By Giamila Fantuzzi

This booklet offers a finished survey of adipose tissue, its physiological capabilities, and its function in sickness. the quantity spans the whole diversity of adipose tissue reports, from uncomplicated anatomical and physiological study to epidemiology and scientific experiences. Groundbreaking fresh experiences are integrated into conventional versions of adipose tissue houses. an outline of the function of macrophages in weight problems and metabolism in integrated.

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Sample text

It binds apoprotein Erich lipoproteins, such as VLDL, chylomicrons, and remnants, and brings them probably in close contact with LPL, facilitating its action. Mice deficient in VLDL receptor have a decreased fat mass and are resistant to diet-induced obesity; moreover, VLDLreceptor deficiency reduces the obesity of ob/ob mice (6). The exact role of this receptor in humans remains to be defined. Whatever their origin, the uptake of long-chain fatty acids by adipocytes requires specific processes in order to allow them to cross the plasma membranes (7,8).

This effect is present only in primates. Atrial natriuretic peptide and brain natriuretic peptide activate guanylate cyclase and stimulate cGMP-dependent protein kinases. They probably play a role in the stimulation of lipolysis during exercise (94). qxd 12/12/06 12:32 PM 28 Page 28 Part I / Adipose Tissue: Structure and Function Dephosphorylation of the regulatory site(s) inhibits HSL. Insulin, the main antilipolytic hormone, acts by phosphorylating and stimulating the activity of phosphodiesterase 3B that breaks down cAMP and reduces thus the phosphorylation of HSL (95).

Last, evidence has been provided that serines 659 and 660 are also phosphorylated by cAMP-dependent protein kinase in vitro in rat adipocytes and that this phosphorylation could also stimulate lipolysis (91). Other pathways of phosphorylation have been described. Increased cAMP concentration can activate the mitogen-activated protein kinase/extracellular-regulated kinase (ERK) pathway (92,93). Activated ERK phosphorylates HSL at serine 600 and increases its activity (92). Finally, the natriuretic peptides atrial natriuretic peptide and brain natriuretic peptide have been shown to phosphorylate HSL and stimulate lipolysis (94).

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