Alterations of the expression levels of CPT-1, SCD1, TRβ-1 and related microRNAs are involved in lipid metabolism impairment in adult rats caused by maternal coconut oil intake during breastfeeding

被引:3
|
作者
Quitete, Fernanda Torres [1 ]
de Moura, Egberto Gaspar [1 ]
Peixoto, Thamara Cherem [1 ]
Torsoni, Adriana Souza [2 ]
Torsoni, Marcio Alberto [2 ]
Milanski, Marciane [2 ]
Ignacio-Souza, Leticia M. [2 ]
Simino, Lais Angelica [2 ]
de Oliveira, Elaine [1 ]
Lisboa, Patricia Cristina [1 ]
机构
[1] Univ Estado Rio De Janeiro, Roberto Alcantara Gomes Biol Inst, Dept Physiol Sci, BR-20551030 Rio De Janeiro, RJ, Brazil
[2] Univ Estadual Campinas, Sch Appl Sci, Lab Metab Disorders, BR-13484350 Limeira, SP, Brazil
关键词
Coconut oil; Metabolic programming; Obesity; Thyroid function; Lipid metabolism; MicroRNA; GENE-EXPRESSION; THYROID-HORMONE; ADIPOSE-TISSUE; FLAXSEED OIL; BODY-WEIGHT; LACTATION; OBESITY; DIET; FAT;
D O I
10.1016/j.jff.2019.103577
中图分类号
TS2 [食品工业];
学科分类号
0832 ;
摘要
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 TR beta-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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页数:8
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