Palmitoleic acid enhances glucose uptake and glycerol‐3‐phosphate generation in adipocytes (LB426)

Palmitoleic acid (16:1n7) enhances whole body glucose disposal, suppresses hepatic steatosis and modulates triacylglycerol (TAG) metabolism in adipocytes. Here, we investigated the effects of 16:1n7 on glucose uptake and TAG synthesis by primary adipocytes. METHODS: Primary epididimal adipocytes from C57BL6 mice treated with 16:1n7 (300 mg/kg/day), oleic acid (18:1n9, 300 mg/kg/day) or water by gavage for 10 days were evaluated for 2‐deoxy‐D‐[3H]‐glucose uptake on basal and insulin‐stimulated (10 nmol/liter) conditions, phosphorylated and total AKT content, 14C‐glucose incorporation into fatty acids or glycerol and 14C‐acetate incorporation into fatty acids. RESULTS: Treatment with 16:1n7 or 18:1n9 did not affect body weight, food intake, masses of white adipose depots and plasma levels of free fatty acids, insulin and glucose. Treatment with 16:1n7 increased basal (~3 fold) and insulin‐stimulated (~2 fold, p<0.05) glucose uptake on epididimal adipocytes compared with water and 18:1n9 treatment. There were no changes on acetate or glucose incorporation into fatty acids among treatments, but the 16:1n7 increased glucose incorporation in glycerol‐TAG (H2O=227.2±9.1; 18:1n9=226.6±24.6; 16:1n7=307.2±19 nmol/106 cells, p<0.05). The treatments did not change the phosphorylated and total AKT content. CONCLUSION: 16:1n7 raised basal and insulin‐stimulated glucose uptake without affecting AKT. Furthermore, 16:1n7 increased the generation of glycerol‐3‐phosphate from glucose on epididimal adipocytes without affecting fatty acid synthesis from this hexose.Grant Funding Source: Supported by FAPESP