Abstract
Insulin stimulates the translocation fatty acid transport protein 1 (FATP1) to plasma membrane, and thus greater free fatty acid (FFA) uptake, in adipocyte cell models. Whether insulin stimulates greater FFA clearance into adipose tissue in vivo is unknown. We tested this hypothesis by comparing direct FFA storage in subcutaneous adipose tissue during insulin versus niacin-medicated suppression of lipolysis. We measured direct FFA storage in abdominal and femoral subcutaneous fat in 10 and 11 adults, respectively, during euglycemic hyperinsulinemia or after oral niacin to suppress FFA compared with 11 saline control experiments. Direct palmitate storage was assessed using a [U-13C]palmitate infusion to measure palmitate kinetics and an intravenous palmitate radiotracer bolus/timed biopsy. Plasma palmitate concentrations and flux were suppressed to 23 ±3 and 26 ±5 mmol $ L-1 (P = 0.91) and 44 ± 4 and 39 ± 5 μmol $ min-1 (P = 0.41) in the insulin and niacin groups, respectively, much less (P < 0.001) than the saline control group (102 ± 8 and 104 ± 12 mmol $ min-1, respectively). In the insulin, niacin, and saline groups, abdominal palmitate storage rates were 0.25 ± 0.05 vs. 0.25 ± 0.07 vs. 0.32 ±0.05 μmol $ kg adipose lipid-1 $ min-1, respectively (P = NS), and femoral adipose storage rates were 0.19 ± 0.06 vs. 0.20 ± 0.05 vs. 0.31 ± 0.05 μmol $ kg adipose lipid-1 $ min-1, respectively (P = NS). In conclusion, insulin does not increase FFA storage in adipose tissue compared with niacin, which suppresses lipolysis via a different pathway.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 2828-2835 |
| Number of pages | 8 |
| Journal | Diabetes |
| Volume | 64 |
| Issue number | 8 |
| DOIs | |
| State | Published - Aug 2015 |
Bibliographical note
Funding Information:Acknowledgments. The authors are indebted to the research volunteers for their participation. The authors are also grateful to Barbara Norby and Carley Vrieze for assistance with nursing care and adipose biopsies and Christy Allred, Debra Harteneck, Darlene Lucas, and Lendia Zhou (Mayo Clinic, Rochester, MN) for assistance with assay development and performance. Funding. This work was supported by grants DK-40484, DK-45343, and DK-50456 from the U.S. Public Health Service and by the Mayo Foundation. The project described was also supported by the National Center for Research Resources and the National Center for Advancing Translational Sciences, National Institutes of Health (NIH), through grant 1-UL1-RR-024150-01.
Publisher Copyright:
© 2015 by the American Diabetes Association.
