Tumor necrosis factor system in insulin resistance in gestational diabetes

G. Winkler, K. Cseh, Éva Baranyi, Zsolt Melczer, G. Speer, Péter Hajós, Ferenc Salamon, Zsuzsa Turi, M. Kovács, P. Vargha, I. Karádi

Research output: Contribution to journalArticle

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Abstract

Objective: The aim of the study was to investigate the pathophysiological role of the tumor necrosis factor (TNF) system in insulin resistance in patients with gestational diabetes (GDM) and during the course of normal pregnancy. Patients and methods: Thirty women with GDM (16-39 gestational weeks), 35 healthy pregnant women (15 first, nine second and 11 third trimester) and 25 healthy age-matched non-pregnant women were studied. Serum TNF-α, and its soluble receptors 1 and 2 (sTNFR-1 and -2) were measured. Results: In non-diabetic pregnant women in the third trimester all measures were significantly higher (P <0.05 or less) than in the first trimester and in non-pregnant women (BMI 27.6 ± 4.1 ( ± S.D.), 24.1 ± 2.6, 22.4 ± 2.4 kg/m2), serum TNF-α (4.6 ± 0.6, 4.1 ± 0.4, 4.1 ± 0.4 ng/l), sTNFR-1 (2.7 ± 0.9, 2.0 ± 0.5, 2.0 ± 0.1 μg/l), sTNFR-2 (5.6 ± 2.6, 4.6 ± 2.1, 3.3 ± 0.2 μg/l), C-peptide (3.1 ± 1.7, 1.1 ± 0.7, 1.1 ± 0.8 μg/l), and C-peptide:blood glucose ratio (0.6 ± 0.2, 0.2 ± 0.1, 0.2 ± 0.1 μg/mmol). In GDM these measures were even higher than in any subgroup of healthy pregnant women (BMI) (33.4 ± 6.4 kg/m2, TNF-α) (6.3 ± 0.6 μg/l), sTNFR-1 (3.0 ± 0.5 μg/l), sTNFR-2 (10.0 ± 6.9 μg/l, C-peptide 6.0 ± 2.7 μg/l, C-peptide:blood glucose ratio: 1.2 ± 0.5 μg/mmol, P <0.01). Significant (P <0.01) positive linear correlations were found in gestational diabetic and non-diabetic women between serum TNF-α, C-peptide levels, and BMI. In gestational diabetic women, in multivariate analysis studying the dependency of C-peptide only BMI remained significant (r2 = 0.67, P = 0.01). Conclusions: Our observation emphasizes the obesity-related component of insulin resistance driven by adipocytokines, such as TNF-α and its receptors during the course of normal pregnancy and GDM.

Original languageEnglish
Pages (from-to)93-99
Number of pages7
JournalDiabetes Research and Clinical Practice
Volume56
Issue number2
DOIs
Publication statusPublished - 2002

Fingerprint

Gestational Diabetes
C-Peptide
Insulin Resistance
Tumor Necrosis Factor-alpha
Pregnant Women
Third Pregnancy Trimester
Blood Glucose
Lymphotoxin-beta
Serum
Pregnancy
Adipokines
Tumor Necrosis Factor Receptors
First Pregnancy Trimester
Multivariate Analysis
Obesity
Observation

Keywords

  • Gestational diabetes
  • Insulin resistance
  • Physiological pregnancy
  • Soluble TNF-receptors
  • Tumor necrosis factor (TNF)-α

ASJC Scopus subject areas

  • Endocrinology
  • Endocrinology, Diabetes and Metabolism

Cite this

Tumor necrosis factor system in insulin resistance in gestational diabetes. / Winkler, G.; Cseh, K.; Baranyi, Éva; Melczer, Zsolt; Speer, G.; Hajós, Péter; Salamon, Ferenc; Turi, Zsuzsa; Kovács, M.; Vargha, P.; Karádi, I.

In: Diabetes Research and Clinical Practice, Vol. 56, No. 2, 2002, p. 93-99.

Research output: Contribution to journalArticle

Winkler, G. ; Cseh, K. ; Baranyi, Éva ; Melczer, Zsolt ; Speer, G. ; Hajós, Péter ; Salamon, Ferenc ; Turi, Zsuzsa ; Kovács, M. ; Vargha, P. ; Karádi, I. / Tumor necrosis factor system in insulin resistance in gestational diabetes. In: Diabetes Research and Clinical Practice. 2002 ; Vol. 56, No. 2. pp. 93-99.
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title = "Tumor necrosis factor system in insulin resistance in gestational diabetes",
abstract = "Objective: The aim of the study was to investigate the pathophysiological role of the tumor necrosis factor (TNF) system in insulin resistance in patients with gestational diabetes (GDM) and during the course of normal pregnancy. Patients and methods: Thirty women with GDM (16-39 gestational weeks), 35 healthy pregnant women (15 first, nine second and 11 third trimester) and 25 healthy age-matched non-pregnant women were studied. Serum TNF-α, and its soluble receptors 1 and 2 (sTNFR-1 and -2) were measured. Results: In non-diabetic pregnant women in the third trimester all measures were significantly higher (P <0.05 or less) than in the first trimester and in non-pregnant women (BMI 27.6 ± 4.1 ( ± S.D.), 24.1 ± 2.6, 22.4 ± 2.4 kg/m2), serum TNF-α (4.6 ± 0.6, 4.1 ± 0.4, 4.1 ± 0.4 ng/l), sTNFR-1 (2.7 ± 0.9, 2.0 ± 0.5, 2.0 ± 0.1 μg/l), sTNFR-2 (5.6 ± 2.6, 4.6 ± 2.1, 3.3 ± 0.2 μg/l), C-peptide (3.1 ± 1.7, 1.1 ± 0.7, 1.1 ± 0.8 μg/l), and C-peptide:blood glucose ratio (0.6 ± 0.2, 0.2 ± 0.1, 0.2 ± 0.1 μg/mmol). In GDM these measures were even higher than in any subgroup of healthy pregnant women (BMI) (33.4 ± 6.4 kg/m2, TNF-α) (6.3 ± 0.6 μg/l), sTNFR-1 (3.0 ± 0.5 μg/l), sTNFR-2 (10.0 ± 6.9 μg/l, C-peptide 6.0 ± 2.7 μg/l, C-peptide:blood glucose ratio: 1.2 ± 0.5 μg/mmol, P <0.01). Significant (P <0.01) positive linear correlations were found in gestational diabetic and non-diabetic women between serum TNF-α, C-peptide levels, and BMI. In gestational diabetic women, in multivariate analysis studying the dependency of C-peptide only BMI remained significant (r2 = 0.67, P = 0.01). Conclusions: Our observation emphasizes the obesity-related component of insulin resistance driven by adipocytokines, such as TNF-α and its receptors during the course of normal pregnancy and GDM.",
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T1 - Tumor necrosis factor system in insulin resistance in gestational diabetes

AU - Winkler, G.

AU - Cseh, K.

AU - Baranyi, Éva

AU - Melczer, Zsolt

AU - Speer, G.

AU - Hajós, Péter

AU - Salamon, Ferenc

AU - Turi, Zsuzsa

AU - Kovács, M.

AU - Vargha, P.

AU - Karádi, I.

PY - 2002

Y1 - 2002

N2 - Objective: The aim of the study was to investigate the pathophysiological role of the tumor necrosis factor (TNF) system in insulin resistance in patients with gestational diabetes (GDM) and during the course of normal pregnancy. Patients and methods: Thirty women with GDM (16-39 gestational weeks), 35 healthy pregnant women (15 first, nine second and 11 third trimester) and 25 healthy age-matched non-pregnant women were studied. Serum TNF-α, and its soluble receptors 1 and 2 (sTNFR-1 and -2) were measured. Results: In non-diabetic pregnant women in the third trimester all measures were significantly higher (P <0.05 or less) than in the first trimester and in non-pregnant women (BMI 27.6 ± 4.1 ( ± S.D.), 24.1 ± 2.6, 22.4 ± 2.4 kg/m2), serum TNF-α (4.6 ± 0.6, 4.1 ± 0.4, 4.1 ± 0.4 ng/l), sTNFR-1 (2.7 ± 0.9, 2.0 ± 0.5, 2.0 ± 0.1 μg/l), sTNFR-2 (5.6 ± 2.6, 4.6 ± 2.1, 3.3 ± 0.2 μg/l), C-peptide (3.1 ± 1.7, 1.1 ± 0.7, 1.1 ± 0.8 μg/l), and C-peptide:blood glucose ratio (0.6 ± 0.2, 0.2 ± 0.1, 0.2 ± 0.1 μg/mmol). In GDM these measures were even higher than in any subgroup of healthy pregnant women (BMI) (33.4 ± 6.4 kg/m2, TNF-α) (6.3 ± 0.6 μg/l), sTNFR-1 (3.0 ± 0.5 μg/l), sTNFR-2 (10.0 ± 6.9 μg/l, C-peptide 6.0 ± 2.7 μg/l, C-peptide:blood glucose ratio: 1.2 ± 0.5 μg/mmol, P <0.01). Significant (P <0.01) positive linear correlations were found in gestational diabetic and non-diabetic women between serum TNF-α, C-peptide levels, and BMI. In gestational diabetic women, in multivariate analysis studying the dependency of C-peptide only BMI remained significant (r2 = 0.67, P = 0.01). Conclusions: Our observation emphasizes the obesity-related component of insulin resistance driven by adipocytokines, such as TNF-α and its receptors during the course of normal pregnancy and GDM.

AB - Objective: The aim of the study was to investigate the pathophysiological role of the tumor necrosis factor (TNF) system in insulin resistance in patients with gestational diabetes (GDM) and during the course of normal pregnancy. Patients and methods: Thirty women with GDM (16-39 gestational weeks), 35 healthy pregnant women (15 first, nine second and 11 third trimester) and 25 healthy age-matched non-pregnant women were studied. Serum TNF-α, and its soluble receptors 1 and 2 (sTNFR-1 and -2) were measured. Results: In non-diabetic pregnant women in the third trimester all measures were significantly higher (P <0.05 or less) than in the first trimester and in non-pregnant women (BMI 27.6 ± 4.1 ( ± S.D.), 24.1 ± 2.6, 22.4 ± 2.4 kg/m2), serum TNF-α (4.6 ± 0.6, 4.1 ± 0.4, 4.1 ± 0.4 ng/l), sTNFR-1 (2.7 ± 0.9, 2.0 ± 0.5, 2.0 ± 0.1 μg/l), sTNFR-2 (5.6 ± 2.6, 4.6 ± 2.1, 3.3 ± 0.2 μg/l), C-peptide (3.1 ± 1.7, 1.1 ± 0.7, 1.1 ± 0.8 μg/l), and C-peptide:blood glucose ratio (0.6 ± 0.2, 0.2 ± 0.1, 0.2 ± 0.1 μg/mmol). In GDM these measures were even higher than in any subgroup of healthy pregnant women (BMI) (33.4 ± 6.4 kg/m2, TNF-α) (6.3 ± 0.6 μg/l), sTNFR-1 (3.0 ± 0.5 μg/l), sTNFR-2 (10.0 ± 6.9 μg/l, C-peptide 6.0 ± 2.7 μg/l, C-peptide:blood glucose ratio: 1.2 ± 0.5 μg/mmol, P <0.01). Significant (P <0.01) positive linear correlations were found in gestational diabetic and non-diabetic women between serum TNF-α, C-peptide levels, and BMI. In gestational diabetic women, in multivariate analysis studying the dependency of C-peptide only BMI remained significant (r2 = 0.67, P = 0.01). Conclusions: Our observation emphasizes the obesity-related component of insulin resistance driven by adipocytokines, such as TNF-α and its receptors during the course of normal pregnancy and GDM.

KW - Gestational diabetes

KW - Insulin resistance

KW - Physiological pregnancy

KW - Soluble TNF-receptors

KW - Tumor necrosis factor (TNF)-α

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