Evidence suggests that ratios of cellular and circulating fatty acids in can have an effect on metabolic regulation. Palmitoleic acid (POA, C16:1 (n-7)) is an omega 7 fatty acid that is produced during de novo lipogenesis in humans. Palmitoleic acid has been shown to be released from the adipose tissue of mice in response to fatty acid synthesis, after which it may play a role in protecting mice from skeletal muscle and hepatic insulin resistance. This protection may arise because POA inhibits hepatic fatty acid synthesis in a negative feedback loop. This evidence suggests that POA has a role as an adipokine, a substance released from the adipose tissue with the function of regulating metabolic activity, in this case by inhibiting further fatty acid synthesis. It is possible that POA achieves this by regulation of glucose and fatty acid metabolism as well as having effects on the β-cells of the pancreas.
In order to elucidate the effects of POA, researchers1 investigated factors associated with POA in 3630 men and women from the United States. Multivariate analysis of the data was used to identify the independent determinants of plasma phospholipid POA levels and multivariate-linear regression was then used to relate POA to metabolic risk factors. Palmitoleic acid made up 0.49% of the mean total plasma fatty acid concentration and so was quantitatively not a major fatty acid. High carbohydrate intakes, high protein intakes, a greater body mass index and alcohol were all independently associated with POA plasma levels. Adjustment for these factors showed that higher POA levels in plasma phospholipids were associated with lower LDL cholesterol concentration, higher HDL cholesterol concentration, a lower total cholesterol concentration, and lower fibrinogen levels. Insulin resistance and high triglycerides were also associated with high levels of POA.
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