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Nutrigenomics pp 181-194 | Cite as

Diabetes

  • Carsten Carlberg
  • Stine Marie Ulven
  • Ferdinand Molnár
Chapter

Abstract

Diabetes is a disease of dys-regulation of glucose and lipid homeostasis that does not only affect the insulin production in the β cells but also the metabolism in organs such as liver, muscle and fat. Worldwide, the prevalence of T2D is rapidly increasing, which, when not properly treated, ultimately leads to reduced life expectancy due to microvascular (retinopathy, nephropathy and neuropathy) and macrovascular (heart disease and stroke (Chap.  11) complications. Like in obesity (Chap.  8), both genetic and environmental factors contribute to the development of diabetes. For example, persons at high risk for developing T2D should benefit from lifestyle changes involving healthy diet, moderate weight loss and increased physical activity. Despite large GWAS screening for risk genes, at present less than 10 % of the inheritance of T2D is understood. Therefore, in addition, epigenome-wide changes, both pre-natal as well as in adult life, are intensively investigated.

In this chapter, we will describe the different forms of diabetes, their diagnosis and the worldwide prevalence of the disease. We will discuss the dys-regulation of glucose homeostasis in T2D. In this context, we will present the genetic and physiologic basis of the disease and again we will highlight chronic inflammation as the core of the disease, this time affecting islets of the pancreas. We will realize that the present understanding of T2D risk genes is insufficient and that most likely epigenetics plays an important role in the disease, as examplified through the thrifty gene hypothesis.

Keywords

T1D T2D OGTT Insulin β cells Liver Skeletal muscle Adipose tissue Inflammation MODY GWAS Epigenetic programming Thrifty gene hypothesis 

Additional Reading

  1. Donath MY (2014) Targeting inflammation in the treatment of type 2 diabetes: time to start. Nat Rev Drug Discov 13:465–476CrossRefPubMedGoogle Scholar
  2. Grayson BE, Seeley RJ, Sandoval DA (2013) Wired on sugar: the role of the CNS in the regulation of glucose homeostasis. Nat Rev Neurosci 14:24–37CrossRefPubMedGoogle Scholar
  3. International Diabetes Federation (IDF): www.idf.org/diabetesatlas
  4. Laakso M, Kuusisto J (2014) Insulin resistance and hyperglycaemia in cardiovascular disease development. Nat Rev Endocrinol 10:293–302CrossRefPubMedGoogle Scholar
  5. Manolio TA, Collins FS, Cox NJ, Goldstein DB, Hindorff LA, Hunter DJ, McCarthy MI, Ramos EM, Cardon LR, Chakravarti A et al (2009) Finding the missing heritability of complex diseases. Nature 461:747–753CrossRefPubMedPubMedCentralGoogle Scholar
  6. Reddy MA, Zhang E, Natarajan R (2015) Epigenetic mechanisms in diabetic complications and metabolic memory. Diabetologia 58:443–455CrossRefPubMedGoogle Scholar

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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