Minireview: The Adipocyte—At the Crossroads of Energy Homeostasis, Inflammation, and Atherosclerosis

Abstract

Adipose tissue evolved to efficiently store energy for times of caloric restriction. The large caloric excess common in many Western diets has negated the need for this thrifty function, leaving adipose tissue ill-equipped to handle this increased load. An excess of adipose tissue increases risk for a number of conditions including coronary artery disease, hypertension, dyslipidemias, type 2 diabetes, and even cancer. Indeed, the ability of the adipocyte to function properly when engorged with lipid can lead to lipid accumulation in other tissues, reducing their ability to function and respond normally. The role of adipose tissue as an endocrine organ capable of secreting a number of adipose tissue-specific or enriched hormones, known as adipokines, is gaining appreciation. The normal balance of these adipose tissue secretory proteins is perturbed in obesity. Paradoxically, the lack of normal adipose tissue, as seen in cases of lipodystrophy and lipoatrophy, is also associated with pathologic sequelae similar to what is seen with obesity. The pathologic findings associated with lack of adipose tissue, largely due to inability to properly store lipids, may also be due to a lack of adipokines. In this review, we highlight the role of adipose tissue as an endocrine organ focusing on some of the recent advances in the identification and pharmacological characterization of adipokines as well as their regulation in the context of obesity and insulin-resistant states.

Relationships among acylation stimulating protein, adiponectin and complement C3 in lean vs obese type 2 diabetes

“…This may have pathophysiological and clinical relevance. Recently, it has been suggested by Pickup and Crook 55 and Pickup et al 56 as well as others, 57,58 that insulin resistance, and ultimately type 2 diabetes, may in part be a manifestation of a chronic acute-phase response. This concept was largely developed from the observations that plasma concentrations of other inflammatory cytokines and acute-phase proteins such as TNF-a, IL-6, and/or CRP are increased in individuals with type 2 diabetes.…”

Prediabetes is associated with abnormal circadian blood pressure variability

“…40 Increased visceral adipose tissue due to the altered distribution pattern impairs adipose tissue function, leading to an increased CVD risk. 41 This is primarily due to altered adipose tissue secretions with auto, para and endocrine effects on multiple metabolic pathways, including those that modulate BP. 42 It is plausible that this altered secretory activity of adipose tissue [43][44][45] unhinges the anti-inflammatory and pro-inflammatory adipokine balance, producing endothelial dysfunction, which over time leads to CVD.…”

Association of hypertension with single nucleotide polymorphisms in the quantitative trait locus for abdominal obesity-metabolic syndrome on chromosome 17

“…10,26 Increased abdominal adiposity leads to a state of chronic low-grade inflammation, insulin resistance and endothelial dysfunction. [27][28][29] Adipocytes in adipose tissues secrete adipokines such as leptin, adiponectin and acylation-stimulating protein (ASP) that regulate obesity. 30 Leptin suppresses appetite, while adiponectin increases insulin sensitivity.…”