Central resistin enhances renal sympathetic nerve activity via phosphatidylinositol 3-kinase but reduces the activity to brown adipose tissue via extracellular signal-regulated kinase 1/2

S Kosari, J A Rathner, Emilio Badoer

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20 Citations (Scopus)

Abstract

Resistin is an adipokine, originally identified in adipose tissue, and its plasma levels are elevated in obesity. Characteristics of obesity include impaired metabolic regulation and cardiovascular dysfunction, such as increased sympathetic nerve activity (SNA) to the kidney and skeletal muscle vasculature. Resistin can affect energy homeostasis through central mechanisms that include reduced food intake and reduced thermogenesis, and can also increase lumbar SNA via a central action. The present study investigated: (i) the effect of centrally-administered resistin on SNA targeting the kidney and (ii) the intracellular signalling pathways mediating the changes in SNA innervating the kidney and brown adipose tissue (BAT) induced by resistin. Intracerebroventricular resistin (7 μg) injected into overnight fasted, anaesthetised rats induced a significant increase in renal SNA by approximately 40%. This response was prevented when phosphatidylinositol 3-kinase (PI3K) was inhibited by i.c.v. administration of LY294002 (5 μg). Resistin reduced BAT SNA and this response was delayed by 150 min when extracellular-regulated kinase (ERK)1/2 was inhibited by i.c.v. administration of U0126. The findings indicate that resistin increases renal SNA via PI3K and reduces BAT SNA via ERK1/2.

Original languageEnglish
Pages (from-to)1432-1439
Number of pages8
JournalJournal of Neuroendocrinology
Volume24
Issue number11
DOIs
Publication statusPublished - Nov 2012
Externally publishedYes

Fingerprint

Phosphatidylinositol 3-Kinase
Resistin
Brown Adipose Tissue
Mitogen-Activated Protein Kinase 3
Mitogen-Activated Protein Kinase 1
Kidney
Obesity
2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one
Adipokines
Thermogenesis
Adipose Tissue
Skeletal Muscle
Homeostasis
Phosphotransferases
Eating

Cite this

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title = "Central resistin enhances renal sympathetic nerve activity via phosphatidylinositol 3-kinase but reduces the activity to brown adipose tissue via extracellular signal-regulated kinase 1/2",
abstract = "Resistin is an adipokine, originally identified in adipose tissue, and its plasma levels are elevated in obesity. Characteristics of obesity include impaired metabolic regulation and cardiovascular dysfunction, such as increased sympathetic nerve activity (SNA) to the kidney and skeletal muscle vasculature. Resistin can affect energy homeostasis through central mechanisms that include reduced food intake and reduced thermogenesis, and can also increase lumbar SNA via a central action. The present study investigated: (i) the effect of centrally-administered resistin on SNA targeting the kidney and (ii) the intracellular signalling pathways mediating the changes in SNA innervating the kidney and brown adipose tissue (BAT) induced by resistin. Intracerebroventricular resistin (7 μg) injected into overnight fasted, anaesthetised rats induced a significant increase in renal SNA by approximately 40{\%}. This response was prevented when phosphatidylinositol 3-kinase (PI3K) was inhibited by i.c.v. administration of LY294002 (5 μg). Resistin reduced BAT SNA and this response was delayed by 150 min when extracellular-regulated kinase (ERK)1/2 was inhibited by i.c.v. administration of U0126. The findings indicate that resistin increases renal SNA via PI3K and reduces BAT SNA via ERK1/2.",
keywords = "Adipose Tissue, Brown, Animals, Arterial Pressure, Down-Regulation, Heart Rate, Injections, Intraventricular, Kidney, MAP Kinase Signaling System, Male, Mitogen-Activated Protein Kinase 3, Phosphatidylinositol 3-Kinase, Rats, Rats, Sprague-Dawley, Resistin, Sympathetic Nervous System, Up-Regulation, Journal Article, Research Support, Non-U.S. Gov't",
author = "S Kosari and Rathner, {J A} and Emilio Badoer",
note = "{\circledC} 2012 The Authors. Journal of Neuroendocrinology {\circledC} 2012 British Society for Neuroendocrinology.",
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T1 - Central resistin enhances renal sympathetic nerve activity via phosphatidylinositol 3-kinase but reduces the activity to brown adipose tissue via extracellular signal-regulated kinase 1/2

AU - Kosari, S

AU - Rathner, J A

AU - Badoer, Emilio

N1 - © 2012 The Authors. Journal of Neuroendocrinology © 2012 British Society for Neuroendocrinology.

PY - 2012/11

Y1 - 2012/11

N2 - Resistin is an adipokine, originally identified in adipose tissue, and its plasma levels are elevated in obesity. Characteristics of obesity include impaired metabolic regulation and cardiovascular dysfunction, such as increased sympathetic nerve activity (SNA) to the kidney and skeletal muscle vasculature. Resistin can affect energy homeostasis through central mechanisms that include reduced food intake and reduced thermogenesis, and can also increase lumbar SNA via a central action. The present study investigated: (i) the effect of centrally-administered resistin on SNA targeting the kidney and (ii) the intracellular signalling pathways mediating the changes in SNA innervating the kidney and brown adipose tissue (BAT) induced by resistin. Intracerebroventricular resistin (7 μg) injected into overnight fasted, anaesthetised rats induced a significant increase in renal SNA by approximately 40%. This response was prevented when phosphatidylinositol 3-kinase (PI3K) was inhibited by i.c.v. administration of LY294002 (5 μg). Resistin reduced BAT SNA and this response was delayed by 150 min when extracellular-regulated kinase (ERK)1/2 was inhibited by i.c.v. administration of U0126. The findings indicate that resistin increases renal SNA via PI3K and reduces BAT SNA via ERK1/2.

AB - Resistin is an adipokine, originally identified in adipose tissue, and its plasma levels are elevated in obesity. Characteristics of obesity include impaired metabolic regulation and cardiovascular dysfunction, such as increased sympathetic nerve activity (SNA) to the kidney and skeletal muscle vasculature. Resistin can affect energy homeostasis through central mechanisms that include reduced food intake and reduced thermogenesis, and can also increase lumbar SNA via a central action. The present study investigated: (i) the effect of centrally-administered resistin on SNA targeting the kidney and (ii) the intracellular signalling pathways mediating the changes in SNA innervating the kidney and brown adipose tissue (BAT) induced by resistin. Intracerebroventricular resistin (7 μg) injected into overnight fasted, anaesthetised rats induced a significant increase in renal SNA by approximately 40%. This response was prevented when phosphatidylinositol 3-kinase (PI3K) was inhibited by i.c.v. administration of LY294002 (5 μg). Resistin reduced BAT SNA and this response was delayed by 150 min when extracellular-regulated kinase (ERK)1/2 was inhibited by i.c.v. administration of U0126. The findings indicate that resistin increases renal SNA via PI3K and reduces BAT SNA via ERK1/2.

KW - Adipose Tissue, Brown

KW - Animals

KW - Arterial Pressure

KW - Down-Regulation

KW - Heart Rate

KW - Injections, Intraventricular

KW - Kidney

KW - MAP Kinase Signaling System

KW - Male

KW - Mitogen-Activated Protein Kinase 3

KW - Phosphatidylinositol 3-Kinase

KW - Rats

KW - Rats, Sprague-Dawley

KW - Resistin

KW - Sympathetic Nervous System

KW - Up-Regulation

KW - Journal Article

KW - Research Support, Non-U.S. Gov't

U2 - 10.1111/j.1365-2826.2012.02352.x

DO - 10.1111/j.1365-2826.2012.02352.x

M3 - Article

VL - 24

SP - 1432

EP - 1439

JO - J. Neuroendocrinol.

JF - J. Neuroendocrinol.

SN - 0953-8194

IS - 11

ER -