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Trigger For T1DM: A Research Map

Scientists have identified the possible trigger for type 1 diabetes mellitus (T1DM).
The T cells of the immune system do not recognise self-antigens, i.e., the body’s own cells. Therefore, they are protected from the attack of the immune system. In T1DM and other autoimmune disorders, this protective system gets disrupted1.

Dr Delong and his colleagues carried out an experiment to study the trigger in T1DM. They isolated T cells from a T1DM mouse model and determined the trigger that is recognised as a foreign body in the insulin-producing β-cells. They recognised a modified version of insulin which acted as an antigen. They also observed that the immune T cells from pancreatic islets of two organ donors with T1DM recognised hybrid insulin peptides (HIPs). This study concluded that these HIPs may have a significant role as a trigger to the immune system and hence attack the body’s insulin-producing pancreatic β-cells, and thus causing T1DM1. Antibodies from the blood of T1DM patients…
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Type 1 Diabetes Mellitus: Aetiology And Pathogenesis

T1DM is allied with the selective destruction of insulin-producing β-cells in the pancreas. The commencement of clinical disease signifies the end stage of β-cell destruction which leads to T1DM. There is marked heterogeneity of the pancreatic lesions, which makes it difficult to follow the pathogenesis of selective β-cell destruction within the islet in T1DM1.

Type 1 Diabetes Mellitus: An Alarming Condition

Diabetes mellitus (DM), a metabolic disorder, is mainly of two types. Type 1 Diabetes Mellitus (T1DM), insulin dependent DM, is an autoimmune reaction to proteins of the islet cells of the pancreas. There is a lack of insulin secretion by β- cells of the pancreas. Type 2 Diabetes Mellitus (T2DM), non-insulin dependent DM, is a combination of genetic factors related to impaired insulin secretion, insulin resistance and environmental factors such as obesity, overeating, lack of exercise, stress, ageing. There is a decreased sensitivity of target tissues to insulin1.