High intakes of fructose in the absence of adequate fibre are known to cause liver overload which stimulates the hepatic de novo lipogenesis pathway. Palmitic acid (PA, C16:0) is a 16 carbon saturated fatty acid that is the end product of de novo lipogenesis. Following synthesis, PA can be desaturated by steroyl CoA desaturase, incorporating a single double bond and thus forming palmitoleic acid (POA, C16:1 (n-7)). Most of the POA in human tissue is derived from this de novo lipogenesis route, because dietary intakes of POA become quickly oxidise following absorption. Rates of de novo lipogenesis are increased in metabolic syndrome, which suggests that production of POA is also increased. Therefore plasma levels of POA could be used as a marker to determine the degree of de novo lipogenesis. High concentration of POA in plasma may therefore be associated with other markers of metabolic syndrome, and could also be a useful predictor of cardiovascular risk.
To these ends, researchers have investigated the association between plasma POA and other markers of metabolic syndrome. For example, in one study1 published in the American Journal of Clinical Nutrition, otherwise healthy Chinese individuals aged 50 to 70 years of age were assessed for plasma concentrations of POA as well as other commonly accepted parameters associated with metabolic syndrome. The results showed that erythrocyte levels of POA were strongly correlated with metabolic syndrome and its components. For example, the extreme quartile for erythrocyte POA concentrations was associated with an increase odds ratio for metabolic syndrome, hypertriglyceridaemia, reduced plasma high density lipoprotein (HDL), central adiposity and elevated blood pressure. This evidence supports a role for plasma levels of POA in determining the presence of metabolic syndrome in humans.
The researchers also reported that POA was inversely associated with adiponectin and positively associated with retinol binding protein 4 (RBP-4) in plasma. Both adiponectin and retinol binding protein 4 are adipokines secreted by adipose tissue. Evidence suggest that they are both involved in the pathogenesis of metabolic syndrome because plasma levels are associated with levels of abdominal adipose tissue. Adiponectin has been reported to be inversely associated with abdominal obesity, with plasma levels falling with increasing visceral, but not subcutaneous, fat stores. Retinol binding protein 4 carries retinol from the liver to peripheral tissue via the plasma. In animal experiments, retinol binding protein 4 may be involved in the development of insulin resistance through the modulation of plasma glucose levels. This may occur mechanistically through the stimulation of cytokine release from adipocytes, which subsequently interfere with the insulin signal cascade.
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