PPAR-δ is a potential modulator of central carbon metabolism in human adipocytes

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

• Level A · Stronger Clinical Evidence
• Level B · Emerging clinical evidence with positive signals
• Level C · Early human research exploring benefits
• Level D · Scientific groundwork from lab and animal studies
• Emerging · Emerging topic under active research

Abstract (original English)

Adipogenesis involves adipocyte differentiation and synthesis and storage of fats. PPAR-γ is the master regulator of adipogenesis and regulates genes for adipocyte differentiation, lipogenesis, adipocyte survival and adipokine secretion. Central carbon metabolism (CCM) comprises of three key pathways glycolysis, tricarboxylic acid (TCA) cycle and pentose phosphate pathway (PPP). CCM utilizes carbon sources to provide energy and building blocks for lipogenesis. Several targets of transcription factor PPAR-γ have been identified in CCM pathways. However, the exact mechanism of PPAR-γ modulation in adipogenesis via CCM remains elusive. Therefore, it is of interest to evaluate the effects of PPAR-γ on CCM in differentiated human SGBS adipocytes by real time-qPCR and metabolomics using its agonist 15d-PGJ2 and antagonist GW9662. Surprisingly, our results suggest that PPAR-δ rather than PPAR-γ is likely to be the key modulator of CCM in differentiated adipocytes at least under current experimental conditions with both 15d-PGJ2 and GW9662 being PPAR-δ agonists, although PPAR-γ plays a crucial role in adipogenesis and lipogenesis. This data provides insight to manage obesity and diabetes using PPAR-δ agonists. Further studies are warranted to explore the regulation of CCM by PPARs in adipocytes.

Evidence level

Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.

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