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Reducing hepatic PKD activity lowers circulating VLDL cholesterol.

Amanda J Genders1,2, Timothy Connor1, Shona Morrison1

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Protein kinase D (PKD) in the liver impacts glucose oxidation and fatty acid metabolism in normal conditions. Hepatic PKD does not significantly affect glucose homeostasis or obesity-related metabolic dysfunction.

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Area of Science:

  • Metabolic regulation
  • Liver function
  • Obesity research

Background:

  • Protein kinase D (PKD) is recognized for its role in energy balance and glucose metabolism.
  • The specific impact of hepatic PKD activity on these metabolic processes remains largely undetermined.

Purpose of the Study:

  • To investigate the role of hepatic PKD activity in regulating glucose metabolism and energy balance.
  • To determine if targeting hepatic PKD can modulate metabolic processes in normal and obese states.

Main Methods:

  • Adeno-associated virus vectors were used to express a dominant-negative (DN) PKD1 in mouse livers, inhibiting all PKD isoforms.
  • Metabolic parameters including glucose tolerance, insulin action, and VLDL cholesterol were assessed in chow-fed and high-fat diet-fed mice.
  • In vitro studies using FAO hepatoma cells were conducted to examine glucose production.

Main Results:

  • In chow-fed mice, hepatic DN PKD expression increased glucose oxidation and reduced VLDL cholesterol, associated with hepatic fatty acid accumulation.
  • Despite reduced gluconeogenic gene expression and enhanced pyruvate tolerance, overall glucose homeostasis was minimally affected.
  • In high-fat diet-induced obesity, hepatic DN PKD had no significant impact on glucose tolerance, insulin action, or plasma VLDL.

Conclusions:

  • Hepatic PKD signaling primarily influences substrate redistribution under normal nutrient availability.
  • PKD activity in the liver does not appear to be a critical regulator of metabolic dysfunction in obesity.
  • Targeting hepatic PKD may offer therapeutic potential for specific metabolic alterations rather than broad obesity-related issues.