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Changes in the unsaturated fatty acid content of the fungusTaphrina deformans as a function of growth, temperature, and sterol content were investigated. It was found that the highest growth rate was accompanied by a relatively high degree of fatty acid unsaturation (18∶1<18∶2+18∶3) and low sterol (brassicasterol) content. Also, a substantial shift in the degree of unsaturation from mainly 18∶2+18∶3 to 18∶1 occurred in the later stages (mid‐linear) of culture development. Cells readily adapted from 18°C to 13°C, and exhibited a higher growth rate at the lower temperature after a period of acclimation. Growth was readily inhibited by the sterol biosynthesis inhibitors propiconazole and naftifine, which blocked brassicasterol biosynthesis at C‐14 demethylation and squalene epoxidation, respectively. Growth was also inhibited by tunicamycin which did so without affecting sterol content. The shift in degree of fatty acid unsaturation did not occur in cells from cultures at reduced temperature or treated with any of the inhibitors. Since tunicamycin did not affect the sterol content, delay in the shift in the degree of fatty acid unsaturation was attributed to factors other than a reduction in sterol content.

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Single nucleotide polymorphisms (SNPs) of fatty acid desaturase (FADS) and n‐3/n‐6 polyunsaturated fatty acids (PUFAs) have been linked to decreased risks of cardiovascular diseases. We aimed to examine whether FADS SNPs (rs2072114, rs1535, and rs174546) interacted with n‐3/n‐6 PUFAs status as plasma levels to affect blood lipid profiles in type 2 diabetes. In 2008, we selected 192 diabetic patients without using lipid‐lowering drugs from a diabetic (DMIDS) cohort established in Taiwan. After adjusting for confounding factors, FADS2 rs2072114 G‐variant correlated significantly with decreased total cholesterol (p‐trend=0.015), LDL (p‐trend=0.009), and HDL (p‐trend=0.007) only in the low (<50 percentile) alpha‐linolenic acid (ALA)/linoleic acids (LA) group but not in the high (≥50 percentile) ALA/LA group (p for interaction= 0.012, 0.012, and 0.181, respectively). Furthermore, the G‐variant was significantly associated with lower total cholesterol (p‐trend=0.049) and HDL (p‐trend=0.024), and marginally with LDL (p‐trend=0.067) in the low n‐3 long chain PUFA (LCPUFAs) group (<50 percentile) but not in the high n‐3 LCPUFAs (≥50 percentile) (p for interaction= 0.170, 0.053, and 0.015, respectively). Genetic variations of FADS2 may interact with n‐3/n‐6 PUFAs to affect cholesterol metabolisms in type 2 diabetes. Further investigation may be needed with larger sample size in this ethnic population.

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