scholarly journals Skin Microcirculation of the Foot in Diabetic Neuropathy

1996 ◽  
Vol 91 (5) ◽  
pp. 559-565 ◽  
Author(s):  
Paetrick M. Netten ◽  
Hub Wollersheim ◽  
Theo Thien ◽  
Jos A. Lutterman
Keyword(s):  
Diabetic Neuropathy ◽  
Laser Doppler ◽  
Diabetic Patients ◽  
Shunt Flow ◽  
Laser Doppler Fluxmetry ◽  
Control Subjects ◽  
Healthy Control ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
And Control

1. In the feet of patients with diabetic neuropathy, total skin blood flow is increased due to an increased shunt flow. The question is, does this increased anastomotic shunt flow lead to either under- or overperfused nutritive capillaries. 2. To solve this question, skin microcirculation tests of the left big toe were performed in 20 healthy control subjects and in 40 insulin-dependent diabetic patients without macroangiopathy, 20 without and 20 with neuropathy. Skin temperature measurements and laser Doppler fluxmetry were performed to record mainly shunt flow and capillaroscopy to study nailfold capillary blood flow. 3. The insulin-dependent diabetic patients with neuropathy had a higher baseline skin temperature (mean ± SEM; 30.0 ± 0.6°C) and laser Doppler fluxmetry [26.2 ± 2.2 perfusion units (pu)] than patients without neuropathy (27.2 ± 0.8°C, P < 0.01; 16.1 ± 2.0 pu, P < 0.01) and healthy control subjects (27.9 ± 0.7°C, P < 0.05; 18.6 ± 2.8 pu, P < 0.05). Sympathetic stimulation (inspiratory gasp) resulted in a smaller laser Doppler fluxmetry decrease in the neuropathic patients (31.4 ± 4.6%) compared with non-neuropathic patients (48.2 ± 5.1%, P < 0.05) and control subjects (49.0 ± 3.8%, P < 0.05), while no difference between the three groups was seen in the laser Doppler fluxmetry decrease during a postural vasoconstriction test. The number of visible capillaries was highest in the neuropathic patients (10.2 ± 0.6/0.5 mm2), when compared with non-neuropathic patients (8.7 ± 1.2/0.5 mm2, P < 0.05) and control subjects (8.3 ± 0.3/0.5 mm2, P < 0.001). Capillary blood-cell velocity was significantly higher in the neuropathic patients (0.32 ± 0.05 mm/s) compared with non-neuropathic patients (0.23 ± 0.03 mm/s, P < 0.05) and control subjects (0.23 ± 0.02 mm/s, P < 0.01). 4. We conclude that there is an overperfused nutritive capillary circulation in the feet of patients with diabetic neuropathy. This is in contradiction to the capillary steal phenomenon and favours the hyperdynamic hypothesis to explain the decreased healing potential in diabetic neuropathic foot ulceration.

Saliva in non-insulin-dependent diabetic patients and control subjects

1998 ◽  
Vol 86 (1) ◽  
pp. 69-76 ◽  
Author(s):  
Jukka H Meurman ◽  
Hanna-Leena Collin ◽  
Leo Niskanen ◽  
Jari Töyry ◽  
Pekka Alakuijala ◽  
...  
Keyword(s):  
Diabetic Patients ◽  
Control Subjects ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
And Control

Inhibition of Nitric Oxide Synthesis in Forearm Vasculature of Insulin-Dependent Diabetic Patients: Blunted Vasoconstriction in Patients with Microalbuminuria

1993 ◽  
Vol 85 (6) ◽  
pp. 687-693 ◽  
Author(s):  
T. G. Elliott ◽  
J. R. Cockcroft ◽  
P.-H. Groop ◽  
G. C. Viberti ◽  
J. M. Ritter
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Healthy Subjects ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Relaxing Factor ◽  
Healthy Control ◽  
Insulin Dependent ◽  
Endothelium Derived Relaxing Factor ◽  
Insulin Dependent Diabetic

1. Microalbuminuria is a risk factor for cardiovascular disease in patients with insulin-dependent diabetes mellitus, and may be a marker of microvascular dysfunction including endothelial damage. The purpose of this study was to determine whether vasoconstrictor responses to NG-monomethyl-L-arginine, an inhibitor of endothelium-derived relaxing factor/nitric oxide biosynthesis, differ between healthy subjects and insulin-dependent patients with or without microalbuminuria. 2. Twenty-eight insulin-dependent diabetic patients (14 with normal albumin excretion, 14 with microalbuminuria) were studied under euglycaemic conditions, together with 14 healthy control subjects. Forearm vascular responses to brachial artery infusions of NG-monomethyl-L-arginine, sodium nitroprusside (an endothelium-independent nitrovasodilator) and carbachol (an endothelium-dependent vasodilator) were determined by strain gauge plethysmography. 3. Basal blood flow and vasodilator responses were similar in each group. NG-Monomethyl-L-arginine reduced blood flow by 41.3 + 2.3% (mean + SEM) in healthy control subjects, 34.0 + 3.4% in diabetic patients without microalbuminuria and 29.2 + 2.0% in diabetic patients with microalbuminuria. Diabetic patients differed from healthy subjects (P = 0.005), due to a difference between control subjects and microalbuminuric diabetic patients (P <0.001). NG-Monomethyl-L-arginine did not influence nitroprusside responses but reduced carbachol responses in control subjects and normoalbuminuric diabetic patients but not in microalbuminuric diabetic patients. 4. These results provide evidence of abnormal endothelium-derived relaxing factor/nitric oxide biosynthesis in insulin-dependent diabetic patients with microalbuminuria.

scholarly journals Cerebral blood flow increases during insulin-induced hypoglycaemia in Type 1 (insulin-dependent) diabetic patients and control subjects

Diabetologia ◽  
1987 ◽  
Vol 30 (5) ◽  
pp. 305-309 ◽  
Author(s):  
H. A. W. Neil ◽  
E. A. M. Gale ◽  
S. J. C. Hamilton ◽  
I. Lopez-Espinoza ◽  
R. Kaura ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic ◽  
And Control

Effect of Posture and Acute Glycaemic Control on the Excretion of Retinol-Binding Protein in Normoalbuminuric Insulin-Dependent Diabetic Patients

1993 ◽  
Vol 84 (4) ◽  
pp. 461-467 ◽  
Author(s):  
Carlo Catalano ◽  
Peter H. Winocour ◽  
Susan Gillespie ◽  
Ian Gibb ◽  
K. George M. M. Alberti
Keyword(s):  
Blood Glucose Concentration ◽  
Excretion Rate ◽  
Binding Protein ◽  
Insulin Dependent Diabetes ◽  
Retinol Binding Protein ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Protein Excretion ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

1. It has been suggested that tubular damage may precede gomerular damage at the onset of diabetic nephropathy. This may be reflected by increased urinary excretion of low-molecular-mass proteins, such as retinol-binding protein. 2. We have measured the urinary excretion rate of retinol-binding protein overnight, during orthostasis and during a hyperinsulinaemic euglycaemic clamp (blood glucose concentration 7.0 mmol/l) with stable diuresis in 34 normotensive, normoalbuminuric insulin-dependent diabetic patients and in 10 normal control subjects. Normal control subjects were not clamped. A further four normoalbuminuric insulin-dependent diabetic patients were rendered euglycaemic without a water load. 3. Overnight retinol-binding protein excretion rate was 58 (16-157) [median(range)] ng/min in patients with insulin-dependent diabetes and 32 (15-72) ng/min in control subjects (P < 0.01). The excretion rate did not change during orthostasis [patients with insulin-dependent diabetes, 67 (3-173) ng/min; control subjects, 23 (5-78) ng/min]. During the euglycaemic clamp retinol-binding protein excretion rate increased to 383 (78-4897) ng/min in patients with insulin-dependent diabetes (P < 0.01). An average increment in retinol-binding protein excretion rate of greater than 4000% was noted after acute euglycaemia in those patients with insulin-dependent diabetes who were not water-loaded. 4. In insulin-dependent diabetes, both overnight and orthostatic retinal-binding protein excretion was not correlated with fasting blood glucose concentration, HbA1, fructosamine or duration of diabetes. The absolute and incremental excretion rates of retinol-binding protein during the clamp were, however, correlated with both fasting blood glucose concentration and glucose excretion rate (rs = 0.41-0.48, P < 0.01). 5. The study demonstrates that retinol-binding protein excretion is increased in insulin-dependent diabetes in the absence of microalbuminuria and that this increase in retinol-binding protein excretion is particularly pronounced after acute euglycaemia. Acute tubular dysfunction related to acute changes in glucose control appears to be the most likely explanation, but established tubular damage could also be implicated. Postural variation in retinol-binding protein excretion was not detected.

scholarly journals Inhibition of TNF-αReverses the Pathological Resorption Pit Profile of Osteoclasts from Patients with Acute Charcot Osteoarthropathy

2015 ◽  
Vol 2015 ◽  
pp. 1-10 ◽  
Author(s):  
Nina L. Petrova ◽  
Peter K. Petrov ◽  
Michael E. Edmonds ◽  
Catherine M. Shanahan
Keyword(s):  
Osteoclast Formation ◽  
Diabetic Patients ◽  
Blood Monocytes ◽  
Control Subjects ◽  
Osteoclastic Resorption ◽  
Healthy Control ◽  
Macrophage Colony ◽  
And Control ◽  
Charcot Osteoarthropathy

We hypothesised that tumour necrosis factor-α(TNF-α) may enhance receptor activator of nuclear factor-κβligand- (RANKL-) mediated osteoclastogenesis in acute Charcot osteoarthropathy. Peripheral blood monocytes were isolated from 10 acute Charcot patients, 8 diabetic patients, and 9 healthy control subjects and culturedin vitroon plastic and bone discs. Osteoclast formation and resorption were assessed after treatment with (1) macrophage-colony stimulating factor (M-CSF) and RANKL and (2) M-CSF, RANKL, and neutralising antibody to TNF-α(anti-TNF-α). Resorption was measured on the surface of bone discs by image analysis and under the surface using surface profilometry. Although osteoclast formation was similar in M-CSF + RANKL-treated cultures between the groups (p>0.05), there was a significant increase in the area of resorption on the surface (p<0.01) and under the surface (p<0.01) in Charcot patients compared with diabetic patients and control subjects. The addition of anti-TNF-αresulted in a significant reduction in the area of resorption on the surface (p<0.05) and under the surface (p<0.05) only in Charcot patients as well as a normalisation of the aberrant erosion profile. We conclude that TNF-αmodulates RANKL-mediated osteoclastic resorptionin vitroin patients with acute Charcot osteoarthropathy.

Effects of somatostatin on the behaviour of thromboxane B2 and β-thromboglobulin in type I diabetes

1985 ◽  
Vol 109 (1) ◽  
pp. 104-107 ◽  
Author(s):  
G. Gragnoli ◽  
A. M. Signorini ◽  
I. Tanganelli
Keyword(s):  
Platelet Function ◽  
Type I Diabetes ◽  
Thromboxane B2 ◽  
Diabetic Patients ◽  
Base Line ◽  
Type I ◽  
Control Subjects ◽  
Pharmacological Studies ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Abstract. Pharmacological studies have shown that the addition of somatostatin to insulin promotes a more rapid recovery from diabetic ketoacidosis. However, contradictory results have been reported concerning the action of somatostatin on platelet function, frequently deranged in diabetes. Therefore the plasma levels of thromboxane B2, a stable metabolite of proaggregatory thromboxane A2 and of β-thromboglobulin, a marker of platelet activation, were studied in 9 control subjects and in 13 insulin-dependent diabetic patients before and during somatostatin injection, administered as an initial 250 μg iv bolus followed by infusion of 300 μg over 3 h. In both groups, after somatostatin infusion thromboxane B2 and β-thromboglobulin levels showed, respectively, a progressive fall and an increase up to the second hour. Over the next hour thromboxane B2 increased and μ-thromboglobulin decreased but their levels did not return to basal values. During this experiment β-thromboglobulin plasma values in diabetic patients did not differ from those of control subjects. In contrast, thromboxane B2, decreased in relation to pharmacological treatment, maintained elevated levels. Our data, however, demonstrate that the dose of somatostatin used, produced in the diabetic patients a normal fall of thromboxane B2 in terms of percentage of base-line values, but increases of β-thromboglobulin lower than in control subjects. It is suggested that platelet function should be evaluated when somatostatin is used in the treatment of poorly controlled type I diabetes.

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