Nutrigenomics pp 141-161 | Cite as


  • Carsten Carlberg
  • Stine Marie Ulven
  • Ferdinand Molnár


Obesity is the consequence of excess WAT accumulation that increases the risk of metabolic diseases (Chap.  12). Adipocytes are the central cellular component of adipose tissue. However, adipose tissue also has a stromal-vascular fraction containing many immune cells, such as macrophages and T cells. WAT is specialized to store and release lipids, while BAT is mainly involved in thermogenesis. Interestingly, some white adipocytes are able to transform to beige adipocytes displaying a phenotype similar to brown adipocytes. During the development of overweight and obesity, adipocytes first grow in size (hypertrophy) and then in number (hyperplasia) attracting a large number of M1-type macrophages. This induces a change in the adipokine production profile of WAT and leads to chronic inflammation in the tissue (Chap.  7). Genetic variations modulate the individual’s susceptibility to obesity in context of the modern obesogenic environment. Studying monogenic forms of obesity provides strong evidence for a central role of appetite regulation in obesity susceptibility with the leptin-melanocortin pathway having an integral role in satiety signaling.

In this chapter, we will define obesity and describe the main functions of adipose tissue and the cells of which the tissue is formed. We will discuss adipogenesis at the example of the conversion of white into beige adipocytes. In this context, we will present the large impact of adipokines during hypertrophy and hyperplasia of WAT and for the communication with the CNS. We will explain how hormonal signals and genetic factors can control food intake and energy expenditure. Variations of the respective genes will be presented as important drivers of monogenetic and common obesity.


BMI Visceral fat Sub-cutaneous fat White, beige and brown adipocytes Adipogenesis Chronic inflammation M1 and M2 macrophages Adipokines Leptin Hindbrain Hypothalamus MC4R FTO 

Additional Reading

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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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