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2015 ; 14
(ä): 110
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Hyperglycemia-induced downregulation of apolipoprotein M expression is not via
the hexosamine pathway
#MMPMID26377577
Jiang B
; Zhang X
; Di D
; Luo G
; Shi Y
; Zhang J
; Berggren-Söderlund M
; Nilsson-Ehle P
; Xu N
Lipids Health Dis
2015[Sep]; 14
(ä): 110
PMID26377577
show ga
BACKGROUND: We previously demonstrated that hyperglycemia could suppress
apolipoprotein M (apoM) synthesis both in vivo and in vitro; however, the
mechanism of hyperglycemia-induced downregulation of apoM expression is unknown
yet. METHODS: In the present study we further examined if hexosamine pathway, one
of the most important pathways of glucose turnover, being involved in modulating
apoM expression in the hyperglycemia condition. We examined the effect of
glucosamine, a prominent component of hexosamine pathway and intracellular
mediator of insulin resistance, on apoM expression in HepG2 cells and in rat's
models. In the present study we also determined apolipoprotein A1 (apoA1) as a
control gene. RESULTS: Our results demonstrated that glucosamine could even
up-regulate both apoM and apoA1 expressions in HepG2 cell cultures. The
glucosamine induced upregulation of apoM expression could be blocked by addition
of azaserine, an inhibitor of hexosamine pathway. Moreover, intravenous infusion
of glucosamine could enhance hepatic apoM expression in rats, although serum apoM
levels were not significantly influences. CONCLUSIONS: It is concluded that both
exogenous and endogenous glucosamine were essential for the over-expression of
apoM, which may suggest that the increased intracellular content of glucosamine
does not be responsible for the depressed apoM expression at hyperglycemia
condition.