Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells

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Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells. / Kappe, Camilla; Holst, Jens Juul; Zhang, Qimin; Sjöholm, Ake.

In: Biochemical and Biophysical Research Communications, Vol. 427, No. 1, 12.10.2012, p. 91-5.

Research output: Contribution to journal › Journal article › Research › peer-review

Harvard

Kappe, C, Holst, JJ, Zhang, Q & Sjöholm, A 2012, 'Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells', Biochemical and Biophysical Research Communications, vol. 427, no. 1, pp. 91-5. https://doi.org/10.1016/j.bbrc.2012.09.010

APA

Kappe, C., Holst, J. J., Zhang, Q., & Sjöholm, A. (2012). Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells. Biochemical and Biophysical Research Communications, 427(1), 91-5. https://doi.org/10.1016/j.bbrc.2012.09.010

Vancouver

Kappe C, Holst JJ, Zhang Q, Sjöholm A. Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells. Biochemical and Biophysical Research Communications. 2012 Oct 12;427(1):91-5. https://doi.org/10.1016/j.bbrc.2012.09.010

Author

Kappe, Camilla ; Holst, Jens Juul ; Zhang, Qimin ; Sjöholm, Ake. / Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells. In: Biochemical and Biophysical Research Communications. 2012 ; Vol. 427, No. 1. pp. 91-5.

Bibtex

@article{f2a0f784406c4a39b0252f9d00fab722,

title = "Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells",

abstract = "Evidence is emerging that elevated serum free fatty acids (hyperlipidemia) contribute to the pathogenesis of type-2-diabetes, and lipotoxicity is observed in many cell types. We recently published data indicating lipotoxic effects of simulated hyperlipidemia also in GLP-1-secreting cells, where the antidiabetic drug metformin conferred protection from lipoapoptosis. The aim of the present study was to identify mechanisms involved in mediating lipotoxicity and metformin lipoprotection in GLP-1 secreting cells. These signaling events triggered by simulated hyperlipidemia may underlie reduced GLP-1 secretion in diabetic subjects, and metformin lipoprotection by metformin could explain elevated plasma GLP-1 levels in diabetic patients on chronic metformin therapy. The present study may thus identify potential molecular targets for increasing endogenous GLP-1 secretion through enhanced viability of GLP-1 secreting cells in diabetic hyperlipidemia and obesity.",

keywords = "Animals, Antioxidants, Apoptosis, Caspase 3, Cell Line, Chromans, Cytoprotection, Fatty Acids, Nonesterified, Glucagon-Like Peptide 1, Hyperlipidemias, Hypoglycemic Agents, MAP Kinase Kinase 3, MAP Kinase Kinase 4, MAP Kinase Kinase 6, Metformin, Mice, Mice, Transgenic, Palmitates, Reactive Oxygen Species, p38 Mitogen-Activated Protein Kinases",

author = "Camilla Kappe and Holst, {Jens Juul} and Qimin Zhang and Ake Sj{\"o}holm",

year = "2012",

month = oct,

day = "12",

doi = "10.1016/j.bbrc.2012.09.010",

language = "English",

volume = "427",

pages = "91--5",

journal = "Biochemical and Biophysical Research Communications",

issn = "0006-291X",

publisher = "Elsevier",

number = "1",

}

RIS

TY - JOUR

T1 - Molecular mechanisms of lipoapoptosis and metformin protection in GLP-1 secreting cells

AU - Kappe, Camilla

AU - Holst, Jens Juul

AU - Zhang, Qimin

AU - Sjöholm, Ake

PY - 2012/10/12

Y1 - 2012/10/12

N2 - Evidence is emerging that elevated serum free fatty acids (hyperlipidemia) contribute to the pathogenesis of type-2-diabetes, and lipotoxicity is observed in many cell types. We recently published data indicating lipotoxic effects of simulated hyperlipidemia also in GLP-1-secreting cells, where the antidiabetic drug metformin conferred protection from lipoapoptosis. The aim of the present study was to identify mechanisms involved in mediating lipotoxicity and metformin lipoprotection in GLP-1 secreting cells. These signaling events triggered by simulated hyperlipidemia may underlie reduced GLP-1 secretion in diabetic subjects, and metformin lipoprotection by metformin could explain elevated plasma GLP-1 levels in diabetic patients on chronic metformin therapy. The present study may thus identify potential molecular targets for increasing endogenous GLP-1 secretion through enhanced viability of GLP-1 secreting cells in diabetic hyperlipidemia and obesity.

AB - Evidence is emerging that elevated serum free fatty acids (hyperlipidemia) contribute to the pathogenesis of type-2-diabetes, and lipotoxicity is observed in many cell types. We recently published data indicating lipotoxic effects of simulated hyperlipidemia also in GLP-1-secreting cells, where the antidiabetic drug metformin conferred protection from lipoapoptosis. The aim of the present study was to identify mechanisms involved in mediating lipotoxicity and metformin lipoprotection in GLP-1 secreting cells. These signaling events triggered by simulated hyperlipidemia may underlie reduced GLP-1 secretion in diabetic subjects, and metformin lipoprotection by metformin could explain elevated plasma GLP-1 levels in diabetic patients on chronic metformin therapy. The present study may thus identify potential molecular targets for increasing endogenous GLP-1 secretion through enhanced viability of GLP-1 secreting cells in diabetic hyperlipidemia and obesity.

KW - Animals

KW - Antioxidants

KW - Apoptosis

KW - Caspase 3

KW - Cell Line

KW - Chromans

KW - Cytoprotection

KW - Fatty Acids, Nonesterified

KW - Glucagon-Like Peptide 1

KW - Hyperlipidemias

KW - Hypoglycemic Agents

KW - MAP Kinase Kinase 3

KW - MAP Kinase Kinase 4

KW - MAP Kinase Kinase 6

KW - Metformin

KW - Mice

KW - Mice, Transgenic

KW - Palmitates

KW - Reactive Oxygen Species

KW - p38 Mitogen-Activated Protein Kinases

U2 - 10.1016/j.bbrc.2012.09.010

DO - 10.1016/j.bbrc.2012.09.010

M3 - Journal article

C2 - 22982676

VL - 427

SP - 91

EP - 95

JO - Biochemical and Biophysical Research Communications

JF - Biochemical and Biophysical Research Communications

SN - 0006-291X

IS - 1

ER -

ID: 45840730