The New Adipose Tissue and Adipocytokines

Abstract

Obesity is a well-known risk factor for the development of insulin resistance, type 2 diabetes, dyslipidemia, hypertension, and cardiovascular disease. Rather than the total amount of fat, central distribution of adipose tissue is very important in the pathophysiology of this constellation of abnormalities termed metabolic syndrome. Adipose tissue, regarded only as an energy storage organ until the last decade, is now known as the biggest endocrine organ of the human body. This tissue secretes a number of substances--adipocytokines--with multiple functions in metabolic profile and immunological process. Therefore, excessive fat mass may trigger metabolic and hemostatic disturbances as well as CVD. Adipocytokines may act locally or distally as inflammatory, immune or hormonal signalers. In this review we discuss visceral obesity, the potential mechanisms by which it would be related to insulin resistance, methods for its assessment and focus on the main adipocytokines expressed and secreted by the adipose tissue. Particularly, we review the role of adiponectin, leptin, resistin, angiotensinogen, TNF-alpha, and PAI-1, describing their impact on insulin resistance and cardiovascular risk, based on more recent findings in this area.

Fenofibrate inhibits adipocyte hypertrophy and insulin resistance by activating adipose PPARα in high fat diet-induced obese mice

“…Visceral fat accumulation due to adipocyte hypertrophy induces changes in the production and secretion of adipokines, such as adiponectin, visfatin, leptin, and TNFα, involved in the development of insulin resistance (Ahima, 2006;Bulcao et al, 2006;Matsuzawa, 2006). Leptin and TNFα are overexpressed in the adipose tissues of obese, insulin-resistant rodents, which have hypertrophic adipocytes (Hotamisligil et al, 1993;Maffei et al, 1995;Okuno et al, 1998;Kralisch et al, 2007).…”

Interleukin-8 and interleukin-10, brain volume and microstructure, and the influence of calorie restriction in old rhesus macaques

“…Excess adipose tissue can also elevate PIC in the systemic circulation (Bulcao et al 2006). We previously reported a small but significant correlation between IL-6 levels near time of scan and the presence of inflammatory disease, while no association was seen between IL-6 and abdominal adiposity as estimated by MRI (Willette et al 2010).…”

Angiopoietin-like 4 Interacts with Matrix Proteins to Modulate Wound Healing*

“…These events are regulated spatiotemporally by several classical growth factors and cytokines, the effects of which have been well documented (2). Less studied are extracellular factors such as matricellular proteins and adipocytokines, both shown to have a profound local impact during wound repair (3,4). Effective directed cell migration requires constant cellular interaction with the extracellular matrix (ECM) 3 in response to the changing wound environment.…”