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Nutritional Programming of Metabolic Syndrome: Role of Nutrients in Shaping the Epigenetics

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Book cover Handbook of Nutrition, Diet, and Epigenetics

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Abstract

Increased prevalence of metabolic syndrome like obesity, heart diseases, and diabetes is an emerging public health problem. Susceptibility to such diseases has always been attributed to environmental and genetic factors which certainly play a pivotal role but cannot be the sole causal factor leading to metabolic syndrome. Epigenetics – a mediator between genetics and environment – is emerging as a potential candidate to explain the increase in the prevalence of such metabolic diseases. Changes in the epigenetic landscape marked by DNA methylation, histone methylation, and acetylation can lead to obesity, insulin resistance, diabetes, and vascular dysfunction in both animals and humans. Nutritional programming during early stages of life can manipulate the metabolism and the physiology of the organism. This is where the importance of optimal maternal nutrition comes into play. Both maternal under- and overnutrition have the potential to adversely affect the etiology of metabolic disorders in the developing fetus by changing the epigenetic marks. Various macronutrients and micronutrients in the maternal diet have also been shown to be exhibiting specific effect on the future health of the offspring. Though the role of epigenetics in fetal programming of metabolic syndrome is constantly being well understood, research on the therapeutic aspect is still in its infancy. Interventions and manipulation of dietary supplementation which potentially can make changes in the epigenetic marks can be the future therapeutic targets for chronic metabolic syndrome.

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Abbreviations

11β-HSD1:

11β-hydroxysteroid dehydrogenase type 1

Agtr1b:

Angiotensin II receptor, type 1b

AMPK:

5′ AMP-activated protein kinase

CEBPB:

CCAAT/enhancer-binding protein beta

G6Pase:

Glucose 6-phosphatase

GHSR:

Growth hormone secretagogue receptor

GLUT4:

Glucose transporter type 4

GR:

Glucocorticoid receptor

HAT:

Histone acetyltransferase

HDAC:

Histone deacetylase

IGF2R:

Insulin-like growth factor 2 receptor

IGFBP3:

Insulin-like growth factor-binding protein-3

IQ:

Intelligence quotient

IUGR:

Intrauterine growth restriction

LINE-1:

Long interspersed nuclear element-1

LXRα:

Liver X receptor alpha

NAD:

Nicotinamide adenine dinucleotide

NOS3:

Nitric oxide synthase

Pdx1:

Pancreatic and duodenal homeobox 1

PEPCK:

Phosphoenolpyruvate carboxykinase

PGC-1α:

PPAR gamma coactivator -1 alpha

PPARα:

Peroxisome proliferator-activated receptor alpha

ROS:

Reactive oxygen species

SIRT1:

Sirtuin 1

TCA:

Tricarboxylic acid

ZFP423:

Zinc finger protein 423

ZFP57:

Zinc finger protein 57

RXRA:

Retinoid X receptor alpha

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Authors and Affiliations

  1. Indian Institute of Chemical Biology, Kolkata, West Bengal, India

    Samit Chattopadhyay

  2. Chromatin and Disease Biology Lab (# 08), National Centre for Cell Science, NCCS Complex, Savitribai Phule Pune University Campus, Pune, Maharashtra, India

    Sonal Patel, Arpankumar Choksi, Richa Pant, Aftab Alam & Samit Chattopadhyay

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  1. Sonal Patel
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  2. Arpankumar Choksi
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  3. Richa Pant
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  4. Aftab Alam
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  5. Samit Chattopadhyay
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Correspondence to Samit Chattopadhyay .

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Editors and Affiliations

  1. School of Life Sciences, University of Westminster, London, UK

    Vinood B. Patel

  2. Diabetes and Nutritional Sciences Research Division, Faculty of Life Sciences and Medicine, King’s College London, London, UK

    Victor R. Preedy

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Patel, S., Choksi, A., Pant, R., Alam, A., Chattopadhyay, S. (2019). Nutritional Programming of Metabolic Syndrome: Role of Nutrients in Shaping the Epigenetics. In: Patel, V., Preedy, V. (eds) Handbook of Nutrition, Diet, and Epigenetics. Springer, Cham. https://doi.org/10.1007/978-3-319-55530-0_42

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