2.3. Roles of white adipose tissue

WAT occurs in virtually all vertebrates, and the physiological basis for its presence has never been investigated thoroughly. Conversely, because of its diverse nature, WAT had been considered to occur almost universally in the animal body and had not been fully recognized as an anatomically organized tissue with site-specific properties until the past few decades (Wasserman 1965, Pond 1978, 1986, 1998, 1999). Although large variability in relative masses of depots and large individual and taxonomical differences are evident, a common pattern of a dozen or so adipose tissue depots can be found in all eutherian and metatherian mammals (Pond 1986). Unilocular white adipocytes are simple by their structure, store large amounts of TAGs during periods of energy excess and deliver fatty acids to other tissues as required. Despite of its simple structure, WAT performs numerous functions in the body that are related but not necessarily restricted with its anatomical locations, such as the provision for lactation (McNamara 1997).

The recently discovered secretory product of white adipocytes, leptin, has been proposed to play a role in the regulation of body weight and the total amount of adipose tissue in the body (Considine & Caro 1997, Schwartz et al. 2000). Leptin is expressed by the ob gene, which has extensive homology among vertebrates (Considine & Caro 1997). The original ‘lipostatic’ concept states that leptin is a hormonal substance that circulates in the blood and provides the brain with a signal about the amount of stored adipose tissue, thereby acting as a satiety factor (Kennedy 1953). Fasting and weight loss decrease the level of leptin in circulation, and weight gain and overfeeding increase it (Considine & Caro 1997, Trayhurn et al. 1998, Schwartz et al. 2000). The exact mechanism of the effect of leptin is not known. The sympathetic nervous system is proposed to play a key role in the regulation of leptin levels, possibly by downregulating leptin production via β₃-adrenoceptors (Trayhurn et al. 1998). Reduced blood leptin and insulin levels presumably increase the activity of anabolic neural pathways in the brain to boost appetite and feed intake, and thereby aim to restore energy homeostasis (Schwartz et al. 2000). Although WAT seems to be the main site of leptin production, leptin is also produced in other tissues, including BAT and placenta (Trayhurn et al. 1998), and may have versatile functions in the body.

Besides leptin, WAT also secretes a large number of other signals that affect energy homeostasis. These include pro-inflammatory cytokines, regulators of lipoprotein metabolism and growth factors, among others (Mohamed-Ali et al. 1998). Catecholamines, insulin and the sympathetic nervous system that modulate the adipocyte function also influence efferent signalling of adipose tissue (Mohamed-Ali et al. 1998, Trayhurn et al. 1998). WAT is thus increasingly being recognised as an active endocrine and paracrine organ, that closely interacts with other organs and tissues, and enables the organism to adapt to a wide range of metabolic challenges.

The lipolysis in WAT is catalyzed by hormone-sensitive lipase and stimulated by catecholamines, NA, and adrenaline (A) mainly via β₁-receptors (Hales et al. 1978). The lipolysis can be activated both by circulating catecholamines and by NA from the sympathetic nerve endings. The sympathetic stimulation of WAT is thought to increase the lipolysis in situations such as exercise, stress and cold exposure (Hales et al. 1978, Garofalo et al. 1996), but sympathetic stimulation has been considered unlikely during starvation, when a fall in circulating insulin has been considered to be a major stimulus (Hales et al. 1978). Recently, it has been shown that prolonged fasting also induces sympathetic activity in WAT (Migliorini et al. 1997). The products of the lipolysis in WAT, or glycerol and FFAs are mainly delivered to the other tissues.