Abstract
The liver is a multifunctional organ that regulates many vital physiological processes. Disruption of hepatic lipid metabolism is often associated with metabolic disturbances. Obesity is closely related to inflammation and insulin resistance and this condition leads to steatosis, considered the hepatic manifestation of metabolic syndrome. It has been proposed that more than a single hepatic insult is necessary to promote the progression of steatosis to steatohepatitis. In this context, exposure to deleterious conditions in uterus has been considered a determining factor in predisposing offspring to the development of liver diseases in later life and miRNA expression seems to participate in metabolic programming in the development of hepatic disorders in adult offspring. So far only few studies have conducted to evaluate miRNA modulation in the liver of offspring of obese dams. Many of these studies indicated that some microRNAs expressed in the liver, such as miR-122 and miR-370, are involved in the control of hepatic lipid metabolism and could be responsible for fatty liver development. Thereby these microRNAs could represent important therapeutical targets to dietary and pharmacologic interventions in the treatment and prevention of hepatic diseases in metabolically programmed offspring.
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Notes
- 1.
The ENCODE project started in September 2003 and was completed in 2012. It brought together an international group of scientists with the goal of identifying all functional elements in the human genome sequence.
Abbreviations
- Acadvl:
-
Acyl-CoA dehydrogenase, very long chain
- Acc1:
-
Acetyl-CoA carboxylase 1
- Agpat1:
-
Acylglycerol-3-phosphate O-acyltransferase 1
- C/EBP-β:
-
CCAAT/enhancer-binding protein-β
- Cpt1-α:
-
Carnitine palmitoyltransferase 1
- DAG:
-
Diacylglycerol
- Dgat1:
-
Diacylglycerol acyltransferase 1
- Fas:
-
Fatty acid synthase
- G6pc:
-
Glucose-6-phosphatase
- GPAM:
-
Glycerol-3-phosphate acyltransferase mitochondrial
- GPAT:
-
Glycerol-3-phosphate acyltransferase
- HCC:
-
Hepatocellular carcinoma
- HFD:
-
High-fat diet
- HIC2:
-
Hypermethylated in cancer 2
- IKK:
-
IkB kinase
- Lclat1:
-
Lysocardiolipin acyltransferase 1
- MAG:
-
Monoacylglycerol
- MAP K1:
-
Mitogen-activated protein kinase 1
- MECP2:
-
Methyl-CpG binding protein 2
- miR/miRNA:
-
microRNA
- Mogat2:
-
Monoacylglycerol acyltransferase 2
- mTOR:
-
Mechanistic target of rapamycin
- NAFLD:
-
Non-alcoholic fatty liver disease
- NASH:
-
Non-alcoholic steatohepatitis
- ncRNA:
-
Non-coding RNA
- NFkB:
-
Nuclear factor kappa B
- p-JNK:
-
c-Jun N-terminal kinase phosphorylated
- Ppar-α:
-
Peroxisome proliferator-activated receptor- α
- Ppar-γ:
-
Peroxisome proliferator-activated receptor-γ
- RISC:
-
RNA-induced silencing complex
- Scd1:
-
Stearoyl-CoA desaturase 1
- Srebp-1c:
-
Sterol regulatory element-binding protein 1c
- TAG:
-
Triacylglycerol
- TNFα:
-
Tumor necrosis factor α
- UTR:
-
Untranslated region
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de Paula Simino, L.A., Torsoni, M.A., Torsoni, A.S. (2017). Obesogenic Programming of Foetal Hepatic Metabolism by microRNAs. In: Rajendram, R., Preedy, V., Patel, V. (eds) Diet, Nutrition, and Fetal Programming. Nutrition and Health. Humana Press, Cham. https://doi.org/10.1007/978-3-319-60289-9_16
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