Nutrigenomics pp 209-222 | Cite as

The Metabolic Syndrome

  • Carsten Carlberg
  • Stine Marie Ulven
  • Ferdinand Molnár


Increased consumption of high-caloric diets combined with reduced physical activity are the main causes for the worldwide dramatic increase in the metabolic syndrome. Obesity (Chap.  8) and insulin resistance (Chap.  9) is initiating the development of the metabolic syndrome, and both significantly increase the risk of T2D (Chap.  10) and CVD (Chap.  11). Insulin plays a central role in regulating energy homeostasis in metabolic tissues. The effects of hyperglycemia and insulin resistance on the risk of CVD are largely pathway- and tissue-specific. The genetic risk for the metabolic syndrome overlaps with that of its major components, such as obesity, T2D and dyslipdemia, but like in these traits, common genetic variations can explain only a minor part of the disease risk. However, there is emerging evidence for an important role of epigenetics, causing heritable changes in gene expression, in the origin and development of the metabolic syndrome.

In this chapter, we discuss the role of insulin resistance and obesity in the major metabolic tissues liver, skeletal muscle, pancreas and WAT causing the metabolic syndrome. We will emphasize pathways that are involved in energy metabolism and will describe how insulin resistance and obesity lead to the metabolic syndrome and its complications. The importance of inflammation and regulation of energy metabolism will be highlighted. In addtion, we will discuss the future challenges and possibilities to treat and prevent the metabolic syndrome by dietary modifications.


Obesity Insulin resistance T2D Metabolic syndrome Liver Adipose tissue Skeletal muscle Pancreas Macrophages Inflammation Epigenetics 

Additional Reading

  1. Desai M, Jellyman JK, Ross MG (2015) Epigenomics, gestational programming and risk of metabolic syndrome. Int J Obes (Lond) 39(4)Google Scholar
  2. Hotamisligil GS (2010) Endoplasmic reticulum stress and the inflammatory basis of metabolic disease. Cell 140:900–917CrossRefPubMedPubMedCentralGoogle Scholar
  3. Huang PL (2009) A comprehensive definition for metabolic syndrome. Dis Model Mech 2:231–237CrossRefPubMedPubMedCentralGoogle Scholar
  4. Keane D, Kelly S, Healy NP, McArdle MA, Holohan K, Roche HM (2013) Diet and metabolic syndrome: an overview. Curr Vasc Pharmacol 11:842–857CrossRefPubMedGoogle Scholar
  5. Lusis AJ, Attie AD, Reue K (2008) Metabolic syndrome: from epidemiology to systems biology. Nat Rev Genet 9:819–830CrossRefPubMedPubMedCentralGoogle Scholar
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Copyright information

© Springer International Publishing Switzerland 2016

Authors and Affiliations

  • Carsten Carlberg
    • 1
  • Stine Marie Ulven
    • 2
  • Ferdinand Molnár
    • 3
  1. 1.Institute of BiomedicineUniversity of Eastern FinlandKuopioFinland
  2. 2.Department of NutritionUniversity of OsloOsloNorway
  3. 3.School of PharmacyUniversity of Easterm FinlandKuopioFinland

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