PMID- 26582989
OWN - NLM
STAT- PubMed-not-MEDLINE
DCOM- 20151120
LR  - 20200930
IS  - 1663-9812 (Print)
IS  - 1663-9812 (Electronic)
IS  - 1663-9812 (Linking)
VI  - 6
DP  - 2015
TI  - HDL and glucose metabolism: current evidence and therapeutic potential.
PG  - 258
LID - 10.3389/fphar.2015.00258 [doi]
LID - 258
AB  - High-density lipoprotein (HDL) and its principal apolipoprotein A-I (ApoA-I) have 
      now been convincingly shown to influence glucose metabolism through multiple 
      mechanisms. The key clinically relevant observations are that both acute HDL 
      elevation via short-term reconstituted HDL (rHDL) infusion and chronically 
      raising HDL via a cholesteryl ester transfer protein (CETP) inhibitor reduce 
      blood glucose in individuals with type 2 diabetes mellitus (T2DM). HDL may 
      mediate effects on glucose metabolism through actions in multiple organs (e.g., 
      pancreas, skeletal muscle, heart, adipose, liver, brain) by three distinct 
      mechanisms: (i) Insulin secretion from pancreatic beta cells, (ii) 
      Insulin-independent glucose uptake, (iii) Insulin sensitivity. The molecular 
      mechanisms appear to involve both direct HDL signaling actions as well as effects 
      secondary to lipid removal from cells. The implications of glucoregulatory 
      mechanisms linked to HDL extend from glycemic control to potential anti-ischemic 
      actions via increased tissue glucose uptake and utilization. Such effects not 
      only have implications for the prevention and management of diabetes, but also 
      for ischemic vascular diseases including angina pectoris, intermittent 
      claudication, cerebral ischemia and even some forms of dementia. This review will 
      discuss the growing evidence for a role of HDL in glucose metabolism and outline 
      related potential for HDL therapies.
FAU - Siebel, Andrew L
AU  - Siebel AL
AD  - Metabolic and Vascular Physiology Laboratory, Baker IDI Heart and Diabetes 
      Institute , Melbourne, VIC, Australia.
FAU - Heywood, Sarah Elizabeth
AU  - Heywood SE
AD  - Metabolic and Vascular Physiology Laboratory, Baker IDI Heart and Diabetes 
      Institute , Melbourne, VIC, Australia.
FAU - Kingwell, Bronwyn A
AU  - Kingwell BA
AD  - Metabolic and Vascular Physiology Laboratory, Baker IDI Heart and Diabetes 
      Institute , Melbourne, VIC, Australia.
LA  - eng
PT  - Journal Article
PT  - Review
DEP - 20151031
PL  - Switzerland
TA  - Front Pharmacol
JT  - Frontiers in pharmacology
JID - 101548923
PMC - PMC4628107
OTO - NOTNLM
OT  - HDL
OT  - apolipoprotein A-I
OT  - cholesterol efflux
OT  - glucose metabolism
OT  - glucose uptake
OT  - insulin secretion
OT  - insulin sensitivity
EDAT- 2015/11/20 06:00
MHDA- 2015/11/20 06:01
PMCR- 2015/10/31
CRDT- 2015/11/20 06:00
PHST- 2015/08/10 00:00 [received]
PHST- 2015/10/19 00:00 [accepted]
PHST- 2015/11/20 06:00 [entrez]
PHST- 2015/11/20 06:00 [pubmed]
PHST- 2015/11/20 06:01 [medline]
PHST- 2015/10/31 00:00 [pmc-release]
AID - 10.3389/fphar.2015.00258 [doi]
PST - epublish
SO  - Front Pharmacol. 2015 Oct 31;6:258. doi: 10.3389/fphar.2015.00258. eCollection 
      2015.