Biomedical Engineering Reference
In-Depth Information
ECM is mainly composed of collagen, fibronectin and secreted protein acidic rich
in cysteine (SPARC). The BM is a thin layer, which mechanically supports (packs)
the adipocytes, comprising laminin, collagen, nidogen/entactic and proteoglycans
[
65
]. Adipose tissues are also highly vascularized such that lean human adipose
tissue receives 3-7 % of the cardiac output [
30
]. In addition to blood vessels,
adipose tissues contain lymph nodes and are influenced by their secretion. While
mesenteric adipose tissues have a high content of lymph nodes, subcutaneous and
perirenal fat pads have either none or very few [
30
]. Additionally adipose tissues
are also innervated by the sympathetic system [
56
,
68
].
3 Distribution of Adipose Tissues in Obesity
The most common pathology related to adipose tissues is obesity, which is a sig-
nificant health problem in developed and developing countries due to its strong
association with metabolic and cardiovascular co-morbidities [
20
,
30
]. In obesity,
the fat mass exceeds 22 and 32 % of the total bodyweight in males and females,
respectively, but it can reach as much as 60-70 % of the bodyweight in massively
obese individuals [
7
,
30
]. During the development of obesity, the adipose tissue
grow through hypertrophy of adipocytes (increase in the size of cells), which is also
accompanied by hyperplasia (increase in number). The hypertrophy results from
excessive triglyceride accumulation in the adipocytes, leading the enlarged cells to
release proliferative paracrine factors (e.g. tumor necrosis factor (TNFa) and insulin
growth factor (IGF1) which are internal controllers of preadipocyte proliferation
[
15
]. The adipocytes would grow until reaching a maximum ''critical cell size''
which is thought to be genetically determined and is specific for each depot [
7
]. The
hyperplasia, which results from proliferation and differentiation of preadipocytes
into new adipocytes is influenced by paracrine and autocrine factors, e.g., insulin and
growth hormones. Combining these, adipose tissues positioned at different ana-
tomical locations do not respond uniformly to stimuli that trigger lipid storage or
mobilization [
7
,
30
,
68
]. In advanced obesity, the increased mass of the adipose
tissues lead to hypoxia in the tissues, resulting in cell death, enhanced chemokine
secretion, and dysregulation in fatty acid fluxes [
73
]. The dead cells stimulate
infiltration of macrophages into the adipose tissues, forming crown-like structures
(CLS) of macrophage aggregations that were observed to surround dead adipocytes
[
1
,
42
,
73
]. The number of the CLS correlates with the level of obesity, and they are
more common in visceral than in subcutaneous adipose tissues [
15
,
42
,
72
]. Inter-
estingly, the metabolic disorders in obese patients are most commonly associated
with visceral compared to subcutaneous fat accumulation [
7
,
49
]. The infiltrating
macrophages fuse to phagocytose the residual LDs, forming large lipid-laden
multinucleated syncytia, a stage that characterizes chronic inflammation [
72
,
73
].
In parallel to that, several ECM components are unregulated during the fat mass
expansion, e.g. elimination of collagen type VI which results in adipose tissue
fibrosis and reduced plasticity [
73
]. This process of ECM remodeling is mediated by
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