Golimumab May Decrease Insulin Dependency in Type 1 Diabetic Patients

The most recent research conducted at the University of Buffalo and Diabetes center by Dr. Teresa Quattrin shows that a monoclonal antibody named Golimumab can be used to improve the response of the diabetic patient’s body towards endogenous insulin. The research was published in the New England Journal of Medicine (NEJM).

The antibody is known to protect the Beta cells of the Islet of Langerhans against the possible destruction being caused to them due to the autoimmune disease in Type 1 diabetes. The antibody not only increases the response to the endogenous insulin but also decreases the requirement of exogenous insulin.

Type 1 diabetes is a form of diabetes mellitus which is frequently observed in youngsters and adults from the age between 6 to 30. The onset of the DM Type 1 occurs after the culmination of lymphocytic infiltration and the destruction of the beta cells in the liver of the diabetic patient which results in low levels of natural insulin production in the body.

The damage to these beta cells in the Islet of Langerhans is caused by the effect of the autoimmune disease which destroys the body’s own cells without the correct sensitization of foreign cells. The insensitive 80-90% Beta cells lead to the failure of glucose catabolic activity. The condition needs to be treated in order to prevent ketosis, decrease the hyperglucagonemia and normalize lipid and protein metabolism.

Golimumab is a type of human monoclonal antibody – a drug which is prepared by the unique type of cloning of the human white blood cells. It is classified as the tumor necrosis factor alpha which means that it plays its role in systemic inflammation. It is one of the cytokines that is involved in the acute phase reactions during cell injury.

Golimumab has been introduced to use in multiple types of autoimmune disorders including rheumatoid arthritis, psoriasis, ankylosing spondylitis as well as Type 1 diabetes mellitus. The drug binds to the human TNFa present both in soluble and transmembrane bioactive forms. This prevents the binding of the TNFa to its receptors thereby inhibiting its biological activity.

The study provided the basis of the findings using a clinical setup where the target type 1 diabetic patients were either subjected to Golimumab or a placebo to study the effects. The trial was conducted on a multicenter, placebo-controlled, double-blind and a parallel-group trial which had a patient of age from 6 to 21 in a ratio of 2:1. The subjects were administered with the drug or the placebo and kept under observation for a period of 52 weeks. The primary endpoint was fixed to be as the area under the curve (AUC) of a 4-hour C-peptide. The second and tertiary endpoints included insulin use, patients’ responses, glycated hemoglobin levels in the blood, any hypoglycemic events and the ratio of fasting proinsulin to C-peptide over time.

The research included a total of 84 participants out of which 6 were given the real drug which is Golimumab and the remaining 28 were given the placebo. The mean standard deviation between the placebo and Golimumab was found to have a great difference of results in primary endpoint. There was no big difference in the levels of glycated hemoglobin. Evidently, the insulin levels in the body were greater in the Golimumab group than in the placebo group. A remission response of 43% and 7% was observed in the Golimumab and the placebo groups respectively. Adverse events like the hypoglycemic effects were only seen in 13 participants. 30 participants showed the titers of Golimumab antibodies in their blood in quantities lower than 1:1000.

Children and young adults who are newly diagnosed with the Type 1 Diabetes Mellitus and considered to show a good deal of response on the introduction of Golimumab in their bodies. This shows a significant improvement not only in the production and the sensitivity of insulin which regulates the blood glucose levels and the other metabolic functions of the patient’s body, but also results in decreased exogenous insulin requirements.

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