Conjugated linoleic acid is a popular supplement because some studies have shown that it may be able to regulate obesity. Animal models have shown conjugated linoleic acid to be effective at decreasing body weight of obese animals, perhaps by regulation of the PPARγ2 transcription factor, although human trials have not been as consistent in their findings. Interestingly, linoleic acid appears to have similar effects on cell biology as conjugated linoleic acid. Linoleic acid is a polyunsaturated fatty acid of the omega 6 series (n-6), but its double bonds are not conjugated (here). Like CLA, linoleic acid can target the PPARγ2 gene and thus regulate adipocyte cell differentiation. This is accomplished by conversion of dietary linoleic acid to arachidonic acid, which is in turn converted to the series 2 eicosanoids (PGE2, PGD2, PGF2α and PGI2) (figure 1).
Figure 1. Possible intracellular regulation of adipocytes by arachidonic acid1. MAPK, mitogen-activated protein kinase. CaMK, calcium/calmodulin-dependent protein kinase
Prostaglandins appears to play a role in the regulation of adipocyte differentiation because prostaglandin F2α is able to interact with a cell surface prostanoid receptor. When activated, the prostanoid receptor increases intracellular calcium levels with a subsequent increase in the calcium/calmodulin-dependent protein kinase (CaMK) secondary messenger system. The result is an increase in DNA synthesis and a decrease adipocyte gene expression. Alternatively, PGF2α can cause inhibitory phosphorylation of the PPARγ2 transcription factor (via the mitogen-activated protein kinase; MAPK), which prevents the turning on of the adipocyte differentiation programme. Linoleic acid therefore appears to regulate the differentiation of adipocytes by both of these intracellular pathways, with the result that differentiation of pre-adipocytes to mature adipocytes is prevented. Non-essential conjugated linoleic acid may therefore have similar intracellular effect to dietary essential linoleic acid.
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