Hello. Sign In
Standards Store

Adipose Tissue and Inflammation

2009 Edition, October 8, 2009

Complete Document

Detail Summary

Active, Most Current

Additional Comments:
ISBN: 978-1-4200-9130-4
Price (USD)
Add to Cart

Product Details:

  • Revision: 2009 Edition, October 8, 2009
  • Published Date: October 8, 2009
  • Status: Active, Most Current
  • Document Language: English
  • Published By: CRC Press (CRC)
  • Page Count: 320
  • ANSI Approved: No
  • DoD Adopted: No

Description / Abstract:


Obesity is a worldwide epidemic disorder that has become recognized in the 21st century as a principal health threat in most countries. Obesity is characterized by accumulation of excess body fat and is quantitatively defined as a body-mass index greater than 30. Several factors contribute to obesity and these can be broadly classified as genetic and environmental. Among the environmental influences, the combination of excess caloric intake and sedentary life contribute most significantly to the incidence of obesity. The American Obesity Association identifies obesity with more than 30 medical conditions. In particular, obesity is a risk factor for the development of common chronic diseases including hypertension, type 2 diabetes, metabolic syndrome, cardiovascular disease, several cancers, and a host of inflammatory disorders. Accumulating evidence implicates inflammation as an essential common thread among these chronic diseases as well as a key feature of obesity-associated morbidities. We must realize that this is not inflammation in the classic sense: obesity and its associated diseases manifest a low-grade, metabolically-associated inflammation; it is inflammation triggered by high caloric diets that involves many of the same mediators associated with classic inflammation.

Concurrent with this understanding of obesity as a chronic low-grade inflammatory disease, it is necessary to recognize adipose tissue as more than a storage site for fat. Adipose tissue is an essential endocrine organ that produces and secretes a host of hormones in response to varying physiologic and pathologic states. Obesity creates an identifiable and characteristic shift in the secreted profiles of these adipose- specific hormones, termed adipokines. These same adipokines promote lowgrade systemic inflammation. For example, obesity and chronic inflammation are accompanied by suppression of adiponectin levels and elevation of resistin levels; the resultant effects on signal transduction converge to increase activation of nuclear factor kappa B (NF-κB) and accelerate production of tumor necrosis factor alpha (TNF-α). In turn, these events alter insulin signaling, decrease Akt activity, and impair translocation of the GLUT-4 glucose transporter to cell surfaces—all events that are characteristic of the insulin-resistant state common in obesity. In addition, the fat cells in obesity recruit macrophages into adipose tissue where they secrete their own host of inflammatory factors.

Adipose Tissue and Inflammation focuses on the contribution of adipose tissue to local and systemic inflammation and allows numerous themes to be drawn. At the start, epidemiologic time–trend analyses in populations worldwide indicate that obesity has increased sharply over the past 10 to 20 years and that in the United States the potential health consequences of this rise have been quantified such that obesity at age 40 is estimated to reduce life expectancy by at least 6 years. From investigative research of the endocrine nature of adipose tissue, we learn here that adipose tissue is better considered as an organ composed of both white and brown adipose tissue contained within two main subcutaneous depots and several specific visceral depots. Analysis of the endocrine nature of the adipose organ, detailed in this volume, reveals that about a quarter of the genes expressed in white adipose tissue encode secreted proteins and that the number of established and putative adipokines identified among these genes exceeds several dozen. The authors, all experts in their fields, report that essential among these adipokines, particularly in regard to their role as modulators of local and systemic inflammation, are leptin, adiponectin, TNF-α, numerous interleukins and prostaglandins, resistin, leukocyte chemoattractants (monocyte chemoattractant protein-1 and macrophage migration inhibitory factor-1), fibrinolytic proteins, and growth factor molecules. Detailed investigations of the inflammatory responses of the adipose organ reveal that classic inflammatory signal transducers such as NF-κB, JNK, PPAR, and iNOS are operative and that their continued regulation of adipose gene expression contributes to chronic inflammatory status in obesity.

We are fortunate to have the contributions from several leading edge experts in the area of obesity and inflammation and they report here their current findings obtained through basic, translational, and clinical research. Insulin is central in this research. Insulin affects adipose inflammation and we learn of the interdependent relationships among insulin resistance, central obesity, and inflammatory processes in adipose tissue. We learn of detailed examinations of the effects of insulin on the levels of key adipokines and the effects of inflammation on insulin sensitivity and other key regulators of glucose homeostasis, cell-cycle progression, and apoptosis in adipose tissue. Experts in their respective fields report on how obesity and adipose inflammation are modulated by systemic and local hormonal factors including growth hormone, glucocorticoids, and prostaglandins; by dietary factors including fatty acids, polyphenols, phytosterols, phytoestrogens, and antioxidants; by life-style changes involving diet, exercise and weight loss; and finally by new and investigative advances in pharmacotherapy.

Adipose Tissue and Inflammation features contributions from international experts in the fields of adiposity, inflammation, adipokines, and pharmaconutrition. We sincerely thank these contributors for sharing their expertise with the scientific community at large through their chapter authorships. In addition, we would like to thank the publisher, Taylor & Francis Group, for agreeing to publish this book. We thank the series editors, Dr. Lester Packer and Dr. Enrique Cadenas for their continued inspiration and our colleague Dr. Mulchard Patel for his enthusiastic encouragement. We also thank the publication staff, whose dedicated work to assist in production resulted in such a well constructed book. Last, but not least, we would like to thank the readers who are interested in learning about the most up-to-date advances in the area of adipose tissue and inflammation.