METHODS AND STUDY DESIGN: We searched Medline, Embase, Cochrane Central Registry of Controlled Trials and CINAHL. Clinical trials were eligible if they compared palm oil-rich diets with diets rich in MUFAs or PUFAs. We pooled results of included studies using a random effects model and assessed the quality of the evidence and certainty of conclusions using the GRADE approach.

RESULTS: Intake of palm oil intake compared to oils rich in MUFA was associated with increased levels of total cholesterol (TC) [mean difference (MD)=0.27 mmol/L; 95% CI 0.08 to 0.45], LDL-C (MD=0.20 mmol/L; 95% CI 0.02 to 0.37) and HDL-C (MD=0.06 mmol/L; 95% CI 0.02 to 0.10). Similarly, for comparison with oils rich in PUFAs, palm oil showed increased in TC (MD=0.38 mmol/L; 95% CI 0.14 to 0.62), LDL-C (MD= 0.44 mmol/L; 95% CI 0.01 to 0.88) and HDL-C (MD=0.08 mmol/L; 95% CI 0.03 to 0.13). For both comparisons, there were no significant effects on triglycerides.

RESULTS: The results showed that lipid content of cell dry weight in Snf-β knockout strain was increased by 32 % (from 19 to 25 %). However, in Snf-β overexpressing strain, lipid content of cell dry weight was decreased about 25 % (from 19 to 14.2 %) compared to the control strain. Total fatty acid analysis revealed that the expression of the Snf-β gene did not significantly affect the fatty acid composition of the strains. However, GLA content in biomass was increased from 2.5 % in control strain to 3.3 % in Snf-β knockout strain due to increased lipid accumulation and decreased to 1.83 % in Snf-β overexpressing strain. AMPK is known to inactivate acetyl-CoA carboxylase (ACC) which catalyzes the rate-limiting step in lipid synthesis. Snf-β manipulation also altered the expression level of the ACC1 gene which may indicate that Snf-β control lipid metabolism by regulating ACC1 gene.