Fat Tissue

To better understand the role played by lipids in disturbances associated with HIV infection and with new antiretroviral therapies, it is necessary to review several concepts regarding fat tissue in humans. Actually, fat tissue seems to be both the main player in and the victim of such disorders. Fat tissue not only stores and mobilises rapidly available energy (~ 9 Kcal/g), but also produces hormone-like substances, such as leptin and adiponectin [91], and, especially, cytokines, such as TNF-a [92] and IL-6 [93]. For these reasons, fat tissue is an important metabolic organ. Leptin regulates hypothalamic centres of hunger and satiety [94, 95]; adiponectin reduces plasma levels of glucose, fatty acids, and triglycerides, thereby preventing fat accumulation in muscles and liver [96, 97]. Some 60% of adipose tissue is composed of adipocytes, the rest being blood cells, pericytes, preadipocytes, and fibroblasts [98]. In the human embryo, fat tissue is observed beginning at the second trimester of pregnancy, and its body distribution remains constant throughout foetal and adult life. At birth, the fatty mass is 14% of body weight, with changes depending on the mother's general condition. During the first year of life, adipocytes undergo hypertrophy, and then replicate until full body development is completed. Only 2% of mature adipocytes undergo mitosis, under appropriate stimulation. Therefore, adipocyte hypertrophy, rather than an increase in their number, seems responsible for the diffuse or localised increases in fatty masses [99]. There is, however, a pool of quiescent or immature adipocytes that can differentiate into mature adipocytes under hormonal and vitamin stimulation [98, 100]. During differentiation, markers such as LPL mRNA, glyc-erol triphosphate dehydrogenase (GPDH), hormone-susceptible lipase (HSL), perilipin, a glucose carrier (GLUT4), and p-3 receptors are acquired. Triglycerides comprise 90% of the mature adipocyte and provide a source of easily available energy through their hydrolysis to fatty acids and glycerol. Mature adipocyte expresses a-2 -adrenergic receptors (a2AR) and adipsin [98]. Adipose tissue secretes LPL, adipsin, complement C3 and B fractions, P450 aromatase, leptin, and growth factors [94, 101]. Its main metabolic functions are lipid hydrolysis and synthesis. Lipolysis is initiated via the activation of p-adrenergic receptors, which in turn activates adenyl cyclase, with subsequent cAMP production via ATP hydrolysis. cAMP activates a protein kinase that, in turn, activates HSL and the hydrolysis of triglyceride to fatty acids and glycerol. The p-1 receptors are epinephrine- and norepinephrine-specific, p-2 receptors are isopre-naline-specific, and p-3 receptors are activated by high doses of catecholamines. a-1 and a-2 receptor activation terminates lipolysis by inhibiting adenyl cyclase. Liposynthesis is driven by LPL, a 55-kDa glycoprotein activated by apoprotein C-II. It hydrolyses circulating triglycerides of chylomi-crons and VLDLs. The distribution of adipose tissue throughout the body depends on genetic and hormonal factors [102]. In females, fat tissue is mainly localised to the thighs, with a central redistribution occurring after menopause. In males, fat tissue has mainly a visceral distribution [103,104]. Excess visceral fat storage is associated with hyperinsulinaemia, diabetes, hyperlipaemia, hypertension, decreased glucose tolerance, and increased cardiovascular disease risk [105]. The metabolic activity of adipose tissue varies according to its anatomic distribution. Epiploic fat is more susceptible to catecholamines than epigas tric fat, because its adipocytes are larger and contain more p-3 receptors. Since there is increased lipolytic hydrolysis in visceral fat, the flow of FFA is directly conveyed to the liver. Hepatic VLDL synthesis increases, whereas the uptake of insulin by the liver decreases. Chronic hyperinsulinaemia induces a peripheral insulin resistance [103], increasing diabetes risk. Subcutaneous thigh fat is less susceptible to catecholamines and has a higher LPL index, implying a greater liposynthetic activity. The number of cortisol and androgen receptors is higher in visceral than in subcutaneous fat [102]; as a consequence, LPL stimulation is stronger. Androgen stimulation of p-receptors increases HSL lipolytic activity. The function of brown adipose tissue (BAT) in humans is still not clear. In many animal species, 25% of body weight consists of BAT, which is involved in thermal homeostasis and heat dispersion when the animal is exposed to low/high temperature or hyper/hypo-feeding. Heat is produced by uncoupling fatty acid oxidation and ATP production in mitochondria through an uncoupling protein (UCP) [106]. In humans, adipocytes identical to those of BAT are observed only in pathological conditions, such as Cushing's syndrome, pheocromocytoma, and multiple symmetric lipomatosis. This last syndrome is characterised by the distribution of multiple, non-encapsulated lipomas to the nape, neck, and supraclavicular and mediastinal regions, along with high LPL activity and decreased lipolysis [107-110]. It has also been suggested that BAT plays a role also in diet-induced thermogenesis.

Fire Up Your Core

Fire Up Your Core

If you weaken the center of any freestanding structure it becomes unstable. Eventually, everyday wear-and-tear takes its toll, causing the structure to buckle under pressure. This is exactly what happens when the core muscles are weak – it compromises your body’s ability to support the frame properly. In recent years, there has been a lot of buzz about the importance of a strong core – and there is a valid reason for this. The core is where all of the powerful movements in the body originate – so it can essentially be thought of as your “center of power.”

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