scholarly journals Diffuse Lymph-Nodes Microangiopathy as Concurrent Cause of Immunodeficiency in Long-Term Insulin-Dependent Diabetic Patients

2019 ◽  
pp. 25-29
Author(s):  
Pietro Muretto

Immune abnormalities have been demonstrated in vitro models in genetic (type1) autoimmune (type 2) and metabolic (type 1 and type 2) Insulin-Dependent Diabetes Mellitus (IDDM). However, the precise reason for increased susceptibility to frequent and protracted infections in diabetic patients is still unclear, despite a multitude of in vitro studies which have focused on the metabolic and functional modifications of immune cells Diabetes microangiopathy, which is a peculiar alteration of the disease, has been extensively described in the retina, renal glomeruli, skin, skeletal muscles, peripheral nerves, and other organs but not in lymph nodes. We report our histological and immunohistochemical observations in lymph-nodes removed in multiple sites during autopsy from four patients with long-term IDDM, severe lymphocytpenia and several infectious diseases during their life. The peculiar microangiopathic modifications made by presence of hyaline substance thickening basal membrane of thin vessels and capillaries appear concurrent with lymphodepletion of B and T cells dependent areas of lymph-nodes and with jointed marked reduction of Follicular Dendritic Reticulum Cells (FDRC). Indeed microangiopathy further compromise the traffic and diapedesis of T and B lymphocytes may prevent the transformation of endothelial cells into FDRC with severe immune failure of lymphoid follicles. The histological and immunohistochemical data in this study could provide additional insights into the complex problem of the immunodeficiency in diabetic patients.

1987 ◽  
Vol 253 (3) ◽  
pp. E300-E304 ◽  
Author(s):  
H. Yki-Jarvinen ◽  
K. Kubo ◽  
J. Zawadzki ◽  
S. Lillioja ◽  
A. Young ◽  
...  

It is unclear from previous studies whether qualitative or only quantitative differences exist in insulin action in adipocytes obtained from obese subjects with non-insulin-dependent diabetes mellitus (NIDDM) when compared with equally obese nondiabetic subjects. In addition, the role of changes in insulin binding as a cause of insulin resistance in NIDDM is still controversial. We compared the sensitivities of glucose transport and antilipolysis to insulin and measured insulin binding in abdominal adipocytes obtained from 45 obese nondiabetic (% fat, 41 +/- 1), 25 obese diabetic (% fat, 40 +/- 1), and 15 nonobese (% fat, 30 +/- 1) female southwestern American Indians. Compared with the nonobese group, the sensitivities of glucose transport and antilipolysis were reduced in both the obese nondiabetic and obese diabetic groups. Compared with the obese nondiabetic subjects, the ED50 for stimulation of glucose transport was higher in the obese patients with NIDDM (171 +/- 38 vs. 92 +/- 10 pM, P less than 0.005). In contrast, the ED50s for antilipolysis were similar in obese diabetic patients (32 +/- 6 pM) and obese nondiabetic subjects (27 +/- 3 pM). No difference was found in insulin binding in patients with NIDDM when compared with the equally obese nondiabetic subjects. These data indicate 1) the mechanism of insulin resistance differs in NIDDM and obesity, and 2) the selective loss of insulin sensitivity in NIDDM precludes changes in insulin binding as a cause of insulin resistance in this disorder.


1992 ◽  
Vol 263 (5) ◽  
pp. E877-E883 ◽  
Author(s):  
G. Biolo ◽  
P. Tessari ◽  
S. Inchiostro ◽  
D. Bruttomesso ◽  
L. Sabadin ◽  
...  

We have investigated postabsorptive and postprandial phenylalanine kinetics in non-obese type 2 diabetic patients [non-insulin-dependent diabetes mellitus (NIDDM)], using a double-isotope technique and the constant oral administration of a synthetic mixed meal. Fasting and postmeal glucose levels were increased (P < 0.01) in NIDDM (165 +/- 16 to 226 +/- 24 mg/dl), with respect to normal controls (85 +/- 3 to 102 +/- 6 mg/dl). Fasting insulin concentrations were comparable in NIDDM (13 +/- 2 microU/ml) and in normals (12 +/- 2 microU/ml), but after the meal it increased less (P < 0.07) in NIDDM vs. normals (to 36 +/- 5 vs. 56 +/- 12 microU/ml, respectively; P < 0.01 vs. basal for both). Postabsorptive phenylalanine rate of appearance (R(a)) in NIDDM (0.63 +/- 0.08 mumol.kg-1 x min-1) was comparable to that of controls (0.73 +/- 0.05 mumol.kg-1 x min-1, not significant). During the meal, total and endogenous phenylalanine R(a), splanchnic uptake, oxidation, and nonoxidative disposal of the ingested phenylalanine were also comparable in the two groups. These data indicate that fasting and postprandial kinetics of the essential amino acid phenylalanine are normal in NIDDM.


2013 ◽  
Vol 10 (1) ◽  
pp. 189-197
Author(s):  
Baghdad Science Journal

The aim of the study was comparative between oxidative stress in diabetes mellitus using the measurement of some biophysical and biochemical parameters on two groups of diabetic patients, were conducted in the Al-Yarmuk Teaching Hospital,30 patients insulin dependent diabetes mellitus (IDDM) or type 1 ,their ages ranged between (15-45) and30 patients non- insulin dependent diabetes mellitus (NIDDM) or type 2,their ages ranged between (42-65).This study has been compared with 30 healthy subjects. The present study was demonstrated to evaluate the alteration in oxidative stress as measured by plasma and red blood cells Malondialdehyde (MDA) andchanges in antioxidant mechanism as measured by plasma and red blood cells Glutathione (GSH) in patients with diabetes mellitus type 1 and type 2,in compares to healthy control group. The results showed significant increment in serum Malondialdehyde (MDA) levels ,and significant decrease in serum glutathione (GSH) levels of Diabetic patients (IDDM), (NIDDM)),compared with control. Total cholesterol (TC), triglyceride (TG) and low density lipoprotein (LDL), high density lipoprotein (HDL), Diabetic patients (IDDM),and (NIDDM)patients showed significant increases in LDL levels. LDLs and very-low-density lipoproteins (VLDLs) the so-called “bad” cholesterols. Unlike HDLs, LDLs and VLDLs are high-cholesterol particles and significant decrease in HDL compared with control Oxidative stress results when free radicals increase more than antioxidants which is naturally synthesis in the body, then causes changing in the cells accure by oxidative stress.


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