 11). In group D3 24-h diastolic blood pressure (85 ± 8 mm Hg) was comparable to the results obtained in D4 (85 ± 8 mm Hg) but significantly higher than in D2 (78 ± 7 mm Hg), D1 (73 ± 7 mm Hg) and C (73 ± 7 mm Hg,p 〈 0.05, Tukey's test). The night/day ratio of diastolic blood pressure was higher in D3 (86 ± 5 %) and D2 (85 ± 7%) than in C (80 ± 7 %,p 〈 0.02). This ratio was also elevated in group D4 (94 ± 8%) compared to D3 (p 〈 0.05) corresponding to a marked smoothing of the diurnal blood pressure curve. The 24-h heart rate (beats per min) was significantly elevated in D3 (84 ± 8) and D2 (80 ± 10) compared with C (73 ± 11,p 〈 0.05 Tukey's test), suggesting the presence of parasympathetic neuropathy In conclusion the normal circadian variation of blood pressure was moderately disturbed in a group of microalbuminuric patients and patients with less advanced overt nephropathy. Patients with advanced diabetic nephropathy receiving antihypertensive therapy showed a marked reduction of nocturnal blood pressure fall, which can only be identified by the application of ambulatory blood pressure measurements to verify the 24-h effectiveness of blood pressure control.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF02221684
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  • 7
    Electronic Resource
    Electronic Resource
    Renal insulin-like growth factor I and growth hormone receptor binding in experimental diabetes and after unilateral nephrectomy in the rat (1991)
    Springer
    Diabetologia 34 (1991), S. 632-639 
    Details
    ISSN: 1432-0428
    Keywords: Renal hypertrophy ; insulin-like growth factor I receptor ; growth hormone receptor ; experimental diabetes ; uninephrectomy
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary We have measured specific binding of insulin-like growth factor I and growth hormone to renal plasma membranes from control, streptozotocin-diabetic, insulin-treated diabetic, uninephrectomised and combined diabetic-uninephrectomised male Wistar rats. Control, insulin-treated and uninephrectomised rats had similar body weights after 7 days (243±2 g), whereas diabetic and diabetic-uninephrectomised animals were significantly lighter (219±4 and 203±4 g, p〈0.05). Blood glucose concentrations were similar in the diabetic and diabetic-uninephrectomised animals (around 26 mmol/l) but significantly lower in the insulin-treated group. Right kidney weight increased by 14% in the control, insulin-treated and sham-nephrectomised animals, by 33% in the diabetic group, 38% in the nephrectomised animals and 60% in the diabetic-nephrectomised group. The renal content of insulin-like growth factor I was similar and stable in the control, insulin-treated and sham-nephrectomised animals (208±14 ng/g wet weight) but rose to a peak of 669±35 ng/g in the diabetic group (p〈0.001), 871±34 ng/g in the nephrectomised animals (p〈0.001) and 1012±43 ng/g in the diabetic-uninephrectomised group (p〈0.001). Maximum binding of insulin-like growth factor I fell on day 1 in the diabetic group (8.3±1.4 vs 5.2±0.71× 10− mol/l; p〈0.01) but thereafter was identical to control animals. In the insulin-treated animals, maximum binding rose to 11.0±1.1×10−11 mol/l, significantly different from control and diabetic animals (p〈0.01). Growth hormone binding fell acutely in both the diabetic and diabetic-nephrectomised animals (3.13±0.58 and 2.83±0.21 vs 7.77±0.68×10−12 mol/l; p〈0.001 for both). Following uninephrectomy, maximum binding of insulin-like growth factor I and growth hormone was unchanged from control values. We conclude that the rise in renal content of insulin-like growth factor I which precedes the compensatory growth seen after induction of diabetes and uninephrectomy is not due to alterations in insulin-like growth factor I receptor binding and is independent of growth hormone binding.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00400992
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  • 8
    Electronic Resource
    Electronic Resource
    Kidney IGF-I mRNA in initial renal hypertrophy in experimental diabetes in rats (1990)
    Springer
    Diabetologia 33 (1990), S. 334-338 
    Details
    ISSN: 1432-0428
    Keywords: Renal hypertrophy ; insulin-like growth factor I ; insulin-like growth factor I mRNA ; streptozotocin diabetes
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary It has recently been demonstrated that immunoassayable kidney insulin-like growth factor I concentration increases 24–48 h after induction of diabetes, preceding the initial renal hypertrophy. To elucidate whether this increase is due to increased local production we studied rat kidney insulin-like growth factor I gene expression during the first four days after induction of streptozotocin diabetes. Eighteen hours after injection with streptozotocin the diabetic animals were divided into two groups, one of which was treated with insulin, and daily for four days animals from each group were taken out for investigation. After four days the wet kidney weight had increased from baseline by 20% (from 687±23 to 827±6mg (mean±SEM), p 〈 0.01) in the untreated diabetic group, while no significant increase occurred in the insulin-treated group (687±23 vs 732±21 mg, NS). Kidney insulin-like growth factor I increased rapidly from baseline, the rise amounting to 52% after 48 h (from 271±11 to 411±32 ng/g, p 〈 0.01) with a decline to control level on day four in the untreated diabetic group. Kidney insulin-like growth factor I remained unchanged in the insulin-treated diabetic group. Insulin-like growth factor I mRNA was measured by solution-hybridization assay. No differences were found in kidney insulin-like growth factor I mRNA between the two diabetic groups over the study period, while in liver, insulin-like growth factor I mRNA tended to be lower on day four in diabetic rats when compared to insulin-treated rats (p=0.07). These results show that the increase in kidney insulin-like growth factor I during initial renal hypertrophy in experimental diabetes is not associated with an elevated level of kidney insulin-like growth factor I mRNA and suggest that other, possibly translational, mechanisms are responsible for insulin-like growth factor accumulation in the kidney.
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/BF00404636
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  • 9
    Electronic Resource
    Electronic Resource
    Thiol group modulation of sodium-lithium countertransport kinetics in diabetic nephropathy (1997)
    Springer
    Diabetologia 40 (1997), S. 1079-1084 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; sodium-lithium countertransport ; thiol group ; N-ethylmaleimide ; erythrocyte ; insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary Abnormal erythrocyte sodium-lithium countertransport (Na-Li CT) activity, traditionally measured at a single sodium concentration of 140 mmol · l–1 (V140), may represent an inherited risk marker for diabetic nephropathy. The membrane defect underlying this association is poorly understood, though modulation by key protein thiol groups appears to be important in essential hypertension. To improve understanding of this abnormality, Na-Li CT kinetics in untreated erythrocytes and after thiol group alkylation with N-ethylmaleimide were investigated in 18 subjects with diabetic nephropathy, 20 normoalbuminuric insulin-dependent diabetic (IDDM) subjects and 18 non-diabetic individuals. Using the traditional assay, V140 was similar in subjects with diabetic nephropathy compared to IDDM control subjects vs 0.311 (0.152–0.475) (0.247 (0.111–0.498) mmol Li · h–1· l erythrocytes–1). Kinetic parameters were abnormal in subjects with diabetic nephropathy compared with diabetic and non-diabetic control subjects, with both Vmax (maximal Na-Li CT activity) (0.454 (0.257–0.963) vs 0.338 (0.183–0.972) vs 0.332 (0.213–0.603) mmol Li · h–1· l erythrocytes–1, p 〈 0.05), and Vmax/Km(So) ratio, reflecting ion association (6.03 (2.3–9.6) vs 4.73 (2.0–10.4) vs 4.48 (1.5–7.1), p 〈 0.01), significantly higher. N-ethylmaleimide decreased Km(So) and Vmax abolishing differences in Vmax/Km(So) ratio between groups (2.45 (1.18–4.21) vs 2.23 (0.96–4.3) vs 2.44 (1.4–3.7), but enhancing the differences in Vmax (0.186 (0.090–0.315) vs 0.120 (0.051–0.256) vs 0.128 (0.080–0.206) mmol Li · h–1· l erythrocytes–1, p 〈 0.0001). Of subjects with diabetic nephropathy, 78 % were outside the 75th percentile of the non-diabetic control subjects when Vmax and Vmax/Km(So) ratio were combined, compared to 20 % of the normoalbuminuric control subjects. We conclude that the traditional assay, V140, is poor at detecting individuals with diabetic nephropathy. Study of the kinetic parameters of the transporter, including thiol group modulation, suggests that increased ion association, Vmax/Km(So) ratio may represent the inherited defect and improves identification of subjects with diabetic nephropathy. [Diabetologia (1997) 40: 1079–1084]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050790
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  • 10
    Electronic Resource
    Electronic Resource
    Abnormal regulation of cell membrane fluidity in diabetic nephropathy (1998)
    Springer
    Diabetologia 41 (1998), S. 337-342 
    Details
    ISSN: 1432-0428
    Keywords: Keywords Diabetic nephropathy ; fluidity ; anisotropy ; N-ethylmaleimide ; erythrocyte ; insulin-dependent diabetes mellitus.
    Source: Springer Online Journal Archives 1860-2000
    Topics: Medicine
    Notes: Summary An abnormality of the physical properties of the cell membrane may underlie the defect that unites the clinical and biochemical abnormalities found in subjects with diabetic nephropathy. The cell membrane is linked both structurally and functionally with the cytoskeleton. The fluorescence anisotropy, a measure of membrane fluidity, was studied at baseline and after modulation of cytoskeletal proteins by thiol group alkylation with N-ethylmaleimide (NEM). 1,6-diphenyl-1,3,5-hexatriene (DPH) was used to assess anisotropy in the deep hydrophobic regions of the lipid bilayer and trimethylammonium-diphenylhexatriene (TMA-DPH) was used to assess the superficial, relatively hydrophilic regions. We compared 17 subjects with insulin-dependent diabetes mellitus (IDDM) and nephropathy with 17 control subjects with IDDM and 24 non-diabetic control subjects. Median TMA-DPH anisotropy (0.271 (0.239–0.332) vs 0.269 (0.258–0.281) vs 0.275 (0.246–0.287)) and DPH anisotropy (0.221 (0.193–0.261) vs 0.227 (0.197–0.253) vs 0.226 (0.193–0.245)) were similar in erythrocytes from the three groups. However after alkylation of protein thiol groups with NEM clear differences emerged. In the control subjects with and without IDDM there was a significant fall in TMA-DPH anisotropy compared to the subjects with diabetic nephropathy in whom the addition of NEM had no effect (ΔTMA-DPH anisotropy –0.005 (–0.020– + 0.006) vs –0.005 (–0.011– + 0.016) vs + 0.002 (–0.010 – + 0.008) p 〈 0.001). This finding was confirmed when the deep regions of the lipid bilayer were assessed using DPH (ΔDPH anisotropy –0.017 (–0.029 –– 0.007.) vs –0.015 (–0.029 – + 0.001) vs + 0.003 (–0.021 – + 0.018) p 〈 0.001). We conclude that cytoskeletal modulation of the physical properties of the cell membrane lipids by proteins is abnormal in subjects with diabetic nephropathy. Such an abnormality could explain some of the clinical and metabolic abnormalities found in this condition. [Diabetologia (1998) 41: 337–342]
    Type of Medium: Electronic Resource
    URL: http://dx.doi.org/10.1007/s001250050912
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