Vitamin D and Obesity

  • Dimiter AvtanskiEmail author
  • Anabel Garcia
  • Emilia Pauline Liao
Part of the Contemporary Endocrinology book series (COE)


Today obesity is epidemic, affecting more than 600 million individuals worldwide, and vitamin D insufficiency is considered to be present in more than half of the world’s population. Overweight status and obesity contribute to the development of type 2 diabetes, atherosclerosis, cancer, and vitamin D deficiency, resulting in increased mortality. The main etiologic factor for obesity is the disturbed balance between energy intake and energy expenditure caused by the modern lifestyle. Adipose tissue is an important endocrine organ producing a variety of cytokines, immune-related proteins, lipids, and enzymes involved in steroid hormone metabolism. Adipose tissue is also the main storage depot for vitamin D and its metabolites, serving as an endogenous source of vitamin D during the winter season. Adipose tissue secretes cytochrome P450 enzymes that are crucial for vitamin D metabolism. Furthermore, adipose tissue is a target for vitamin D, which is required for the normal function of both adipose cells (adipocytes) and adipose immune cells. Thus, obesity-induced vitamin D deficiency has an impact on adipose secretory functions. Vitamin D modulates adipocyte differentiation through mechanisms dependent or independent on vitamin D receptor (VDR). Signaling mediators of vitamin D involve the nuclear corepressor (NCoR) and silencing mediator for retinoid and thyroid hormone receptors (SMRT) which affect chromatin remodeling and gene transcription. Although it is tempting to suggest that overweight status or obesity can be reversed by vitamin D supplementation, experimental data do not support such a notion. In this chapter we summarize the current knowledge about the molecular mechanisms of vitamin D action in adipose tissue supported by data from clinical observational and basic science experimental studies.


Obesity Adipocyte Vitamin D Vitamin D receptor (VDR) Inflammation 


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Copyright information

© Springer International Publishing AG, part of Springer Nature 2018

Authors and Affiliations

  • Dimiter Avtanski
    • 1
    Email author
  • Anabel Garcia
    • 2
  • Emilia Pauline Liao
    • 3
  1. 1.Endocrine Research Laboratory, Department of MedicineLenox Hill HospitalNew YorkUSA
  2. 2.Division of EndocrinologyLenox Hill HospitalNew YorkUSA
  3. 3.Division of Endocrinology, Department of MedicineHofstra Northwell School of Medicine, Lenox Hill Hospital, Northwell HealthNew YorkUSA

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