By Saverio Cinti MD (auth.), Giamila Fantuzzi PhD, Theodore Mazzone MD (eds.)
This publication offers a entire survey of adipose tissue, its physiological services, and its position in disorder. the quantity spans the whole variety of adipose tissue reviews, from simple anatomical and physiological study to epidemiology and medical reviews. The authors are exotic researchers, clinicians and epidemiologists. they've got integrated groundbreaking contemporary experiences into conventional versions of adipose tissue homes.
Chapters on recognized homes of adipokines leptin and adiponectin are complemented by way of an creation to a unique view of adipose tissue as a dynamic organ that regulates systemic substrate availability and metabolism, besides numerous different discrete capabilities. This novel notion is improved.
Worldwide developments in weight problems are mentioned from an evolutionary point of view and reasons of the present weight problems epidemic are postulated. also, researchers and clinicians study the organization and power position of adipose tissue in affliction mediation and provide epidemiological proof. This quantity concludes with a considerate and leading edge dialogue of assorted techniques to inducing and maintaining weight reduction in overweight
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Additional resources for Adipose Tissue and Adipokines in Health and Disease
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WAT has high expression of 4E-BP1, a protein important for the posttranscriptional regulation of protein synthesis. Mice lacking 4E-BP1show a reduction of the total fat mass and a brown phenotype of their adipose organ, suggesting that a posttranscriptionally regulated protein can be responsible for the white phenotype. The author suggests that PGC1 (a cofactor of PPARL) is the protein whose posttranscriptional synthesis is blocked by 4E-BP1 (55). We recently reported a completely new example of adipose organ plasticity, with reversible transdifferentiation of adipocytes into epithelial cells.
This action involves probably both SREBP-1c (39) and LXRF, although the actual role of SREBP-1c has been questioned (40). Glucose also stimulates lipogenesis in adipocytes (41) and, as in liver, a full stimulation requires the simultaneous presence of insulin and glucose. The action of glucose could be transmitted by ChREBP, as this transcription factor is expressed in adipocytes (24,35,42,43); however, a stimulatory effect of glucose on ChREBP translocation to nucleus and DNA binding activity in adipocytes has not yet been demonstrated.