Discoidal HDL and apoA-I-derived peptides improve glucose uptake in skeletal muscle

Dalla-Riva, Jonathan; Stenkula, Karin G.; Petrlová, Jitka; Lagerstedt, Jens O.

doi:10.1194/jlr.m032904

Cited by 50 publications

(56 citation statements)

References 37 publications

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“…Using L6 myotubes and myofi bers studied ex vivo, it has been found that the effect of reconstituted HDL on glucose uptake is comparable to that observed with insulin, and that it is associated with increased plasma membrane GLUT4 ( 93 ). ApoA-I/HDL also promotes glycogen synthesis in myocytes in association with increases in glycogen synthase kinase 3 (GKS3) phosphorylation ( 37 ).…”

Section: Skeletal Muscle Myocytesmentioning

confidence: 93%

Regulation of signal transduction by HDL

Mineo

Shaul

2013

Journal of Lipid Research

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which HDL serves to shuttle cholesterol from peripheral tissues or cells to the liver. This review highlights recent advances in our knowledge of HDL-initiated processes mediated by changes in intracellular signaling in numerous cell types of relevance to both cardiovascular and metabolic conditions, which represent actions of the lipoprotein beyond its classical role in global cholesterol homeostasis. The evidence that HDL infl uences cardiovascular and metabolic health and disease will fi rst be briefl y summarized. Responses to HDL or to apoA-I, its major apolipoprotein, in cellular targets directly involved in vascular biology will then be reviewed, followed by a summary of the mechanisms that HDL infl uences in cell types participating in energy and glucose homeostasis. The processes underlying apoA-I-or HDL-induced changes in intracellular signaling will then be discussed, and fi nally presently unanswered questions in this realm of HDL biology will be considered. Although HDL cargo molecules can contribute to cellular responses to the lipoprotein ( 1, 2 ), herein emphasis will be placed primarily on signaling events directly induced by apoA-I or HDL, which are likely occurring in response to cholesterol effl ux. To help leverage our present understanding of apoA-I-or HDL-initiated signaling in future studies, the signaling events and the proteins or mediators whose abundance or activity is altered by apoA-I or HDL in various cell types are summarized in Tables Abbreviations: AMPK, AMP-activated protein kinase; CaMKK, calcium/calmodulin-dependent protein kinase kinase; COX-2, cyclooxygenase type 2; DHCR24, 3 ␤ -hydroxysteriod-⌬ 24 reductase; eNOS, endothelial nitric-oxide synthase; EPC, endothelial progenitor cell; GKS3, glycogen synthase kinase 3; HO-1, heme oxygenase-1; ICAM-1, intercellular adhesion molecule-1; JAK2, Janus kinase 2; LKB1, liver kinase B1; MCP-1, monocyte chemoattractant protein-1; PKA, protein kinase A; PKC, protein kinase C; RCT, reverse cholesterol transport; ROS, reactive oxygen species; S1P, sphingosine-1-phosphate; SAA3, serum amyloid A3; SR-BI, scavenger receptor class B, type I; VCAM-1, vascular cell adhesion molecule-1; VSM, vascular smooth muscle.

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Section: Skeletal Muscle Myocytesmentioning

confidence: 93%

Regulation of signal transduction by HDL

Mineo

Shaul

2013

Journal of Lipid Research

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“…The rate of transport of [ While previous studies have suggested HDL can improve glucose transport via increasing cell surface GLUT4 levels [5,6], these studies were conducted in vitro and did not observe increased glucose transport with apoA-I treatment. HDL has previously been reported to increase GLUT4 translocation to the cell surface via SR-BI and Akt [6].…”

Section: Discussionmentioning

confidence: 99%

“…Therapeutic interventions that increase plasma HDL levels improve glycaemic control in patients with type 2 diabetes [2,3], and treatment with HDL or apoA-I has been shown to increase glucose uptake into skeletal muscle [4,5] and adipose tissue [6]. Furthermore, treatment with HDL or apoA-I increases insulin secretion and production in isolated pancreatic islets and insulinoma beta cell lines [7,8].…”

Section: Introductionmentioning

confidence: 99%

In vivo PET imaging with [18F]FDG to explain improved glucose uptake in an apolipoprotein A-I treated mouse model of diabetes

et al. 2016

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Aims/hypothesis Type 2 diabetes is characterised by decreased HDL levels, as well as the level of apolipoprotein A-I (apoA-I), the main apolipoprotein of HDLs. Pharmacological elevation of HDL and apoA-I levels is associated with improved glycaemic control in patients with type 2 diabetes. This is partly due to improved glucose uptake in skeletal muscle. Methods This study used kinetic modelling to investigate the impact of increasing plasma apoA-I levels on the metabolism of glucose in the db/db mouse model.

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“…HDLs and apoA-I also protect ␤ -cells from apoptosis in vitro ( 111 ), while treatment with the apoA-I mimetic peptide L-4F has been reported to decrease insulin resistance in obese mice ( 112 ). The C-terminal domain of apoA-I has also been shown to increase glucose uptake in vitro into cultured L6 skeletal muscle myotubes ( 113 ). These fi ndings are consistent with reports of mice deficient in apoA-I and apoA-II having compromised glycemic control ( 62,114 ) and mice overexpressing apoA-I having improved insulin sensitivity ( 115 ).…”

Section: Effects Of Specifi C Hdl Constituents and Subpopulations In mentioning

confidence: 99%

Cardioprotective functions of HDLs

Rye

Barter

2014

Journal of Lipid Research

249

170

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This article is available online at http://www.jlr.org inverse predictors of the risk of having a cardiovascular event ( 1-5 ); moreover, a low concentration of HDL cholesterol remains predictive of increased cardiovascular risk, even when low density lipoprotein (LDL) cholesterol has been reduced to very low levels by treatment with statins ( 6 ); ii ) HDLs have several well-documented functions with the potential to protect against cardiovascular disease ( 7,8 ); iii ) interventions that increase the concentration of HDLs inhibit the development and progression of atherosclerosis in several animal models ( 9-12 ); and iv ) in "proofof-concept" studies in humans, intravenous infusions of reconstituted HDLs (rHDLs) consisting of apoA-I complexed with phospholipids promote regression of coronary atheroma as assessed by intravascular ultrasound ( 13,14 ).However, interventions that increase the concentration of HDL cholesterol in humans have not yet been shown to translate into a reduction in clinical cardiovascular events. Indeed, recent human clinical trials investigating the effects of raising the level of HDL cholesterol by treatment with cholesteryl ester transfer protein (CETP) inhibitors or with niacin failed to demonstrate any clinical cardiovascular benefi t ( 15-17 ) (http://www.thrivestudy. org), and in one case, the treatment caused harm ( 15 ). A reasonable assumption that has been made from these studies is that the cholesterol content of HDLs is not the factor that protects. Thus, if HDLs do have direct cardioprotective properties, it follows from the human population studies that, while the concentration of HDL cholesterol is generally an excellent marker of the HDL functions that do protect, it does not invariably refl ect their cardioprotective functions. This is consistent with the fi nding in a recent Mendelian randomization study that some genetic mechanisms that raise the concentration of HDL cholesterol appear not to lower the risk of myocardial infarction ( 18 ). The authors of this analysis concluded that, while The proposition that high density lipoproteins (HDLs) protect against the development of cardiovascular diseases is based on a number of robust and consistent observations: i ) numerous human population studies have shown that the plasma concentrations of both HDL cholesterol and the major HDL apolipoprotein, apoA-I, are independent, Abbreviations: CETP, cholesteryl ester transfer protein; HO-1, heme oxygenase-1; PON-1, paraoxonase-1; rHDL, reconstituted HDL; SR-B1, scavenger receptor-B1; VCAM-1, vascular cell adhesion molecule-1.

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Discoidal HDL and apoA-I-derived peptides improve glucose uptake in skeletal muscle

Cited by 50 publications

References 37 publications

Regulation of signal transduction by HDL

Regulation of signal transduction by HDL

In vivo PET imaging with [18F]FDG to explain improved glucose uptake in an apolipoprotein A-I treated mouse model of diabetes

Cardioprotective functions of HDLs

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