**3. Conclusion**

Endocrine-metabolic alterations associated to obesity are related to WAT dysfunction, mainly VAT. However, the increase of VAT mass per se is not an unequivocal indication of VAT dysfunction, whereas the adipocyte size actually is. Therefore, the balance between hypertrophy and hyperplasia will determine the appearance of enlarged adipocytes and, consequently, the development of VAT dysfunction. There are many factors that regulate this balance in WAT expansion. In this chapter, we have addressed three of them: fructose intake, GCs and testosterone. Both, fructose intake and GCs, stimulate adipogenesis by modulating APCs competency and number, and thus terminal differentiation. However, in both cases the chronic exposure to these factors led to hypertrophic adipocytes, and therefore to an unhealthy WAT expansion. Chronic exposure to high GC levels seems to induce a resistance state in APCs that would limit their adipogenic potential, partially by a lower response to GCs stimuli due to MR expression decrease. Conversely, testosterone is an anti-adipogenic factor that favours unhealthy expansion. Obesity is associated with reduced testosterone levels, which would promote adipogenesis; however, much extensive research is needed to determine the role of androgens in APCs adipogenic potential in obesity. Finally, factors inducing adipogenesis could become a therapeutic target against Dietary and Hormonal Factors Involved in Healthy or Unhealthy Visceral Adipose Tissue Expansion http://dx.doi.org/10.5772/65927 177

**Figure 2.** The analysis of three different factors regulating adipogenesis and VAT expansion shows differential effects, depending on the factor analysed. Early GC excess and FRD intake make APCs more competent, this means favouring their ability to differentiate into mature adipocytes, consequently increasing adipogenesis. Nevertheless, this increased adipogenesis occurs in parallel with hypertrophic VAT expansion. GCs chronic excess causes APCs competency to decrease, adipogenesis to fall and VAT expansion mainly by the hypertrophy of preexistent adipocytes. Effects of low testosterone levels associated to obesity need to be further studied. Nonetheless, it is already known that testosterone is an anti-adipogenic factor involved in unhealthy VAT expansion, favouring adipocyte hypertrophy. In summary, all three factors are involved in increased hypertrophy/hyperplasia balance, generating a dysfunctional VAT.

endocrine-metabolic disorders, favouring WAT healthy expansion and thus mitigating obesity-associated pathologies (**Figure 2**).
