Palmitoleic (16:1 cis-9) and cis-vaccenic (18:1 cis-11) acid alter lipogenesis in bovine adipocyte cultures.

Our objectives were to: (1) confirm elongation products of palmitoleic acid (16:1 cis-9) elongation in vitro using stable isotopes and (2) evaluate if exogenous supplementation of palmitoleic acid, elongation products, or both are responsible for decreased desaturation and lipogenesis rates observed with palmitoleic acid supplementation in bovine adipocytes. Stromal vascular cultures were isolated from adipose tissue of two beef carcasses, allowed to reach confluence, held for 2 days, and differentiated with a standard hormone cocktail (day 0). On day 2, secondary differentiation media containing 1 of 4 fatty acid treatments [0 µM fatty acid (control), or 150 µM palmitic (16:0), palmitoleic, or cis-vaccenic (18:1 cis-11)] was added for 4 days. On day 6, cells were incubated with [(13)C] 16:1, [(13)C] 2, or [(13)C] 18:0 to estimate elongation, lipogenic, and desaturation rates using gas chromatography-mass spectrometry. Enrichment of [(13)C] 18:1 cis-11 confirmed 18:1 cis-11 is an elongation product of 16:1. Additionally, [(13)C] label was seen in 20:1 cis-13 and cis-9, cis-11 CLA. Synthesis of [(13)C] 16:0 from [(13)C] 2 was reduced (P < 0.05) in palmitoleic acid and cis-vaccenic acid-treated compared with control cells following 36 h incubation. By 12 h of [(13)C] 18:0 incubation, cells supplemented with palmitoleic acid had reduced (P < 0.05) [(13)C] 18:1 cis-9 compared with all other treatments. Gene expression and fatty acid results support isotopic data for lipogenesis and desaturation. Therefore, palmitoleic acid is actively elongated in vitro and its elongation product, cis-vaccenic acid, can also reduce lipogenesis. However, inhibition of desaturation can be directly attributed to palmitoleic acid and not its elongation products, 18:1 cis-11 or 20:1 cis-13.