Which statement best describes Type 1 diabetes mellitus pathophysiology?

Which statement best describes Type 1 diabetes mellitus pathophysiology?

• A. Insulin resistance with preserved beta cell function.
• B. Autoimmune destruction of alpha cells causing impaired glucagon response.
• C. Pancreatic beta cell destruction leading to absolute insulin deficiency.
• D. Secondary diabetes due to pancreatic damage without beta cell loss.

Answer: (C)

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency. Without insulin, glucose cannot enter most cells, so blood glucose rises despite ongoing hepatic glucose production. The lack of insulin also removes inhibition of lipolysis, causing increased free fatty acids and ketone production, which can lead to diabetic ketoacidosis if not treated. Autoimmune destruction is often associated with B-cell–targeted autoantibodies (such as GAD65, IA-2, ZnT8) and typically presents in younger individuals, though it can occur at any age. Because endogenous insulin production is essentially stopped, lifelong insulin therapy is required. This contrasts with type 2 diabetes, where insulin resistance with a relative rather than absolute insulin deficiency is the main issue, and with pancreatic damage without beta-cell loss or alpha-cell destruction, which are not characteristic of classic type 1 diabetes.

Type 1 diabetes results from autoimmune destruction of pancreatic beta cells, leading to absolute insulin deficiency. Without insulin, glucose cannot enter most cells, so blood glucose rises despite ongoing hepatic glucose production. The lack of insulin also removes inhibition of lipolysis, causing increased free fatty acids and ketone production, which can lead to diabetic ketoacidosis if not treated. Autoimmune destruction is often associated with B-cell–targeted autoantibodies (such as GAD65, IA-2, ZnT8) and typically presents in younger individuals, though it can occur at any age. Because endogenous insulin production is essentially stopped, lifelong insulin therapy is required. This contrasts with type 2 diabetes, where insulin resistance with a relative rather than absolute insulin deficiency is the main issue, and with pancreatic damage without beta-cell loss or alpha-cell destruction, which are not characteristic of classic type 1 diabetes.