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Obesogenic Programming of Foetal Hepatic Metabolism by microRNAs

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Book cover Diet, Nutrition, and Fetal Programming

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. 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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Correspondence to Adriana Souza Torsoni PhD .

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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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  • DOI: https://doi.org/10.1007/978-3-319-60289-9_16

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