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Source comparison

Tesamorelin NAFLD: Type Comparison

Metabolic Syndrome NAFLD Insulin resistance, visceral adiposity, hepatic lipogenesis High (35–50% hepatic fat reduction) HOMA-IR >3.0, VAT >160 cm², hepatic fat >10% Best-characterized population. Strongest clinical evidence from HIV trials generalizes well Le

This comparison does not assign a generated winner or score.

  • Metabolic Syndrome NAFLD
  • Insulin resistance, visceral adiposity, hepatic lipogenesis
  • High (35–50% hepatic fat reduction)
  • HOMA-IR >3.0, VAT >160 cm², hepatic fat >10%
  • Best-characterized population. Strongest clinical evidence from HIV trials generalizes well
  • Lean NAFLD
  • Genetic (PNPLA3), dietary (fructose), mitochondrial dysfunction
  • Low-Moderate (15–25% reduction)
  • BMI <25, normal VAT, normal insulin sensitivity
  • Mechanism misalignment. GH-mediated lipolysis addresses a pathway that isn't the primary driver
  • HIV-Associated NAFLD
  • Antiretroviral toxicity, immune activation, lipodystrophy
  • High (30–40% reduction)
  • Published trial population. Elevated VAT, insulin resistance
  • Only population with randomized controlled trial data as of 2026
  • NASH with Fibrosis (F0–F2)
  • Inflammation, hepatocyte ballooning, early fibrosis
  • Moderate (25–35% fat reduction, inflammation markers improve)
  • ALT >60 U/L, NAS score ≥4, fibrosis F0–F2
  • Hepatic fat and inflammation improve; fibrosis reversal requires >2 years of sustained metabolic correction
  • Advanced Fibrosis (F3–F4)
  • Cirrhosis, stellate cell activation, portal hypertension
  • Unknown. Excluded from trials
  • Fibrosis F3–F4 by biopsy or elastography
  • No safety data. Theoretical risk of GH stimulating fibrotic pathways limits use
  • Tesamorelin works best when NAFLD is driven by insulin resistance and visceral adiposity. The exact metabolic state where GH's lipolytic and insulin-sensitizing effects are most beneficial. Patients with lean NAFLD or advanced fibrosis fall outside the established evidence base.