Type 1 vs. Type 2 Diabetes: Autoimmunity vs. Insulin Resistance

Diabetes mellitus comprises distinct pathophysiological entities. The two main types differ fundamentally in etiology.

Type 1 Diabetes (T1D)

• Autoimmune destruction of pancreatic β-cells by T lymphocytes.
• Absolute insulin deficiency.
• Onset often childhood/adolescence, but can occur at any age (LADA in adults).
• Requires lifelong exogenous insulin.
• Associated with HLA-DR3/DR4, other autoimmune conditions (thyroiditis, celiac).

Type 2 Diabetes (T2D)

• Insulin resistance in muscle, liver, adipose tissue + progressive β-cell dysfunction/failure.
• Relative insulin deficiency (initially hyperinsulinemia).
• Strong genetic predisposition + lifestyle factors (obesity, inactivity, diet).
• Onset typically >40 years, but rising in youth with obesity.
• Managed with lifestyle, oral agents (metformin first-line), GLP-1 RAs, SGLT2 inhibitors, insulin as needed.

Key Distinctions

Feature	Type 1	Type 2
Primary defect	Autoimmune β-cell destruction	Insulin resistance + β-cell failure
Insulin level	Absent/very low	High → normal → low over time
Ketosis risk	High (DKA common at onset)	Low (unless severe stress)
Autoantibodies	Present (GAD65, IA-2, ZnT8, IAA)	Absent
Body habitus	Often lean	Often overweight/obese

Accurate classification guides therapy. Misdiagnosis (e.g., LADA as T2D) delays insulin initiation, risking DKA.