A Prospective Study: Latent Autoimmune Diabetes in Adults and Beta-Cell Function

By Lauren Thayer from In The Cloud Copy

Latent autoimmune diabetes in adults or LADA is a slow progressing form of autoimmune diabetes. Similar to type 1 diabetes, also an autoimmune disease, in LADA, the pancreas stops producing insulin in adequate qualities. The insulin-producing cells of the pancreas, called beta cells, a type of islet cell, are slowly damaged, ultimately causing this decline in insulin production.

How does LADA Differ from Type 1 Diabetes?

LADA and type 1 diabetes are both autoimmune diseases, but they differ in that patients with LADA often do not require insulin for months to years after a diagnosis, while those with a type 1 diabetes diagnosis will require replacement insulin immediately, as their pancreas produces very little or no insulin.

The age at diagnosis also varies from a LADA diagnosis and a type 1 diabetes diagnosis. A patient with LADA is typically over the age of 30 at diagnosis, while those with type 1 diabetes are often much younger, with a peak diagnosis age of around 14.

People with LADA are often misdiagnosed with type 2 diabetes as the pancreas is still producing some insulin.

Beta Cell Function

Beta cells are located in the pancreas in the islets of Langerhans. The main function of a beta cell is to produce and secrete insulin into the body, thereby regulating the levels of glucose in the body.
Beta cells release C-peptide, which works to prevent various symptoms of vascular deterioration related to diabetes, including neuropathy. The level of C-peptide measured in a person’s body can also give insight into the viable beta cell mass available.

Possible Determinants of Beta-Cell Function Progression in Patients with LADA

An 8-year prospective study was done to assess patterns of the progression of beta cell function. Failure of beta cell function was defined by fasting C-peptide (FCP) < 75 pmol/L. Other characteristics of patients were analyzed to attempt to identify possible determinants of beta-cell function progression. Characteristics included BMI, age of onset of disease, and glutamic acid decarboxylase autoantibody (GADA) titer.

The study, “Decline Pattern of Beta-cell Function in Adult-onset Latent Autoimmune Diabetes: an 8-year Prospective Study,” found that found that 29 of the 101 test subjects did develop failure of their beta cells. The C-peptide in LADA patients were biphasic, meaning it had two phases. Initially it showed a fast paced linear progression and then entered a period of stability.

The GADA titer, discussed earlier, was valuable in identifying those who face an elevated risk of beta cell dysfunction. Those with a high GADA titer were more likely to show beta-cell function failure compared to those with a low GADA titer. In fact, 71.3% of patients with high-GADA titers showed failure compared to only 6.2% of patients with a low GADA titer.

While the function of GADA and its effects on LADA patients is still being thoroughly studied, this study further supports that theory that a GADA titer of less than 173.5 WHO units/mL is essential to maintain function of the B cells. Without B cells the body is unable to produce sufficient insulin to prevent a hyperglycemic state in the patient. Preservation of the B cells could help to slow or stop the development of progression of LADA in future patients.

Learn more about this study here.

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