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In these age groups, CVD mortality increased significantly for the first time in over 2 decades.
It is characterised by accumulation of fat in the central part of the body and correlates with insulin resistance IR.
Visceral adipocytes are large, insulin-resistant and highly active metabolically. Through the production of a variety of adipokines, adipocytes play a role in the pathogenesis of inflammation, dyslipidaemia and hypertension.
In these disorders, the phenotype of dyslipidaemia is highly atherogenic. IR appears to play an important role in the pathogenesis of this type of dyslipidaemia.
IR is associated with enhanced lipolysis as well as reduced FFA uptake and esterification leading to an increased flux of FFA into non-adipose tissues, including the liver and muscle.
Since FFA compete with glucose for cellular uptake and metabolism, they can further reduce insulin sensitivity, instituting a vicious cycle.
Excessive visceral adiposity increases the availability of FFA through the hydrolysis of adipocyte TG by a variety of lipases, including triglyceride lipase, lipoprotein lipase LpL, hormone-sensitive lipase and endothelial lipase.
Such increases in circulating FFA lead to TG accumulation in muscle and liver fatty liver and raise circulating TG levels due to enhanced hepatic production of very low density lipoprotein VLDL cholesterol.
When influx of FFA to the liver exceeds efflux, there is increased hepatic FFA uptake, synthesis and secretion that can lead to hepatic steatosis, which in turn exacerbates IR, giving rise to a new vicious cycle.
In addition, overloading of the white adipose tissue WAT beyond its storage capacity can also adversely affect skeletal and cardiac muscle, liver as well as pancreatic function.
Cholesteryl ester transfer protein CETP is secreted by the adipose tissue and is an important determinant of lipoprotein composition because it mediates the transfer of cholesteryl esters CE from CE-rich lipoproteins to TG-rich lipoproteins in exchange for TG.
In obese patients, CETP activity and mass are increased.
Several studies showed that hepatic apoB secretion is metabolically regulated. The apoB gene is constitutively expressed and in most cases the modulation of apoB production does not involve changes in apoB mRNA levels.Dommedagsprofetiene forskyves i takt med tiden.
These observations suggest that post-translational mechanisms play a role in the regulation of apoB levels, including endoplasmic reticulum translocation and protein degradation. Thus, reduced apoB degradation might be the main contributor to the increase in plasma apoB levels.
On the other hand, hepatic IR can lead to increased availability of apoB and might predispose to higher rates of hepatic VLDL assembly and secretion, the key steps in the development of metabolic dyslipidaemia. Problema 2 02.
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