Disentangling the neuroendocrine systems that regulate energy homeostasis and
adiposity has been a long-standing challenge in pathophysiology, with obesity
being an increasingly important public health problem. Adipose tissue is no
longer considered a passive bystander in body-weight regulation. It actively
secretes a large number of hormones, growth factors, enzymes, cytokines,
complement factors and matrix proteins, at the same time as expressing receptors
for most of these elements, which influence fuel storage, mobilisation and
utilisation at both central and peripheral sites. Thus, an extensive cross talk
at a local and systemic level in response to specific external stimuli or
metabolic changes underpins the multifunctional characteristics of adipose
tissue. In addition to the already-known adipokines, such as IL, TNFα,
leptin, resistin and adiponectin, more recently attention has been devoted to
‘newcomers’ to the ‘adipose tissue arena’, which
include aquaporin, caveolin, visfatin, serum amyloid A and vascular endothelial
growth factor. While in vitro and in vivo experiments have provided extremely
valuable information, the advances in genomics, proteomics and metabolomics are
offering a level of information not previously attainable to help unlock the
molecular basis of obesity. The potential and power of combining
pathophysiological observations with the wealth of information provided by the
human genome, knock-out models, transgenesis, DNA microarrays, RNA silencing and
other emerging technologies offer a new and unprecedented view of a complex
disease, conferring novel insights into old questions by identifying new pieces
to the unfinished jigsaw puzzle of obesity.