## Discriminating Feature: Preserved Endogenous Insulin Secretion **Key Point:** The hallmark difference between type 2 and type 1 diabetes is the presence of residual beta cell function in type 2, evidenced by detectable C-peptide, versus near-complete beta cell destruction in type 1. ### Pathophysiology Comparison | Feature | Type 1 Diabetes | Type 2 Diabetes | |---------|-----------------|------------------| | **Beta cell mass** | <10% remaining (autoimmune destruction) | 40–60% remaining (dysfunction) | | **Fasting C-peptide** | <0.3 ng/mL (absent/minimal) | 0.8–3.1 ng/mL (preserved) | | **Fasting insulin** | <2 µIU/mL | Often normal or elevated | | **Primary defect** | Insulin deficiency | Insulin resistance + relative deficiency | | **Glucagon response** | Exaggerated (loss of beta-cell inhibition) | Often elevated but blunted | | **Hepatic glucose output** | Elevated (unopposed glucagon) | Elevated (glucagon + insulin resistance) | **High-Yield:** C-peptide is the gold-standard marker of endogenous insulin secretion because it is cleaved 1:1 from proinsulin and is NOT affected by exogenous insulin therapy. A detectable C-peptide in a hyperglycemic patient almost always indicates type 2 diabetes (or MODY, latent autoimmune diabetes in adults [LADA], or secondary diabetes). ### Clinical Significance **Clinical Pearl:** A type 2 diabetic with C-peptide >0.3 ng/mL retains some beta cell reserve and may respond to oral agents or GLP-1 agonists; a type 1 diabetic with C-peptide <0.3 ng/mL requires insulin from diagnosis. This single test guides therapy. **Mnemonic:** **C-peptide = Clue to endogenous production** — if present, think type 2 (or LADA); if absent, think type 1. [cite:Harrison 21e Ch 417; Endocrine Society Guidelines on T1DM vs T2DM]
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