TNF- inhibits insulin action in liver and adipose tissue

A model of metabolic syndrome

S. S. Solomon, O. Odunusi, D. Carrigan, G. Majumdar, D. Kakoola, N. I. Lenchik, Ivan Gerling

Research output: Contribution to journalArticle

27 Citations (Scopus)

Abstract

Several studies suggest that TNF- contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-α. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-α. Twenty-six of these 33 genes created a single network centered around: insulin, TNF-α, p38-MAPK, TGFb1; SMAD and STAT1; and enzymes and cytokines involved in apoptosis (CASP3, GADD45B, IL2, TNF-α, etc.). We analyzed our data together with other data of gene expression in adipocytes and found a number of processes common to both, for example, cell death and inflammation; intercellular signaling and metabolism; G-Protein, IL-10 and PTEN signaling. Moreover, the two datasets combined generated a single molecular network that further identified PTEN (a phosphatase) as a unique new link between insulin signaling, IR, and apoptosis reflecting the pathophysiology of metabolic syndrome.

Original languageEnglish (US)
Pages (from-to)115-121
Number of pages7
JournalHormone and Metabolic Research
Volume42
Issue number2
DOIs
StatePublished - Feb 12 2010

Fingerprint

Liver
Adipose Tissue
Insulin
Tissue
Insulin Resistance
PTEN Phosphohydrolase
Apoptosis
Gene Expression
Gene expression
p38 Mitogen-Activated Protein Kinases
GTP-Binding Proteins
Adipocytes
Caspase 3
Interleukin-10
Interleukin-2
Cell Death
Cell death
Cytokines
Inflammation
Phosphoric Monoester Hydrolases

All Science Journal Classification (ASJC) codes

  • Endocrinology, Diabetes and Metabolism
  • Biochemistry
  • Endocrinology
  • Clinical Biochemistry
  • Biochemistry, medical

Cite this

TNF- inhibits insulin action in liver and adipose tissue : A model of metabolic syndrome. / Solomon, S. S.; Odunusi, O.; Carrigan, D.; Majumdar, G.; Kakoola, D.; Lenchik, N. I.; Gerling, Ivan.

In: Hormone and Metabolic Research, Vol. 42, No. 2, 12.02.2010, p. 115-121.

Research output: Contribution to journalArticle

Solomon, SS, Odunusi, O, Carrigan, D, Majumdar, G, Kakoola, D, Lenchik, NI & Gerling, I 2010, 'TNF- inhibits insulin action in liver and adipose tissue: A model of metabolic syndrome', Hormone and Metabolic Research, vol. 42, no. 2, pp. 115-121. https://doi.org/10.1055/s-0029-1241834
Solomon SS, Odunusi O, Carrigan D, Majumdar G, Kakoola D, Lenchik NI et al. TNF- inhibits insulin action in liver and adipose tissue: A model of metabolic syndrome. Hormone and Metabolic Research. 2010 Feb 12;42(2):115-121. https://doi.org/10.1055/s-0029-1241834
Solomon, S. S. ; Odunusi, O. ; Carrigan, D. ; Majumdar, G. ; Kakoola, D. ; Lenchik, N. I. ; Gerling, Ivan. / TNF- inhibits insulin action in liver and adipose tissue : A model of metabolic syndrome. In: Hormone and Metabolic Research. 2010 ; Vol. 42, No. 2. pp. 115-121.
@article{a66f12333a0e49f089e6a273d69cd9f8,
title = "TNF- inhibits insulin action in liver and adipose tissue: A model of metabolic syndrome",
abstract = "Several studies suggest that TNF- contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-α. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-α. Twenty-six of these 33 genes created a single network centered around: insulin, TNF-α, p38-MAPK, TGFb1; SMAD and STAT1; and enzymes and cytokines involved in apoptosis (CASP3, GADD45B, IL2, TNF-α, etc.). We analyzed our data together with other data of gene expression in adipocytes and found a number of processes common to both, for example, cell death and inflammation; intercellular signaling and metabolism; G-Protein, IL-10 and PTEN signaling. Moreover, the two datasets combined generated a single molecular network that further identified PTEN (a phosphatase) as a unique new link between insulin signaling, IR, and apoptosis reflecting the pathophysiology of metabolic syndrome.",
author = "Solomon, {S. S.} and O. Odunusi and D. Carrigan and G. Majumdar and D. Kakoola and Lenchik, {N. I.} and Ivan Gerling",
year = "2010",
month = "2",
day = "12",
doi = "10.1055/s-0029-1241834",
language = "English (US)",
volume = "42",
pages = "115--121",
journal = "Hormone and Metabolic Research",
issn = "0018-5043",
publisher = "Georg Thieme Verlag",
number = "2",

}

TY - JOUR

T1 - TNF- inhibits insulin action in liver and adipose tissue

T2 - A model of metabolic syndrome

AU - Solomon, S. S.

AU - Odunusi, O.

AU - Carrigan, D.

AU - Majumdar, G.

AU - Kakoola, D.

AU - Lenchik, N. I.

AU - Gerling, Ivan

PY - 2010/2/12

Y1 - 2010/2/12

N2 - Several studies suggest that TNF- contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-α. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-α. Twenty-six of these 33 genes created a single network centered around: insulin, TNF-α, p38-MAPK, TGFb1; SMAD and STAT1; and enzymes and cytokines involved in apoptosis (CASP3, GADD45B, IL2, TNF-α, etc.). We analyzed our data together with other data of gene expression in adipocytes and found a number of processes common to both, for example, cell death and inflammation; intercellular signaling and metabolism; G-Protein, IL-10 and PTEN signaling. Moreover, the two datasets combined generated a single molecular network that further identified PTEN (a phosphatase) as a unique new link between insulin signaling, IR, and apoptosis reflecting the pathophysiology of metabolic syndrome.

AB - Several studies suggest that TNF- contributes to the development of insulin resistance (IR). We compared transcriptional profiles of rat H-411E liver cells exposed to insulin in the absence or presence of TNF-α. We identified 33 genes whose expression was altered by insulin, and then reversed by TNF-α. Twenty-six of these 33 genes created a single network centered around: insulin, TNF-α, p38-MAPK, TGFb1; SMAD and STAT1; and enzymes and cytokines involved in apoptosis (CASP3, GADD45B, IL2, TNF-α, etc.). We analyzed our data together with other data of gene expression in adipocytes and found a number of processes common to both, for example, cell death and inflammation; intercellular signaling and metabolism; G-Protein, IL-10 and PTEN signaling. Moreover, the two datasets combined generated a single molecular network that further identified PTEN (a phosphatase) as a unique new link between insulin signaling, IR, and apoptosis reflecting the pathophysiology of metabolic syndrome.

UR - http://www.scopus.com/inward/record.url?scp=76149109500&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=76149109500&partnerID=8YFLogxK

U2 - 10.1055/s-0029-1241834

DO - 10.1055/s-0029-1241834

M3 - Article

VL - 42

SP - 115

EP - 121

JO - Hormone and Metabolic Research

JF - Hormone and Metabolic Research

SN - 0018-5043

IS - 2

ER -