Download Adipose Tissue and Adipokines in Health and Disease by Saverio Cinti MD (auth.), Giamila Fantuzzi PhD, Theodore PDF

By Saverio Cinti MD (auth.), Giamila Fantuzzi PhD, Theodore Mazzone MD (eds.)

This e-book offers a entire survey of adipose tissue, its physiological features, and its position in disorder. the amount spans the total variety of adipose tissue experiences, from uncomplicated anatomical and physiological study to epidemiology and medical reports. The authors are wonderful researchers, clinicians and epidemiologists. they've got included groundbreaking contemporary reviews into conventional versions of adipose tissue houses.

Chapters on famous houses of adipokines leptin and adiponectin are complemented via an creation to a unique view of adipose tissue as a dynamic organ that regulates systemic substrate availability and metabolism, besides quite a few different discrete services. This novel proposal is improved.

Worldwide tendencies in weight problems are mentioned from an evolutionary viewpoint and motives of the present weight problems epidemic are postulated. also, researchers and clinicians study the organization and strength function of adipose tissue in disorder mediation and provide epidemiological facts. This quantity concludes with a considerate and cutting edge dialogue of varied ways to inducing and maintaining weight reduction in overweight

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Extra info for Adipose Tissue and Adipokines in Health and Disease

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These mice have a brown phenotype of abdominal fat and resistance to obesity (52). FOXC2 is a gene for a transcription factor that is exclusively expressed in adipose tissue. Its transgenic expression in the adipose tissue in mice results in a lean, obesityresistant, and insulin-sensitive phenotype. The adipose organ of these mice has a browner phenotype than that of controls (53). Of note, humans with insulin resistance have a reduction of FOXC2 expression in biopsies from the abdominal subcutaneous adipose tissue, together with a reduction of other genes of brown adipocyte phenotype (54).

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Its expression is increased during fasting and reduced by refeeding and insulin (69), whereas thiazolidinediones stimulate it (70). Deletion of AQPap in mice induces a lack of plasma glycerol increase in response to G-adrenergic stimulation and during fasting, with hypoglycemia during fasting (71), and results in obesity (72). Missense mutations resulting in the loss of transport activity have been described in humans (73). One subject homozygous for such a mutation had a normal body weight and normal basal plasma glycerol concentration but a lack of increase during exercise (73), suggesting that AQPap has a role in glycerol efflux in humans but is not the only mechanism.

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