Aims: To investigate, in the liver of adult offspring, the possible effects of melatonin supplementation in the obese mother during pregnancy and lactation.
Main methods: C57BL/6 females were fed with a control (C) or a high-fat (HF) diet and supplemented with melatonin (Mel) during the pregnancy and lactation, forming the groups: C, CMel, HF, and HFMel. After weaning until three months old, the offspring only received the C diet.
Key findings: The HF mothers and their offspring showed higher body weight (BW) than the C mothers and offspring. However, at 3-mo-old, BW was reduced in HFMel vs. HF offspring. Also, plasmatic and liver lipid markers increased in HF vs. C offspring but were reduced in HFMel vs. HF offspring. Liver lipid content was lessened in HFMel vs. HF offspring by 50 %. Also, lipid metabolism, pro-inflammatory and endoplasmic reticulum (ER) stress genes were higher expressed in HF vs. C offspring but reduced in HFMel vs. HF offspring. Contrarily, beta-oxidation and antioxidant enzyme genes were less expressed in HF vs. C offspring but improved in HFMel vs. HF offspring. Finally, AMPK/mTOR pathway genes, initially dysregulated in the HF, were restored in the HFMel offspring.
Significance: The obese mother leads to liver alterations in the offspring. Current findings demonstrated the maternal melatonin supplementation during pregnancy and lactation in adult offspring's liver. Consequently, the effects were seen in mitigating the liver's AMPK/mTOR pathway genes, lipogenesis, beta-oxidation, inflammation, oxidative stress, and ER stress, preventing liver disease progression in the offspring.
Keywords: Epigenetics; Fetal programming; Inflammation; Liver steatosis; Maternal obesity.
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