Abstract

Abstract We studied the molecular and epigenetic mechanisms associated with dysfunctions caused by postnatal coconut oil exposure. Lactating dams were divided into soybean oil (SO) and coconut oil (CO) groups (0.5 g/kg/gavage). Half of the CO offspring received CO in their chow throughout their lifetime (CO + C). Adult CO offspring had higher liver TRβ-1 mRNA, which is consistent with lower miR-181a and lower DIO2 mRNA in brown adipose tissue (BAT) and higher CPT-1 mRNA in white adipose tissue (WAT). CO + C offspring exhibited higher BAT miR-382*, but DIO2 was unaltered. This group also had higher liver SCD1, miR-122 expression, and WAT SCD1 mRNA. CO and CO + C offspring had lower hepatic CPT-1 mRNA. The disturbances in CO offspring may be partially attributed to alterations in the enzymes involved in lipid metabolism, which may be mediated via mechanisms associated with miR-122. Continuous exposure to CO prohibits some of these changes.

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