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Apolipoprotein CIII and Angiopoietin-like Protein 8 are Elevated in Lipodystrophy and Decrease after Metreleptin.

Marissa Lightbourne1, Anna Wolska2, Brent S Abel3

  • 1Eunice Kennedy Shriver National Institute of Child Health and Human Development, National Institutes of Health, Bethesda, MD, USA.

Journal of the Endocrine Society
|January 14, 2021
PubMed
Summary
This summary is machine-generated.

Elevated levels of lipoprotein lipase (LPL) inhibitors, apolipoprotein C-III and angiopoietin-like protein 8, contribute to hypertriglyceridemia in lipodystrophy. Metreleptin treatment may reduce these inhibitors, offering a therapeutic strategy.

Keywords:
angiopoietin like proteinapolipoproteinhypertriglyceridemialeptinlipodystrophylipoprotein lipase

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Area of Science:

  • Endocrinology
  • Metabolic Disorders
  • Lipid Metabolism

Background:

  • Lipodystrophy syndromes are characterized by severe hypertriglyceridemia.
  • Leptin therapy, specifically metreleptin, has shown efficacy in improving hypertriglyceridemia in these patients.
  • The precise mechanisms underlying hypertriglyceridemia and its resolution with metreleptin remain unclear.

Purpose of the Study:

  • To investigate the relationship between circulating lipoprotein lipase (LPL) modulators and hypertriglyceridemia.
  • To compare LPL modulator levels in healthy controls versus patients with lipodystrophy.
  • To assess changes in LPL modulators following metreleptin treatment in lipodystrophy patients.

Main Methods:

  • Cross-sectional study comparing lipodystrophy patients (n=14) with healthy controls (n=28).
  • Longitudinal analysis of lipodystrophy patients before and after 2 weeks and 6 months of metreleptin treatment.
  • Quantification of LPL stimulators (apoC-II, apoA-V) and inhibitors (apoC-III, ANGPTLs 3, 4, 8) and assessment of ex vivo LPL activity.

Main Results:

  • Lipodystrophy patients exhibited significantly higher levels of most LPL modulators, including ANGPTL8 (>300-fold) and apoC-III (4-fold), compared to controls.
  • Elevated LPL inhibitors (apoC-III, ANGPTL8) positively correlated with triglyceride levels at baseline.
  • Metreleptin treatment reduced apoC-II, apoC-III, and ANGPTL8 levels, with significant decreases observed by 6 months for ANGPTL8.

Conclusions:

  • Increased levels of LPL inhibitors, specifically apolipoprotein C-III and angiopoietin-like protein 8, likely contribute to hypertriglyceridemia in lipodystrophy.
  • These LPL inhibitors may mediate the triglyceride-lowering effects of metreleptin.
  • ApoC-III and ANGPTL8 are potential therapeutic targets for managing hypertriglyceridemia in lipodystrophy.