Comparison of BT-PABA test and fecal chymotrypsin measurements in normal subjects and diabetic patients

1990 ◽  
Vol 27 (2) ◽  
pp. 157-163
Author(s):  
Giuseppe Montalto ◽  
Antonio Carroccio ◽  
Giovanni Marino ◽  
Maurizio Soresi ◽  
Cesare Marco ◽  
...  
Keyword(s):  
Normal Subjects ◽  
Diabetic Patients ◽  
Fecal Chymotrypsin

Insulin resistance is localized to skeletal but not heart muscle in type 1 diabetes

1993 ◽  
Vol 264 (5) ◽  
pp. E756-E762 ◽  
Author(s):  
P. Nuutila ◽  
J. Knuuti ◽  
U. Ruotsalainen ◽  
V. A. Koivisto ◽  
E. Eronen ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Glucose Uptake ◽  
Compartment Model ◽  
Normal Subjects ◽  
Whole Body ◽  
Diabetic Patients ◽  
Uptake Rates ◽  
Arm Muscles ◽  
Type 1 Diabetic Patients

To determine the tissue localization of insulin resistance in type 1 diabetic patients, whole body and regional glucose uptake rates were determined under euglycemic hyperinsulinemic conditions. Leg, arm, and heart glucose uptake rates were measured using positron emission tomography-derived 2-deoxy-2-[18F]-fluoro-D-glucose kinetics and the three-compartment model described by Sokoloff et al. (L. Sokoloff, M. Reivich, C. Kennedy, M.C. DesRosiers, C.S. Patlak, K.D. Pettigrew, O. Sakurada, and M. Shinohara. J. Neurochem. 28: 897–916, 1977) in eight type 1 diabetic patients and eight matched normal subjects. Whole body glucose uptake was quantitated by the euglycemic insulin clamp technique. Whole body glucose uptake was approximately 31% lower in the diabetic patients (P < 0.01) than in the normal subjects, thus confirming the presence of whole body insulin resistance. The rate of glucose uptake was approximately 45% lower in leg muscle when measured in the femoral region (55 +/- 7 vs. 102 +/- 13 mumol.kg muscle-1.min-1, diabetic patients vs. normal subjects, P < 0.05) and approximately 27% lower in the arm muscles (66 +/- 4 vs. 90 +/- 13 mumol.kg muscle-1.min-1, respectively, P < 0.05), whereas no difference was observed in heart glucose uptake [789 +/- 80 vs. 763 +/- 58 mumol.kg muscle-1.min-1 not significant (NS)]. Whole body glucose uptake correlated with glucose uptake in femoral (r = 0.93, P < 0.005) and arm muscles (r = 0.66, P < 0.05) but not with glucose uptake in the heart (r = 0.04, NS). We conclude that insulin resistance in type 1 diabetic patients is localized to skeletal muscle, whereas heart glucose uptake is unaffected.(ABSTRACT TRUNCATED AT 250 WORDS)

scholarly journals Intralesional Infiltrations of Cell-Free Filtrates Derived from Human Diabetic Tissues Delay the Healing Process and Recreate Diabetes Histopathological Changes in Healthy Rats

2021 ◽  
Vol 2 ◽  
Author(s):  
Jorge Berlanga-Acosta ◽  
Maday Fernández-Mayola ◽  
Yssel Mendoza-Marí ◽  
Ariana García-Ojalvo ◽  
Raymond J. Playford ◽  
...  
Keyword(s):  
Healing Process ◽  
Normal Subjects ◽  
Nerve Degeneration ◽  
Tissue Homogenate ◽  
Diabetic Rat ◽  
Metabolic Memory ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Medical Interventions ◽  
Tissue Homogenates

Lower limb ulcers in type-2 diabetic patients are a frequent complication that tributes to amputation and reduces survival. We hypothesized that diabetic healing impairment and other histopathologic hallmarks are mediated by a T2DM-induced tissue priming/metabolic memory that can be transferred from humans to healthy recipient animals and consequently reproduce diabetic donor’s phenotypes. We examined the effect of human T2DM tissue homogenates injected into non-diabetic rat excisional wounds. Fresh granulation tissue, popliteal artery, and peroneal nerve of patients with T2DM were obtained following amputation. Post-mammoplasty granulation and post-traumatic amputation-tissue of normal subjects acted as controls. The homogenates were intralesionally injected for 6–7 days into rats’ excisional thickness wounds. Infiltration with the different homogenates caused impaired wound closure, inflammation, nerve degeneration, and arterial thickening (all P &lt; 0.01 vs relevant control) resembling histopathology of diabetic donor tissues. Control materials caused marginal inflammation only. Infiltration with glycated bovine albumin provoked inflammation and wound healing delay but did not induce arterial thickening. The reproduction of human diabetic traits in healthy recipient animals through a tissue homogenate support the notion on the existence of tissue metabolic memory-associated and transmissible factors, involved in the pathogenesis of diabetic complications. These may have futuristic clinical implications for medical interventions.

Head-space gas-chromatographic determination of 3-hydroxybutyrate in plasma after enzymic reactions, and the relationship among the three ketone bodies.

1985 ◽  
Vol 31 (4) ◽  
pp. 596-598 ◽  
Author(s):  
M Kimura ◽  
K Kobayashi ◽  
A Matsuoka ◽  
K Hayashi ◽  
Y Kimura
Keyword(s):  
Ketone Bodies ◽  
Normal Subjects ◽  
Chromatographic Determination ◽  
Diabetic Patients ◽  
Head Space ◽  
Analytical Recovery ◽  
Acetoacetate Decarboxylase ◽  
Reproducible Method ◽  
The Relationship

Abstract In this sensitive, reproducible method for determination of D-3-hydroxybutyrate (3-OHB) in plasma, it is converted to acetone by use of 3-hydroxybutyrate dehydrogenase (EC 1.1.1.30)/lactate dehydrogenase (EC 1.1.1.27) coupled with acetoacetate decarboxylase (EC 4.1.1.4). The resulting acetone is detected by head-space gas chromatography. The lowest concentration of 3-OHB detectable in plasma was 2 mumol/L. The calibration curve showed a linear relationship for 3-OHB concentration from 0 to 5 mmol/L (r = 0.999). Analytical recovery of 3-OHB (50 mumol/L) was 97.9 (SD 3.8)%. The method was developed for determination of the three ketone bodies in plasma. The ratio of acetone to acetoacetate was not significantly different (p greater than 0.2) between normals (n = 31) and diabetics (n = 86). In normal subjects, the ratio of 3-OHB to acetoacetate was 1.20 (SD 0.44). In diabetic patients, the ratio correlated with the logarithm of the total ketone body concentration (r = 0.828).

Evidence of Abnormal Factor: VIII Related Protein in Diabetes Mellitus

1979 ◽  
Author(s):  
E. Cacciola ◽  
R. Giustolisi ◽  
T. Lombardo ◽  
R. Musso ◽  
M. Russo ◽  
...  
Keyword(s):  
Factor Viii ◽  
Vascular Complications ◽  
Normal Subjects ◽  
Diabetic Patients ◽  
Related Protein ◽  
Biological Functions ◽  
Biophysical Properties ◽  
Con A ◽  
Crossed Immunoelectrophoresis ◽  
Ristocetin Cofactor

Biochemical and functional properties of Factor VIII related protein (VIII:RP) have been studied in the plasma from two groups of diabetic patients with or without vascular complications compared to normal subjects.The Factor VIII related antigen (VIIIR:AG) was performed by Laurell’s electroimmunoassay (LA) and electrophoretic mobility (EM) by two dimensional crossed Immunoelectrophoresis (2 DC IE). Biophysical properties were evaluated by cryoprecipitation and concanavalin A (Con A) treatment at different concentrations. Biological functions were determined using the ristocetin cofactor (RiCoF ) assay on fixed-washed platelets and procongulant activity (F VIII:C).In diabetic patients, particularly in the ones at higher thrombogenic risk, the evaluation of VIII:C/VIIIR; AG and VIII:vWF/VIIIR;AG ratios showed a significant (P<0.001) increased VIIIR:AG with a higher co-ristocelin activity than the procoagulant one. Furthermore, biophysical and bio chemical modifications of diabetic Factor VIIIR;AG, mainly a lower EM on 2 DCIE, were found. These results suggest that the Factor VIIIR:AG abnormality, detectable in diabetic plasma, can be related with an abnormal glycoprotein biosynthesis.

Prostaglandins and Platelet Function in Diabetes

1979 ◽  
Author(s):  
J. García-Conde ◽  
J.A. Amado ◽  
J. Merino ◽  
I. Benet
Keyword(s):  
Platelet Aggregation ◽  
Platelet Rich Plasma ◽  
Normal Subjects ◽  
Inhibitory Effect ◽  
Rat Aorta ◽  
Diabetic Group ◽  
Diabetic Patients ◽  
Prostaglandin I2 ◽  
Induced Aggregation ◽  
Normal Controls

We have studied platelet aggregation induced by 0,5 mM. Araquidonic acid (AA) addition to platelet-rich-plasma (PRP) from 21 insulin treated diabetic patients and in 21 non-diabetic controls. The velocity of aggregation was significantly higher in the diabetic group. There was no differences in the velocity of aggregation in patients with or without retinopathy.The incubation of PRP of normal subjects at 37- during 5 minutes with 5,8 10-4 M. Imidazole changed the pattern of aggregation: The velocity of aggregation was slower and appeared a wave of disaggregation. Imida zole had not effect on aggregation in the diabetic group. This data add support to the findings published by COLWLLL showing that platelets from diabetics have hyperactive AA metabolism. Prostaglandin I2 (PGI2) obtained from rat aorta shows an inhibitory effect on ADP or AA induced aggregation. This effect is less marked in diabetic PRP than in PRP of normal controls. PGI2 release in platelet-poor-plasma from diabetics is normal. This can represent a resistance ot diabetic platelet to the anti aggregating effect of PGI 2. A similar finding was also appreciated with the PGE1 in three out of six patients so tar stu

Haemoglobin and flow-mediated vasodilation

2006 ◽  
Vol 110 (4) ◽  
pp. 467-473 ◽  
Author(s):  
Per Lav Madsen ◽  
Michaela Scheuermann Freestone ◽  
Stefan Neubauer ◽  
Keith Channon ◽  
Kieran Clarke
Keyword(s):  
Radial Artery ◽  
Vascular Endothelium ◽  
Type Ii Diabetes ◽  
Normal Subjects ◽  
Diabetic Patients ◽  
Type Ii ◽  
Peripheral Vasodilation ◽  
Hb Concentration ◽  
Flow Mediated Vasodilation ◽  
The Relationship

A low [Hb] (Hb concentration) is out-balanced by peripheral vasodilation via mechanisms that are incompletely understood. Peripheral vasodilation is influenced by NO (nitric oxide) released from vascular endothelium in response to increased vessel wall shear stress, and absorption by Hb is the main mechanism by which the bioactivity of NO is disarmed. Thus we propose that graded NO absorption is the mechanism through which a low [Hb] is related to peripheral vasodilation. In the present study, we examined the relationship between [Hb] and FMD (flow-mediated vasodilation; 5 min of cuff ischaemia) of the radial and brachial arteries in 33 normal subjects and in 13 patients with Type II diabetes, known to have impaired NO-mediated vasodilation. The smaller radial artery provided the more sensitive test, as it had a 2-fold larger FMD than the brachial artery (22±18% compared with 9±18% respectively, in normal subjects; means±S.D., P<0.05). FMD of the radial artery had a negative correlation with [Hb] (r2=−0.66, P<0.05; n=27). In subjects with [Hb] below and above the median of 14.1 g/dl, the radial artery FMD was 30±22% compared with 13±12% respectively (P<0.05). In diabetic patients, FMD was lower and a co-variation with [Hb] could not be established. Thus, in normal subjects, NO-mediated endothelium-related vasodilation at least partly out-balanced the ‘added burden’ of a low [Hb] during post-ischaemic reperfusion.

Effects of exogenous growth hormone pretreatment on the pituitary growth hormone response to growth hormone-releasing hormone alone or in combination with pyridostigmine in Type I diabetic patients

1991 ◽  
Vol 125 (5) ◽  
pp. 510-517 ◽  
Author(s):  
Andrea Giustina ◽  
Simonetta Bossoni ◽  
Corrado Bodini ◽  
Antonino Cimino ◽  
Giuseppe Pizzocolo ◽  
...  
Keyword(s):  
Growth Hormone ◽  
Blood Glucose ◽  
Normal Subjects ◽  
Diabetic Patients ◽  
Type I ◽  
Gh Secretion ◽  
Glucose Levels ◽  
Group A ◽  
Group B ◽  
And Control

Abstract. We evaluated the effects of iv pretreatment with exogenous GH on the GH response to GHRH either alone or in combination with pyridostigmine in 14 Type I diabetic patients and 6 normal subjects. All the subjects received an iv bolus injection of biosynthetic human GH, 2 IU; 2 h later they received either a. pyridostigmine, 120 mg orally, or b. placebo, 2 tablets orally, followed 1 h later by iv injection of GHRH(1-29) NH2, 100 μg. In normal subjects the median GH peak after GH+GHRH was 1.8, range 1.2-6.9 μg/l. Pyridostigmine enhanced the GH response to GHRH in all subjects. The median GH peak after pyridostigmine+ GH+GHRH was 32.7, range 19.8-42.1 μg/l (p<0.001 vs GHRH alone). Seven diabetic subjects had median GH peaks after GH+GHRH >6.9 μg/l (the maximum GH peak after GH+GHRH in normal subjects) (group A: median GH peak 35.7, range 21.7-55 μg/l). The other diabetic subjects had GH peak lower than 6.9 μg/l (group B: median GH peak 4.4, range 2.1-6.5 μg/l). Pyridostigmine significantly increased the GH response to GHRH in group B patients (median GH peak 29.3, range 15.7-93.4 μg/l, p<0.001 vs GH+GHRH alone), but not in group A patients (median GH peak 39.9, range 21.9-64.9 μg/l). Group A diabetic patients were younger and had higher HbA1c and blood glucose levels than group B patients. In those diabetic patients with an exaggerated GH response to GH+GHRH, pyridostigmine failed to cause the increase in GH secretion observed in diabetic and control subjects with no responses to GH+GHRH. It can be suggested that elevated 24-h GH levels in some Type I diabetic patients may be due to decreased somatostatinergic tone which in turn causes altered autoregulation of GH secretion. We hypothesize that this finding is a consequence of a reset of the hypothalamic control of GH secretion caused by a chronically elevated blood glucose level in this subpopulation.

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