When the energy balance is positive, the adipose organ prevalently undergoes an increment in its white component. White adipocytes become hypertrophic and subsequently hyperplastic (likely due to a close causal relationship). In fact, it has been suggested that adipocytes are unable to expand beyond a given maximum volume, or 'critical size', which is genetically determined and specific for each depot . Adipocytes that have reached the critical size trigger an increase in cell number [78-80]. In a recent review, Hausman et al. , after considering the evidence for this theory, conclude that not only paracrine factors, but also circulating factors as well as neural influences may play a large role in regulating adipose tissue development and growth. They suggest that in the development of obesity, enlarged fat cells produce and release proliferative paracrine factors as internal controllers of preadipocyte proliferation, and that their proliferative response is modulated by neural inputs to fat tissue and/or serum factors. In any case, paracrine factors appear to play a pivotal role. Adipose tissue expresses numerous factors that could be implicated in the modulation of adi-pogenesis: IGF-1, TGF-a, TNF-a, macrophage colony-stimulating factor (MCSF), angiotensin II, autotaxin-lysophosphatidic acid (ATX-LPA), lep-tin,resistin,etc. .
Of note, in genetically obese ob/ob mice (lacking leptin) and in other types of genetic and diet-induced obesity, the fat mass is hypertrophic and hyperplastic, while in genetically obese db/db mice (lacking leptin receptor) the fat mass is increased only by a hypertrophic mechanism ( and our unpublished observations). Therefore, the pres ence of leptin receptor seems to be essential to induce hyperplasia. In the subcutaneous adipose tissue of a massively obese patient lacking leptin receptor , we recently observed that mean adipocyte volume was about half that usually seen in the same depot of patients with similar BMI due to 'primitive obesity'.
A recent study showed that obesity induced by a high-fat diet in mice is hypertrophic, while that induced by hypothalamic lesion due to administration of monosodium glutamate is hyperplastic .
A positive energy balance also affects the organ's brown component. The brown adipocytes of obese animals are generally similar to white cells. Prevalently unilocular cells are observed at the sites where brown adipocytes are normally found, but these cells often exhibit typical mitochondria distinct from the 'normal' organelles of white fat cells. They usually - though modestly -express UCP1 as well as the typical protein of white adipocytes: leptin . Interestingly, the large amount of TNF-a found in obese mice induces an increased rate of apoptosis of brown fat cells .
Transgenic animals lacking |31, 2 and 3 receptors become massively obese eating the same amount of food as lean ones . In such animals, brown adipocytes are identical to those found in the genetically obese (ob/ob) and db/db mice described above: they are unilocular and show leptin expression and modest UCP1 activity in mitochondria with the typical morphology. This is in line with the fact that obesity due to lack of lep-tin (ob/ob) or its receptor (db/db) is accompanied by reduced BAT adrenergic stimulation owing to the absence of the stimulus normally exerted by the hormone on hypothalamic orthosympathetic centres.
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