Biomedical Engineering Reference
In-Depth Information
proteolytic enzymes, e.g., plasminogen and matrix metalloproteinase, where genetic
variations in their activity contribute to inter-individual variation in the capacity for
adipose tissue expansion [ 42 ].
4 Pathophysiology of Adipose Tissue
The low-grade chronic inflammation in dysfunctional adipose tissues characterizing
obesity is associated with the ''metabolic syndrome'', which clusters several met-
abolic abnormalities, including hypertension, dyslipidemia, glucose intolerance and
insulin resistance, malfunctions that increase the risk of developing type-2 diabetes
and related cardiovascular diseases [ 28 , 48 , 51 ]. The infiltrating macrophages
constitute a major source of inflammatory mediators, especially the TNFa, which
impair adipocyte differentiation, promote lipolysis and secretion of free fatty acids,
and contribute to insulin resistance [ 28 , 48 ]. Similar to TNFa, other adipokines with
pro-inflammatory activity (e.g. IL-6 and monocyte chemoattractant protein-1
(MCP-1)) or adipokines that are involved in thrombosis and hypertension (e.g.
plasminogen activator inhibitor-1 (PAI-1) and angiotensinogen) are also overpro-
duced with increasing adiposity [ 48 ]. On the contrary, secretion of some adipokines
with anti-inflammatory and anti-oxidant properties (e.g. adiponectin) is decreased
[ 48 ]. Growth of visceral fat is in particular a risk factor for these pathologies,
compared to excess subcutaneous adipose tissues, as the visceral fat tissues secrete
higher levels of the aforementioned complement pro-inflammatory factors [ 28 , 48 ,
51 ]. The appearance of dysfunctional adipose tissues is also associated with accu-
mulation of ectopic fat in other tissues e.g. skeletal muscle and viscera, which
eventually impairs systemic processes in the liver, pancreas, heart and brain.
5 Estrogen and Adipose Tissues
5.1 Estrogen Consumption
The industrialized diet, particularly in poor populations, is often cheap, calorie-
dense food, rich in fat, salt, simple carbohydrates and sugars, and, importantly,
hormones [ 60 ]. Hence, rapid urbanization and the increase in demand for agri-
cultural products are largely responsible for the worldwide increasing prevalence
of obesity. Large food corporations are extensively using hormones, particularly
estrogen, in order to increase production of milk and cause poultry, cattle, and
other livestock to grow bigger in size and weight. There are evidence in the
literature that commercial cow milk and beef contain large amounts of estrogen
[ 47 ]. Indeed, consumption of these products accounts for approximately 60-80 %
of the estrogen hormone in adult western diets [ 55 ]. Even though the estrogen
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