Dr. Stokes, the loss of lipin-1 results in an increase in glycolysis and a shift to lipid synthesis. We believe that lipin-1 deficient macrophages are using incoming lipid for lipid synthetic events thus processing the lipid in another way. The WT macrophages have not switched their metabolism to compensate yet.
We believe etomoxir treatment further pushes the cells in a glycolytic and lipid synthetic phenotype in the knockouts thus increasing their efferocytic ability.
very nice Robert. Why is the ETO having opposite effects on the WT and KO in final fig?
Dr. Stokes, the loss of lipin-1 results in an increase in glycolysis and a shift to lipid synthesis. We believe that lipin-1 deficient macrophages are using incoming lipid for lipid synthetic events thus processing the lipid in another way. The WT macrophages have not switched their metabolism to compensate yet.
We believe etomoxir treatment further pushes the cells in a glycolytic and lipid synthetic phenotype in the knockouts thus increasing their efferocytic ability.
Does the type of fat (saturated vs unsaturated) affect the process of efferocytosis in macrophages?
I do not know that answer but I imagine it does. Different fats result in more pro-inflammatory or anti-inflammatory responses.