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. 2011 Mar 8;7(1):8–20. doi: 10.5114/aoms.2011.20598

Figure 1.

Figure 1

Block diagram of proposed sequence of events leading to MetS. (1) Serum LDL (L) becomes glycated due to exposure to glucose and fructose. (2) Adipocytes depend upon apoE (E) to scavenge glycated LDL-C and transport it into HDL-A1 (H). (3) ApoE becomes damaged and adipocytes accumulate lipid droplets (F) and excess cholesterol (C) in their endoplasmic reticulum (ER). Meanwhile, plasma membrane becomes cholesterol-depleted. Stressed adipocytes release angiotensin-II (AT-II) which leads to sodium-hoarding and hypertension. (4) Macrophages enter adipose tissue to engulf cell debris from accumulating dead adipocytes, forming multi-nucleated giant cells. (5) Due to insufficient HDL-C, fatty deposits accumulate ectopically to buffer cholesterol supplies to the major organs