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Funding. This work was supported by National Institutes of Health (NIH) National Heart, Lung, and Blood Institute grant HL-130146 (to B.S.J.D.), NIH National Institute of Diabetes and Digestive and Kidney Diseases grants DK-095132 (to J.S.) and DK-113007 (to J.S.), and American Diabetes Association Research Foundation grant 1-16-IBS-272 (to J.S.).
Author Contributions. L.Q., S.K.S., K.M.S., and J.-S.W. contributed research data. L.Q., B.S.J.D., and J.S. designed the study and wrote the manuscript. J.S. is the guarantor of this work and, as such, had full access to all of the data in the study and takes responsibility for the integrity of the data and the accuracy of the data analysis.
Loss of adipocyte ANGPTL4 in the context of HFD had an interesting effect on LPL activity and adipose triglyceride uptake. On a chow diet, the increase in adipose LPL activity in Angptl4AdipoKO mice led to a corresponding increase in adipose tissue uptake of triglycerides. This connection between increased LPL activity and increased triglyceride uptake in adipose tissue was lost in mice fed a HFD. Adipose tissue LPL activity remained higher in Angptl4AdipoKO mice fed a HFD compared to floxed control mice, but the enhanced adipose tissue uptake observed on chow diet was largely lost. These data suggest that on a chronic high-fat diet, LPL activity is no longer rate-limiting for the entry of triglyceride-derived fatty acids into adipose tissues. Why this would be the case is not clear. One possibility is that LPL-mediated lipolysis continues to occur, but uptake of these fatty acids into tissues is now limiting. The mechanisms by which fatty acids released by vascular lipolysis traverse capillary endothelial cells and are then taken up by adipocytes are not well understood. We measured gene expression of several genes associated with fatty acid uptake, but did not observe changes in expression that would clearly indicate a reduction in fatty acid uptake. However, our analysis did not encompass all genes associated with uptake, nor does gene expression necessarily corelate with functionality. Moreover, in our analysis we did not differentially analyze cell types within adipose tissues. A dramatic change in fatty acid uptake genes in endothelial cells might be masked by the lack of change or even increase in these same genes in adipocytes. Further, more targeted research will be needed to understand how fatty acid uptake is altered by long term high fat feeding and whether this may contribute to adipose dysfunction. Alternatively, it could be that changes in fatty acid uptake pathways are not responsible for the similar uptake in Angptl4fl/fl and Angptl4AdipoKO mice. It is possible that in Angptl4AdipoKO mice other tissues uptake sufficient TGs to reduce the supply available to white adipose tissue. Although we did not see evidence of this in our uptake assays, it is important to note that we did not measure uptake in all tissues. The fact that Angptl4AdipoKO mice fed a chronic HFD cleared plasma TGs somewhat faster and had lower plasma TG levels than Angptl4fl/fl mice on the same diet suggest that there may indeed be tissues in Angptl4AdipoKO mice that take up more TGs.
Body composition (fat and lean mass) was determined using nuclear magnetic resonance (NMR) in mice following 11 weeks on diet in the 12-week diet cohort and 25 weeks on diet in the 6-month diet cohort. Mice were weighed before being placed in a restraint tube without anesthesia and placed into either a Bruker LF50 (for mice under 50 g) or a Bruker LF90 (for mice over 50 g). Following NMR scanning mice were immediately returned to their cages. Body composition measurements were performed in the Fraternal Order of the Eagles Diabetes Research Center Metabolic Phenotyping Core.
This work was supported by grants from the National Institutes of Health (R01HL130146 [BSJD]). We thank the University of Iowa Genome Editing Facility for assistance in generating the ANGPTL4 floxed allele and the Fraternal Order of Eagles Diabetes Research Center Metabolic Phenotyping Core Laboratory for assistance is collecting metabolic caging data.
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Feature papers represent the most advanced research with significant potential for high impact in the field. A FeaturePaper should be a substantial original Article that involves several techniques or approaches, provides an outlook forfuture research directions and describes possible research applications.
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