Adipose tissue dysfunction in obesity, diabetes, and vascular diseases

Abstract

The classical perception of adipose tissue as a storage place of fatty acids has been replaced over the last years by the notion that adipose tissue has a central role in lipid and glucose metabolism and produces a large number of hormones and cytokines, e.g. tumour necrosis factor-alpha, interleukin-6, adiponectin, leptin, and plasminogen activator inhibitor-1. The increased prevalence of excessive visceral obesity and obesity-related cardiovascular risk factors is closely associated with the rising incidence of cardiovascular diseases and type 2 diabetes mellitus. This clustering of vascular risk factors in (visceral) obesity is often referred to as metabolic syndrome. The close relationship between an increased quantity of visceral fat, metabolic disturbances, including low-grade inflammation, and cardiovascular diseases and the unique anatomical relation to the hepatic portal circulation has led to an intense endeavour to unravel the specific endocrine functions of this visceral fat depot. The objective of this paper is to describe adipose tissue dysfunction, delineate the relation between adipose tissue dysfunction and obesity and to describe how adipose tissue dysfunction is involved in the development of diabetes mellitus type 2 and atherosclerotic vascular diseases. First, normal physiology of adipocytes and adipose tissue will be described.

Adipose tissue quantity and composition contribute to adipokine concentrations in the subclavian vein and the inferior mesenteric vein

“…Various beneficial characteristics have been attributed to adiponectin, such as insulin sensitizing, anti-atherosclerotic and anti-inflammatory properties. 22 Differing from other adipokines, adiponectin levels typically decrease in obese states 23 and with increasing subcutaneous adipocyte size. 24 The current data show that increased SAT and VAT mass and increased subcutaneous and visceral adipocyte size result in lower adiponectin concentrations.…”

Childhood obesity–related endothelial dysfunction: an update on pathophysiological mechanisms and diagnostic advancements

“…In childhood obesity, hypertrophic adipose tissue is invaded by macrophages, resulting in the upregulation of adipocyte adhesion molecules. This process leads to the diapedesis of monocytes and initiates a vicious circle of adipogenesis and inflammation (41). Several adipokines have a direct effect on endothelial function, including leptin and adiponectin (42,43).…”

Increased aldosterone in patients with metabolic syndrome; an additional risk factor

“…This may reflect a mild variant of primary aldosteronism supports the hypothesis of factors released from fat cells directly or indirectly stimulating aldosterone secretion. In another words, dysfunctional adipose tissue can secrete aldosterone independently from renin stimulation [27].…”