ABSTRACT
Background: Advanced glycation end products are associated with chronic complications of diabetes mellitus. This glycation process renders many proteins immunogenic. Aim: To detect the presence of antibodies against albumin, collagen and low density lipoprotein glycation products in boys and teenagers with diabetes mellitus. Patients and methods : Thirty one patients with diabetes mellitus type I, aged 11ñ3.8 years and with a mean duration of disease of 3.7ñ2.7 years and 31 healthy controls aged 12.4ñ5.3 years were studied. Antibodies against glycation end products were detected by ELISA and results were expressed as a ratio of the optical density of the glycated protein/optical density of the native protein. Results : Diabetic patients and healthy controls did not have antibodies against albumin glycation end products. Diabetics had higher levels of antibodies than controls for collagen glycation end products (2.6ñ0.4 and 1.8ñ0.2 respectively, p< 0.01) and low density lipoprotein glycation end products (3.07ñ0.92 and 2.2ñ0.72 respectively, p< 0.05). Conclusions: The biological role of these antibodies is not clear. They could be a depuration mechanism for glycation end products or contribute to chronic complications of diabetes mellitus
Subject(s)
Humans , Male , Female , Child, Preschool , Adolescent , Autoantibodies/blood , Diabetes Mellitus, Type 1/immunology , Glycation End Products, Advanced/immunology , Enzyme-Linked Immunosorbent Assay , Case-Control StudiesABSTRACT
Background: immune cells participate in the formation of atheromatous plate, however little is known about the effects of native or oxidatively modified lipoproteins on these cells. Aim: To study the effects of lipoproteins on in vitro mononuclear cell proliferation. Material and methods: peripheral blood mononuclear cells were obtained from 10 patients with type 2 diabetes mellitus (aged 52 ñ 9 years old with a disease duration of 8.2 ñ 5.7 years and a mean glycosilated hemoglobin of 9.3 ñ 2.2 percent) and 10 non diabetic healthy controls (aged 50.3 ñ 7.1 years old). These were stimulated with phytohemagglutinin (PHA) alone or in the presence of native LDLS, malondialdehyde modified LDLs or glycated LDLs. Proliferation was measured as 3H-thymidine incorporation and expressed as Stimulation Index (SI). Results: SI of patients and healthy subjects, after PHA stimulation were similar: (57.5 ñ 29.8 and 61.1 ñ 23.5) respectively LDLs did not induce proliferation in neither group. Native LDLs produced a 98 percent inhibition of PHA induced proliferation. Malondialdehyde modified and glycated LDLs caused a 50 percent inhibition. The suppressive effect was maintained when lipoproteins were incorporated to culture media 60 min prior or after PHA stimulation. Conclusions: Lipoproteins inhibit in vitro PHA induced peripheral blood mononuclear cell proliferation both in diabetic and in non diabetic subjects
Subject(s)
Humans , Male , Female , Adult , Middle Aged , Diabetes Mellitus, Type 2/immunology , Immunosuppression Therapy , In Vitro Techniques , Lipoproteins, LDL/immunology , Phytohemagglutinins/pharmacology , Lymphoproliferative Disorders/immunology , Lymphocyte ActivationABSTRACT
La diabetes mellitus es una enfermedad poco frecuente en pediatría, cuyo diagnóstico debe sospecharse frente a un paciente con compromiso del estado general, poliuria y polidipsia y frente a todo paciente que ingresa en coma de causa no precisada. En los últimos años los avances en los estudios inmunológicos, genéticos y epidemiológicos han determinado que la destrucción de las células de los islotes de Langerhans, responsable de la diabetes infantil, es un proceso inmunológico regulado por una susceptibilidad genética. En este artículo se describe una actualización en los conocimientos de la etiopatogenia de la diabetes insulinodependiente o tipo I
Subject(s)
Humans , Infant , Diabetes Mellitus, Type 1/etiology , Diabetes Mellitus, Type 1/classification , Diabetes Mellitus, Type 1/diagnosis , Islets of Langerhans/immunologyABSTRACT
LDLs obtainded from blood of healthy subjects, were glycated or altered with malondialbehyde and used as antigens. Serum autoantibodies against these LDLs were measured by ELISA in 22 patients with non insulin dependent diabetes mellitus aged 46 to 67 years old and 13 healthy controls aged 41 to 64 years old. Basal and LDL stimulated tumor necrosis factor production in vitro, by peripheral leukocytes of diabetics and controls was also measured. Results: The ratio of glycated LDL/native LDL antibodies was higher in diabetics than in controls (9.37 ñ 2.72 and 0.41 ñ 0.11 respectively p < 0.05) and the ratio of MDA modified LDL/native LDL antibodies was not significantly different (8.64 ñ 3.83 and 2.14 ñ 1.26 respectively, NS). Tumor necrosis or production by leukocytes was higher in diabetics than in controls in basal conditions (53.3 ñ 15.3 and 26.9 ñ 14.7 arbitrary units (a.u.) respectively), when stimulated withnative LDL (46.5 ñ 5 and 24.3 ñ 9.4 a.u. respectively), when stimulated with malondialdehyde modified LDL (50 ñ 16.2 and 24.4 ñ 7.7 a.u. respectively) or when stimulated with glycated LDL (38.3 ñ 8.8 and 14.4 ñ 7.5 a.u. respectively). Conclusions: Diabetic patients have an enhanced immune response against low density lipoproteins, factor that could contribute to the accelared atherogenesis of this disease