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Cellular and humoural autoimmunity markers in type 2 (non-insulin-dependent) diabetic patients with secondary drug
A V Zavala1, L E Fabiano de Bruno, A I Cardoso
1Cátedra de Nutrición, Hospital de Clínicas General José de San Martín, Universidad de Buenos Aires, Argentina.
Abstract:
In some cases patients with Type 2 (non-insulin-dependent) diabetes mellitus fail to respond to treatment with oral hypoglycaemic agents. These patients may respond in the same way as Type 1 (insulin-dependent) diabetic patients. Cellular immune aggression (defined as the capacity of peripheral mononuclear cells to inhibit stimulated insulin secretion by dispersed rat islet cells), insulin autoantibodies, C-peptide response and HLA antigens were determined in 31 Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents and in 22 control subjects. Nine (29.03%) of the 31 Type 2 diabetic patients showed positive cellular immune aggression (2 SD below control group) and 22 (70.97%) presented no cellular immune aggression. There was a relationship between positive cellular immune aggression and each of the following parameters: age, body mass index and microangiopathy. No correlation was found between positive cellular immune aggression and glycaemia, HbA1, blood lipids or atherosclerosis. Patients with positive cellular immune aggression showed a significantly lower glucagon-stimulated C-peptide response vs those with no cellular immune aggression. Within a sub-group of patients who had never been treated with insulin, insulin autoantibodies were present in four of six patients with positive cellular immune aggression. DR2 antigen was found with decreased frequency in patients whereas no DR3/DR4 heterozygotes were observed. Our data support the hypothesis that a group of Type 2 diabetic patients with secondary failure to oral hypoglycaemic agents presented autoimmunity towards pancreatic Beta cells.
Insights
Some Type 2 diabetes patients failing oral medication show signs of autoimmunity. This cellular immune aggression targets pancreatic beta cells, impacting C-peptide response and autoantibody presence.
Area of Science:
- Immunology
- Endocrinology
- Diabetology
Background:
- Type 2 diabetes mellitus (T2DM) patients sometimes fail oral hypoglycaemic agents, exhibiting responses similar to Type 1 diabetes.
- Secondary failure in T2DM suggests potential underlying mechanisms beyond typical insulin resistance.
Purpose of the Study:
- To investigate cellular immune aggression and related markers in T2DM patients with secondary failure to oral hypoglycaemic agents.
- To explore the association between cellular immune aggression and clinical/immunological parameters in this patient group.
Main Methods:
- Assessed cellular immune aggression (peripheral mononuclear cell inhibition of insulin secretion) in 31 T2DM patients and 22 controls.
- Measured insulin autoantibodies, C-peptide response, and HLA antigens.
- Correlated cellular immune aggression with age, BMI, microangiopathy, glycaemia, HbA1, lipids, and atherosclerosis.
Main Results:
- 29% of T2DM patients with secondary failure exhibited positive cellular immune aggression.
- Positive cellular immune aggression correlated with age, BMI, and microangiopathy, but not glycaemia or lipids.
- Patients with positive cellular immune aggression had a significantly lower glucagon-stimulated C-peptide response and increased insulin autoantibodies in a subgroup.
Conclusions:
- A subset of T2DM patients with secondary failure demonstrates autoimmunity against pancreatic beta cells.
- Cellular immune aggression may contribute to the progressive beta-cell dysfunction observed in these patients.
- These findings suggest a potential autoimmune component in some T2DM cases, warranting further investigation.