LDL but not HDL increases adiponectin release of primary human adipocytes

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• 作者：Sabrina Krautbauer ; Markus Neumeier ; Kristina Eisinger ; Yvonne Hader ; Ashraf Dada ; Gerd Schmitz ; Charalampos Aslanidis ; Christa Buechler
• 关键词：Lipoprotein ; LDL apheresis ; Familial hypobetalipoproteinemia
• 刊名：Experimental and Molecular Pathology
• 出版年：December, 2013
• 年：2013
• 卷：95
• 期：3
• 页码：325-329
• 全文大小：441 K

文摘

Adipocytes in obesity have inappropriately low cholesterol while adiponectin release is reduced. Cholesterol shortage may contribute to low adiponectin and 3T3-L1 cells treated with lovastatin have diminished adiponectin in cell supernatants. LDL and HDL deliver cholesterol to adipocytes. LDL but not HDL increases adiponectin in cell supernatants of primary human adipocytes. The effect of LDL is not blocked by receptor associated protein suggesting that members of the LDL-receptor family are not involved. To evaluate whether these in vitro observations translate into changes in systemic adiponectin, adiponectin was measured in serum of three patients before, immediately after and 3 d after LDL-apheresis. Whereas circulating lipoproteins are reduced immediately after apheresis adiponectin is not changed. Therefore, acute lowering of lipoproteins does not affect systemic adiponectin also excluding that plenty of adiponectin is bound to lipoprotein particles. Accordingly, levels of adiponectin in purified lipoproteins are quite low. Familial hypobetalipoproteinemia (FHBL) is a rare disorder associated with low plasma LDL. Serum adiponectin is, however, similar compared to healthy controls. Thus, neither LDL nor HDL directly contributes to circulating adiponectin concentrations.