Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Mazzanti, Laura; Rabini, R. A.; Testa, I; Bertoli, Enrico

doi:10.1111/j.1365-2362.1989.tb00200.x

Cited by 31 publications

(15 citation statements)

References 40 publications

(18 reference statements)

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“…The patients studied by Hill et al [10] had a similar duration of diabetes but were younger (9-19 years) and some patients had microvascular disease. The patients studied by Testa et al [5], Mazzanti et al [6], Juhan-Vague et al [7] and Rahmani-Jourdheuil et al [8] however, all had IDDM of similar duration and age to those patients in the present study, but some of the patients in these previous studies had diabetic complications. The results in the present study demonstrate that the presence of diabetic complications could affect membrane fluidity as those patients with diabetic nephropathy had lower membrane fluidity compared to their uncomplicated counterparts although this was not different when compared to normal control subjects.…”

Section: Discussioncontrasting

confidence: 51%

“…As anisotropy and fluidity are inversely related, this indicates increased fluidity in the deep hydrophobic regions of the erythrocyte membrane. This has been reported in previous studies [5][6][7][8], although others have also reported normal [9,10] or lower fluidity [11][12][13] as assessed by DPH in diabetes. The reason for these differences is not entirely clear.…”

Section: Discussionmentioning

confidence: 60%

“…Membrane fluidity has also been studied in diabetes but patient groups have varied and the results have been inconsistent [5][6][7][8][9][10][11][12][13]. The sodium-lithium countertransporter is a transmembrane protein with increased activity in some diabetic patients but its character has not been studied in relation to membrane fluidity in diabetes.…”

Section: -400]mentioning

confidence: 99%

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Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients

et al. 1994

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Summary Sodium-lithium countertransport (SLC) activity at a standard physiological sodium concentration is raised in uncomplicated IDDM, for which the kinetic mechanism is a raised maximum velocity (Vmax). Diabetic patients with nephropathy do not have raised values for Vmax but a low Michaelis constant (kin). Transporter activity could be influenced by its membrane lipid environment. This was assessed in 21 control subjects, 32 uncomplicated diabetic patients, 17 patients with diabetic nephropathy and 11 patients with nondiabetic nephropathy by measuring the fluorescence anisotropy of DPH and TMA-DPH to assess different membrane regions. Standard SLC was higher in all the patient groups compared to the control subjects: 0.307 ___ 0.020 mmol Li/h x 1 cells in uncomplicated IDDM; 0.300 + 0.032 in diabetic nephropathy patients and 0.276 + 0.019 in non-diabetic nephropathy patients vs 0.216 + 0.011 mmol Li/h x 1 cells in control subjects (p < 0.001, p < 0.05, p < 0.05, respectively). This was due to raised Vm,x values in the uncomplicated group: 0.528 + 0.035 vs 0.385 + 0.022 mmol Li/h x 1 cells in control subjects (p = 0.001) and low values for km in the diabetic nephropathy group: 58 (27-170) vs 106 (81-161) mmol/1 in control subjects (p <0.001). Raised SLC in the non-diabetic nephropathy group was largely due to raised Vmax: 0.460 + 0.030 mmol Li/h x 1 cells; p = 0.053, with no difference in kin: 99.5 (74-137). DPH anisotropy was lower in the uncomplicated diabetic patients (0.210 + 0.0009) compared to the control subjects (0.214 + 0.0007:p = 0.006) and was related to both standard SLC (rs = -0.68, p < 0.001) and Vm= (rs = --0.77, p < 0.001). Though DPH anisotropy in the diabetic nephropathy group was not different from normal control subjects, it also correlated with SLC (rs = -0.72, p < 0.001) due to the same relationship with Urea x (FS = --0.73, p < 0.001) as in uncomplicated diabetes. TMA-DPH anisotropy showed no difference between the four groups and was not related to either standard SLC, Vmax or kin. Therefore, changes in membrane fluidity in the hydrophobic regions of the erythrocyte membrane may be responsible for some of the differences in SLC in IDDM. [Diabetologia (1994) 37: 394-400]

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Section: Discussioncontrasting

confidence: 51%

Section: Discussionmentioning

confidence: 60%

Section: -400]mentioning

confidence: 99%

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Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients

et al. 1994

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“…It has been reported that erythrocytes from diabetic patients have a higher intracellular Na + concentration (4). Several mechanisms may account for the observed Ca 2+ increase.…”

Section: Discussionmentioning

confidence: 91%

Altered Cellular Ca2+ and Na+ Transport in Diabetes Mellitus

et al. 1990

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Platelet intracellular Ca2+ concentration ([Ca2+]i) and its response to stimuli (ADP and thrombin) were studied in 15 insulin-dependent and 22 non-insulin-dependent diabetes mellitus patients with the fluorescent probe Fura 2. The activity of Ca2(+)-ATPase and Na(+)-K(+)-ATPase, membrane fluidity, and cholesterol and phospholipid content were also determined in platelet membranes. Compared with control subjects, diabetic patients showed 1) increased platelet [Ca2+]i in the resting state, 2) higher Ca2+ levels after stimulation with thrombin and ADP, due entirely to increased resting concentrations, 3) reduced activity of Na(+)-K(+)-ATPase, 4) increased activity of Ca2(+)-ATPase, 5) higher fluidity of the platelet membrane, and 6) increased membrane concentration of total phospholipids. Na(+)-K(+)-ATPase activity was inversely related to platelet [Ca2+]i in each group studied, whereas Ca2(+)-ATPase activity was positively correlated with intracellular Ca2+ levels. The data obtained in diabetic subjects suggest an abnormality in Ca2+ and Na+ transport across the platelet membrane that might be responsible for the reported platelet hyperreactivity to stimuli in diabetes.

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“…In Siena consensus paper; a grade A was assigned to calcium dobesilat, MPFF, and O-(betahydroxyethyl) rutosides (HR)-oxerutins, a grade B to escin and ruscus extracts and a grade C to the remaining VADS (21). Recently published Society for Vascular Surgery and the American Venous Forum guideline suggested that diosmin, hesperidin, rutoside, micronized purified flavonoid fraction or horse chestnut seed extract (escin) must be used in addition to compression therapy for chronic venous disease (Grade 2, Evidence level B) (22). Table 1.…”

Section: Introductionmentioning

confidence: 99%

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Kahramanmaraş Sütçü İmam Üniversitesi Tıp Fakültesi Dergisi

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ÖzetVenöz ülserler anlamlı morbiditeye sebep olan önemli tıbbi sorunlardır. Primer venöz yetmezliğin ileri evrelerinde veya venöz yetmezliğe bağlı oluşan posttrombotik sendrom sonucunda gelişir. Tedavisi kompresyon, bacak elevasyonu, local yara bakımı, ilaç tedavisi ve altta yatan venöz patolojinin cerrahi veya girişimsel olarak düzeltilmesidir. Diğer tedavi yöntemleri eğer kompresyon tedavisi ile birlikte uygulanırsa başarılı olabilir. Biz burada venöz ülser tedavisinde venoaktif ilaçların etkinliğini bilimsel kanıtlar eşliğinde tartıştık.Anahtar Kelimeler: Venöz ülser; venoaktif ilaçlar; venöz yetersizli AbstractVenous ulcers are important medical problem that caused significant morbidity. They develop as a result of advanced chronic venous insufficiency, caused most frequently by primary venous incompetence or the post thrombotic syndrome. Treatment of venous ulcers include compression therapy, leg elevation, local ulcer and skin care, drug treatment, and correction of the underlying venous pathology with surgical and endovenous interventions. Primary and sine qua non method to cure venous ulcer is compression treatment. Other treatment modalities can be successful if only they have performed with compression treatment. In here we discuss the scientific evidence on efficacy of venoactive drug therapy on treatment of venous ulcer.

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Modifications induced by diabetes on the physicochemical and functional properties of erythrocyte plasma membrane

Cited by 31 publications

References 40 publications

Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients

Erythrocyte sodium-lithium countertransport activity is related to membrane fluidity in IDDM patients

Altered Cellular Ca2+ and Na+ Transport in Diabetes Mellitus

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