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Serum CCN6 levels are significantly reduced in non-alcoholic fatty liver disease (NAFLD) patients. Lower CCN6 is associated with increased NAFLD risk and metabolic dysfunction, highlighting its potential role in disease pathogenesis.

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Area of Science:

  • Metabolic pathways
  • Adipokine family
  • Pathogenesis of liver disease

Background:

  • CCN6/WISP3, a CCN family adipokine, influences metabolic pathways.
  • The role of CCN6 in non-alcoholic fatty liver disease (NAFLD) pathogenesis is not well understood.
  • This study investigates CCN6 serum levels in NAFLD patients versus healthy controls.

Purpose of the Study:

  • To compare serum CCN6 levels between NAFLD patients and healthy individuals.
  • To explore the association between CCN6 levels and NAFLD risk factors.
  • To elucidate the potential role of CCN6 in NAFLD development.

Main Methods:

  • Case-control study involving 88 NAFLD patients and 88 controls.
  • Serum levels of CCN6, TNF-α, IL-6, adiponectin, and fasting insulin measured by ELISA.
  • Biochemical variables (AST, ALT, lipids, FBG) analyzed using an autoanalyzer.

Main Results:

  • Significantly lower CCN6 levels observed in NAFLD patients (1501.95 ± 483.41 pg/ml) compared to controls (1899.49 ± 559.70 pg/ml, P < 0.001).
  • Negative correlations found between CCN6 and insulin, HOMA-IR, and TNF-α in NAFLD patients.
  • CCN6 levels showed a significant association with NAFLD risk (OR = 0.867, P < 0.001) after adjusting for confounders.

Conclusions:

  • NAFLD patients exhibit significantly reduced serum CCN6 levels.
  • Decreased CCN6 levels are linked to an increased risk of developing NAFLD.
  • CCN6 may play a protective role in NAFLD pathogenesis.