Endocrinology

Diabetes Types

Type 1, type 2, gestational, MODY — same hyperglycemia, different mechanisms

Diabetes is chronic hyperglycemia from impaired insulin action. Type 1 (~10%) is autoimmune destruction of pancreatic β-cells; presents in childhood with absolute insulin deficiency, DKA. Type 2 (~85-90%) is insulin resistance plus relative deficiency; tied to obesity and lifestyle. Gestational diabetes appears in pregnancy, often resolves postpartum but flags lifetime risk. MODY (~1-5%) is monogenic — autosomal dominant β-cell defect, often misdiagnosed as type 1 or 2. Diagnosis: HbA1c ≥6.5%, fasting glucose ≥126, random ≥200 with symptoms, or 2-hour OGTT ≥200.

  • Type 1Autoimmune; absolute insulin deficiency
  • Type 2Insulin resistance + relative deficiency
  • GestationalPregnancy onset; ~50% develop T2DM in 10y
  • MODYMonogenic, autosomal dominant
  • Diagnosis HbA1c≥6.5%
  • Goal HbA1c<7% (most adults)

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Why diabetes biology matters

  • Cardiovascular protection. Diabetes is a coronary equivalent; SGLT2i/GLP-1RA reduce MACE.
  • Renal protection. Empagliflozin slows CKD progression in diabetic and non-diabetic kidney disease.
  • Obesity treatment. Semaglutide (Wegovy), tirzepatide (Mounjaro) — GLP-1/GIP analogs revolutionizing weight management.
  • Pre-diabetes intervention. Lifestyle prevents 58% of progression; metformin 31% (DPP trial).
  • Hospital glucose management. Hyperglycemia in inpatients raises infection, mortality.
  • Pregnancy planning. Pre-conception HbA1c <6.5% reduces malformation risk in T1/T2DM.
  • Continuous glucose monitoring. Time-in-range (70-180 mg/dL >70%) supplements HbA1c.

Common misconceptions

  • "Sugar causes diabetes." Excess calories and obesity drive Type 2; sucrose itself isn't uniquely toxic.
  • Type 2 is "mild" diabetes. Same complications as Type 1 with longer asymptomatic phase.
  • Insulin means failure. Insulin is the most effective glucose-lowering agent; some patients need it.
  • HbA1c alone tells you control. Time-in-range and hypoglycemia exposure also matter.
  • SGLT2 inhibitors only lower glucose. They reduce CV death, HF hospitalization, CKD progression independently.
  • Lean people can't have Type 2. 10-20% of T2DM are lean; consider MODY, LADA, secondary diabetes.

Frequently asked questions

How does Type 1 differ from Type 2?

Type 1: autoimmune (anti-GAD, anti-IA-2, anti-ZnT8 antibodies positive in 90%); HLA-DR3/DR4 risk; lean; presents young (peak 4-7 and 10-14); requires insulin from diagnosis; ketosis-prone. Type 2: insulin resistance + β-cell decline; obesity, sedentary lifestyle, family history; usually adult onset (now seen in adolescents); managed with lifestyle, metformin, then add agents; ketosis less common but possible.

How is HbA1c interpreted?

HbA1c reflects average glucose over preceding 8-12 weeks (RBC lifespan ~120 days). Each 1% increase ≈ 28 mg/dL average glucose. 5.7-6.4%: prediabetes. ≥6.5%: diabetes. Goal <7% for most adults; <6.5% if achievable safely; <8% in elderly/comorbid. Confounded by hemoglobinopathies, anemia, recent transfusion, pregnancy — use fructosamine or CGM in those cases.

How is Type 2 treated?

Step 1: lifestyle (Mediterranean diet, 150 min/week exercise, 5-10% weight loss). Step 2: metformin (decreases hepatic glucose output, weight neutral, possibly cardioprotective). Step 3: add SGLT2 inhibitor (empagliflozin) if CV/renal disease, GLP-1 receptor agonist (semaglutide) for obesity/CV protection. Insulin when β-cell function severely declined or HbA1c >10%. Sulfonylureas, DPP-4i are alternatives.

What is DKA?

Diabetic ketoacidosis: insulin deficiency leads to lipolysis, ketogenesis (β-hydroxybutyrate, acetoacetate), metabolic acidosis. Glucose >250, pH <7.3, anion gap >12, ketones positive. Typical T1DM but increasingly seen in T2DM (especially with SGLT2 inhibitors — euglycemic DKA). Treatment: IV fluids, insulin drip, K+ replacement, identify trigger (infection, missed insulin, MI).

What about gestational diabetes?

Screen at 24-28 weeks with 50g OGTT challenge or 75g fasting test. Insulin resistance peaks late pregnancy due to placental hormones. Risks: macrosomia, shoulder dystocia, neonatal hypoglycemia, preeclampsia. Treatment: diet, exercise, metformin, insulin if needed. Postpartum: 75g OGTT at 6-12 weeks; lifelong T2DM risk ~50% over 10 years; lifestyle screening annually.

What is MODY?

Maturity-onset diabetes of the young — autosomal dominant β-cell defect. 14 subtypes; HNF1A (MODY3) most common. Features: diagnosis <25 years, autoantibody negative, family history in three consecutive generations, residual β-cell function. Subtype matters: MODY2 (glucokinase) needs no treatment; MODY1/3 (HNF) very sensitive to sulfonylureas (off insulin possible). Genetic testing changes management.

What complications develop?

Microvascular (glycemic control matters most): retinopathy (#1 cause adult blindness), nephropathy (#1 cause ESRD), neuropathy (foot ulcers, gastroparesis, autonomic). Macrovascular (BP/lipids matter more): MI, stroke, PAD. Other: NAFLD, infections, dementia. Tight HbA1c plus BP <130/80 plus statin reduce events. SGLT2i and GLP-1RA add cardiorenal protection beyond glucose lowering.