In recent years, nutrition research has moved from epidemiology and physiology to molecular genetics. In this context, omics studies are emerging as an appealing tool for nutritional scientists. It is known that nutrients can interact with genes affecting transcription factors, protein expression and metabolite production. Nutritional genomics (nutrigenomics) is seen as a bridge between health diet and genotype. Dietary components affect gene expression patterns (transcriptome), chromatin organisation (epigenome) and protein expression patterns, including posttranslational modifications (proteome) and metabolite profiles (metabolome).

Key Concepts

  • Dietary habits are one of the crucial exogenous factors impacting health and incidence of several chronic diseases, including obesity, type 2 diabetes, cardiovascular diseases, metabolic syndrome and cancer.
  • Several lines of evidence indicate that nutrients can interact with genes, affecting gene transcription, protein expression and metabolite production.
  • Nutrigenomic studies describe the effect of food on gene expression, thus providing insight into how diet and genotype interactions affect physical and mental health.
  • Macronutrients may directly act as ligands for transcription factors or alter signal transduction pathways responsible for modifications in gene expression.
  • Glucose, in the presence of insulin, induces the expression of genes encoding for glycolytic and lipogenic enzymes, thereby regulating glucose homeostasis.
  • Dietary fats deeply change gene expression, triggering an adaptive response to fluctuations in the quantity and quality of fat ingested.
  • Both quantity and quality of ingested proteins influence the expression of several genes.
  • In addition, micronutrients (vitamins and minerals) and phytochemicals exert a health‐promoting action by modulating distinct signal transduction pathways via direct interaction with transcription factors or via epigenetic modifications of target promoters.
  • Gene–diet interaction is a complex network, where food components usually act in concert; therefore, it is not easy to translate scientific evidence into nutritional advice.

Keywords: nutrient–gene interaction; genotype; transcription factors; macronutrients; diet‐related diseases; personalised nutrition; omics

Figure 1. OMICs technologies applied to nutritional research.
Figure 2. Glucose‐dependent regulation of glycolytic and lipogenic genes in hepatic cells. Enzymes indicated in red are those whose gene transcription is upregulated by glucose. See text for further details. ACC, acetyl‐CoA carboxylase; ChoRE, carbohydrate‐response elements; ChREBP, carbohydrate‐response element‐binding protein; Elovl6, Elongase 6; FAS, fatty acid synthase; F6P, fructose‐6‐phosphate; F2,6BP, fructose‐2,6‐bisphosphate; G, glucose; G6P, glucose‐6‐phosphate; GK, glucokinases; GLUT‐2, glucose transporter‐2; LPK, liver pyruvate kinase; PEP, phosphoenolpyruvate; SCD1, stearoyl‐CoA desaturase and X5P, xylulose‐5‐phosphate.
Figure 3. Proteolytic activation of SREBPs by cholesterol and unsaturated fatty acids. See text for further details. ACS, acetyl‐CoA synthetase; bHLH, basic helix‐loop‐helix domain; ER, endoplasmic reticulum; FAS, fatty acid synthase; HMG‐CoA, 5‐hydroxy‐3‐methylglutaryl‐coenzyme A; INSIG, insulin‐induced protein; LDLR, low‐density lipoprotein receptor; PCSK9, proprotein convertase subtilisin/kexin type 9; Reg, regulatory domain; SCAP, SREBP cleavage‐activating protein; SP1, site‐1 protease; SP2, site‐2 protease; SRE, sterol‐responsive element and SREBP, sterol‐responsive element‐binding protein.


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Gasperi, Valeria, Vangapandu, Chaitanya, Catani, Maria Valeria, and Savini, Isabella(Aug 2017) Nutrigenomics. In: eLS. John Wiley & Sons Ltd, Chichester. [doi: 10.1002/9780470015902.a0021027]