The Elovl3 gene belongs to a highly conserved family of microsomal enzymes involved in the formation of very long-chain fatty acids (VLCFAs). The recognized role for the enzyme is to control the elongation of saturated and monounsaturated fatty acids up to 24 carbons in length. Elovl3 was originally identified as a highly expressed gene in brown adipose tissue (BAT) upon cold exposure, however significant amounts of transcript can also be found in liver, kidney, white adipose tissue (WAT), heart and in the sebaceous glands of the skin. We have recently seen that Elovl3 ablation gives rise to diminished body weight. These mice are resistant to diet-induced obesity and both female and male knockout mice have reduced hepatic lipogenic gene expression and TG secretion as well as a decreased ratio between energy intake and energy expenditure.
In an attempt to identify early markers of metabolic disturbance, we used mice at an age before the onset of impaired weight gain is recognized to analyze the expression of genes involved in lipid metabolism in liver, brown and inguinal white adipose tissue, where Elovl3 is significantly expressed under normal conditions. Furthermore, we analyzed the expression under conditions when energy intake exceeds energy expenditure and during increased energy demand.
Here we show that besides BAT, Elovl3 expression is also regulated in depot specific adipose tissue at different ambient temperatures. We also show that, in addition to impaired expression of both liver (MUP1) and adipose derived (leptin and adiponectin) factors, the Elovl3-/- mice have decreased adipose mass and TG levels already at 30°C, suggesting that factors other than skin barrier dysfunction are involved in the metabolic disturbance associated with Elovl3 ablation.