Effects of leptin and adiponectin on pancreatic β-cell function

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Effects of leptin and adiponectin on pancreatic β-cell function. / Lee, Yong-ho; Magkos, Faidon; Mantzoros, Christos S; Kang, Eun Seok.

In: Metabolism, Vol. 60, No. 12, 2011, p. 1664-1672.

Research output: Contribution to journalReviewResearchpeer-review

Harvard

Lee, Y, Magkos, F, Mantzoros, CS & Kang, ES 2011, 'Effects of leptin and adiponectin on pancreatic β-cell function', Metabolism, vol. 60, no. 12, pp. 1664-1672. https://doi.org/10.1016/j.metabol.2011.04.008

APA

Lee, Y., Magkos, F., Mantzoros, C. S., & Kang, E. S. (2011). Effects of leptin and adiponectin on pancreatic β-cell function. Metabolism, 60(12), 1664-1672. https://doi.org/10.1016/j.metabol.2011.04.008

Vancouver

Lee Y, Magkos F, Mantzoros CS, Kang ES. Effects of leptin and adiponectin on pancreatic β-cell function. Metabolism. 2011;60(12):1664-1672. https://doi.org/10.1016/j.metabol.2011.04.008

Author

Lee, Yong-ho ; Magkos, Faidon ; Mantzoros, Christos S ; Kang, Eun Seok. / Effects of leptin and adiponectin on pancreatic β-cell function. In: Metabolism. 2011 ; Vol. 60, No. 12. pp. 1664-1672.

Bibtex

@article{9f8306b39c084bd2b19ca6b50e18fa58,
title = "Effects of leptin and adiponectin on pancreatic β-cell function",
abstract = "Leptin and adiponectin are hormones secreted from adipocytes that have important roles in metabolism and energy homeostasis. This review evaluates the effects of leptin and adiponectin on β-cell function by analyzing and compiling results from human clinical trials and epidemiologic studies as well as in vitro and in vivo experiments. Leptin has been shown to inhibit ectopic fat accumulation and thereby prevent β-cell dysfunction and protect the β-cell from cytokine- and fatty acid-induced apoptosis. However, leptin suppresses insulin gene expression and secretion as well as glucose transport into the β-cell. Adiponectin stimulates insulin secretion by enhancing exocytosis of insulin granules and upregulating the expression of the insulin gene; however, this effect depends on the prevailing glucose concentration and status of insulin resistance. In addition, adiponectin has antiapoptotic properties in β-cells. Available evidence concerning the role of these adipokines on insulin secretion, insulin gene expression, and apoptosis is not always entirely consistent; and many fundamental questions remain to be answered by future studies.",
keywords = "Adiponectin/metabolism, Animals, Apoptosis/drug effects, Clinical Trials as Topic, Epidemiologic Studies, Gene Expression Regulation/drug effects, Humans, Insulin/metabolism, Insulin Resistance, Insulin Secretion, Insulin-Secreting Cells/drug effects, Leptin/metabolism",
author = "Yong-ho Lee and Faidon Magkos and Mantzoros, {Christos S} and Kang, {Eun Seok}",
note = "Copyright {\textcopyright} 2011 Elsevier Inc. All rights reserved.",
year = "2011",
doi = "10.1016/j.metabol.2011.04.008",
language = "English",
volume = "60",
pages = "1664--1672",
journal = "Metabolism",
issn = "0026-0495",
publisher = "Elsevier",
number = "12",

}

RIS

TY - JOUR

T1 - Effects of leptin and adiponectin on pancreatic β-cell function

AU - Lee, Yong-ho

AU - Magkos, Faidon

AU - Mantzoros, Christos S

AU - Kang, Eun Seok

N1 - Copyright © 2011 Elsevier Inc. All rights reserved.

PY - 2011

Y1 - 2011

N2 - Leptin and adiponectin are hormones secreted from adipocytes that have important roles in metabolism and energy homeostasis. This review evaluates the effects of leptin and adiponectin on β-cell function by analyzing and compiling results from human clinical trials and epidemiologic studies as well as in vitro and in vivo experiments. Leptin has been shown to inhibit ectopic fat accumulation and thereby prevent β-cell dysfunction and protect the β-cell from cytokine- and fatty acid-induced apoptosis. However, leptin suppresses insulin gene expression and secretion as well as glucose transport into the β-cell. Adiponectin stimulates insulin secretion by enhancing exocytosis of insulin granules and upregulating the expression of the insulin gene; however, this effect depends on the prevailing glucose concentration and status of insulin resistance. In addition, adiponectin has antiapoptotic properties in β-cells. Available evidence concerning the role of these adipokines on insulin secretion, insulin gene expression, and apoptosis is not always entirely consistent; and many fundamental questions remain to be answered by future studies.

AB - Leptin and adiponectin are hormones secreted from adipocytes that have important roles in metabolism and energy homeostasis. This review evaluates the effects of leptin and adiponectin on β-cell function by analyzing and compiling results from human clinical trials and epidemiologic studies as well as in vitro and in vivo experiments. Leptin has been shown to inhibit ectopic fat accumulation and thereby prevent β-cell dysfunction and protect the β-cell from cytokine- and fatty acid-induced apoptosis. However, leptin suppresses insulin gene expression and secretion as well as glucose transport into the β-cell. Adiponectin stimulates insulin secretion by enhancing exocytosis of insulin granules and upregulating the expression of the insulin gene; however, this effect depends on the prevailing glucose concentration and status of insulin resistance. In addition, adiponectin has antiapoptotic properties in β-cells. Available evidence concerning the role of these adipokines on insulin secretion, insulin gene expression, and apoptosis is not always entirely consistent; and many fundamental questions remain to be answered by future studies.

KW - Adiponectin/metabolism

KW - Animals

KW - Apoptosis/drug effects

KW - Clinical Trials as Topic

KW - Epidemiologic Studies

KW - Gene Expression Regulation/drug effects

KW - Humans

KW - Insulin/metabolism

KW - Insulin Resistance

KW - Insulin Secretion

KW - Insulin-Secreting Cells/drug effects

KW - Leptin/metabolism

U2 - 10.1016/j.metabol.2011.04.008

DO - 10.1016/j.metabol.2011.04.008

M3 - Review

C2 - 21632069

VL - 60

SP - 1664

EP - 1672

JO - Metabolism

JF - Metabolism

SN - 0026-0495

IS - 12

ER -

ID: 290039407