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Background  Dietary salts are important factors in metabolic disorders. They are vital components of enzymes, vitamins, hormones, and signal transduction that act synergistically to regulate lipid metabolism. Our previous studies have identified that Krüppel-like factor −3 (KLF-3) is an essential regulator of lipid metabolism. However, it is not known if KLF-2 also regulates lipid metabolism and whether KLF-2 and −3 mediate the effects of dietary salts on lipid metabolism.    Methods  In this study, we used  klf  mutants [homozygous  klf-2  (ok1043) V and  klf-3  (ok1975) II mutants] to investigate the role of dietary salts in lipid metabolism. All gene expression was quantified by qRT-PCR. Localization of KLF-2 was analyzed by the expression of  klf-2 :: gfp  (in pPD95.75 vector) using a fluorescent microscope. Fat storage was measured by Oil Red O staining.    Results    Klf-2  was identified to express in the intestine during all stages of  Caenorhabditis elegans  development with peak expression at L3 stage. Mutation of  klf-2  increased fat accumulation. Under regular growth media free of Ca 2+,  the expression of both  klf-2  and − 3  was inhibited slightly; further their expression reduced significantly in WT worms fed on 10X Ca 2+  diet. When  klf-3  was mutated, the expression of  klf-2  increased under 10X Ca 2+  diet; but when  klf-2  was mutated, the expression of  klf-3  was not altered under 10X Ca 2+  diet. Overall, Mg 2+  and K +  were less effective on the gene expression of  klfs . KLF target gene  Ce -C/EBP-2 showed elevated expression in WT and  klf-3  (ok1975) worms with changed Ca 2+  concentrations but not in  klf-2  (ok1043) worms. However, high Ca +2  diet exhibited inhibitory effect on  Ce -SREBP expression in WT worms.    Conclusion  Dietary Ca 2+  is most effective on fat storage and  klf-2  expression, wherein high Ca 2+  diet decreased  klf-2  expression and reduced fat buildup. Mechanistic study identified  Ce -C/EBP (C48E7.3;  lpd-2 ) and Ce-SREBP (Y47D3B.7;  lpd-1 ) as the target genes of  klf-2  and/or  klf-3  to mediate lipid metabolism. This study identifies a new function of  klf-2  in inhibiting fat buildup and reveals the interplay between dietary salts and  klf-2  and  klf-3  in lipid metabolism.

Defective lipid metabolism associated with mutation in klf-2 and klf-3: important roles of essential dietary salts in fat storage