Progression from high insulin resistance to type 2 diabetes does not entail additional visceral adipose tissue inflammation
Obesity is associated with a low-grade chronic inflammation state. As a consequence, adipose tissue expresses pro-inflammatory cytokines that propagate inflammatory responses systemically elsewhere, promoting whole-body insulin resistance and consequential islet β-cell exhaustation. Thus, insulin resistance is considered the early stage of type 2 diabetes. However, there is evidence of obese individuals that never develop diabetes indicating that the mechanisms governing the association between the increase of inflammatory factors and type 2 diabetes are much more complex and deserve further investigation. We studied for the first time the differences in insulin signalling and inflammatory pathways in blood and visceral adipose tissue (VAT) of 20 lean healthy donors and 40 equal morbidly obese (MO) patients classified in high insulin resistance (high IR) degree and diabetes state. We studied the changes in proinflammatory markers and lipid content from serum; macrophage infiltration, mRNA expression of inflammatory cytokines and transcription factors, activation of kinases involved in inflammation and expression of insulin signalling molecules in VAT. VAT comparison of these experimental groups revealed that type 2 diabetic-MO subjects exhibit the same pro-inflammatory profile than the high IR-MO patients, characterized by elevated levels of IL-1β, IL-6, TNFα, JNK1/2, ERK1/2, STAT3 and NFκB. Our work rules out the assumption that the inflammation should be increased in obese people with type 2 diabetes compared to high IR obese. These findings indicate that some mechanisms, other than systemic and VAT inflammation must be involved in the development of type 2 diabetes in obesity.
Medienart: |
E-Artikel |
---|
Erscheinungsjahr: |
2012 |
---|---|
Erschienen: |
2012 |
Enthalten in: |
Zur Gesamtaufnahme - volume:7 |
---|---|
Enthalten in: |
PloS one - 7(2012), 10 vom: 01., Seite e48155 |
Sprache: |
Englisch |
---|
Beteiligte Personen: |
Barbarroja, Nuria [VerfasserIn] |
---|
Links: |
---|
Anmerkungen: |
Date Completed 26.04.2013 Date Revised 21.10.2021 published: Print-Electronic Citation Status MEDLINE |
---|
doi: |
10.1371/journal.pone.0048155 |
---|
funding: |
|
---|---|
Förderinstitution / Projekttitel: |
|
PPN (Katalog-ID): |
NLM222221046 |
---|
LEADER | 01000naa a22002652 4500 | ||
---|---|---|---|
001 | NLM222221046 | ||
003 | DE-627 | ||
005 | 20231224053748.0 | ||
007 | cr uuu---uuuuu | ||
008 | 231224s2012 xx |||||o 00| ||eng c | ||
024 | 7 | |a 10.1371/journal.pone.0048155 |2 doi | |
028 | 5 | 2 | |a pubmed24n0740.xml |
035 | |a (DE-627)NLM222221046 | ||
035 | |a (NLM)23110196 | ||
040 | |a DE-627 |b ger |c DE-627 |e rakwb | ||
041 | |a eng | ||
100 | 1 | |a Barbarroja, Nuria |e verfasserin |4 aut | |
245 | 1 | 0 | |a Progression from high insulin resistance to type 2 diabetes does not entail additional visceral adipose tissue inflammation |
264 | 1 | |c 2012 | |
336 | |a Text |b txt |2 rdacontent | ||
337 | |a ƒaComputermedien |b c |2 rdamedia | ||
338 | |a ƒa Online-Ressource |b cr |2 rdacarrier | ||
500 | |a Date Completed 26.04.2013 | ||
500 | |a Date Revised 21.10.2021 | ||
500 | |a published: Print-Electronic | ||
500 | |a Citation Status MEDLINE | ||
520 | |a Obesity is associated with a low-grade chronic inflammation state. As a consequence, adipose tissue expresses pro-inflammatory cytokines that propagate inflammatory responses systemically elsewhere, promoting whole-body insulin resistance and consequential islet β-cell exhaustation. Thus, insulin resistance is considered the early stage of type 2 diabetes. However, there is evidence of obese individuals that never develop diabetes indicating that the mechanisms governing the association between the increase of inflammatory factors and type 2 diabetes are much more complex and deserve further investigation. We studied for the first time the differences in insulin signalling and inflammatory pathways in blood and visceral adipose tissue (VAT) of 20 lean healthy donors and 40 equal morbidly obese (MO) patients classified in high insulin resistance (high IR) degree and diabetes state. We studied the changes in proinflammatory markers and lipid content from serum; macrophage infiltration, mRNA expression of inflammatory cytokines and transcription factors, activation of kinases involved in inflammation and expression of insulin signalling molecules in VAT. VAT comparison of these experimental groups revealed that type 2 diabetic-MO subjects exhibit the same pro-inflammatory profile than the high IR-MO patients, characterized by elevated levels of IL-1β, IL-6, TNFα, JNK1/2, ERK1/2, STAT3 and NFκB. Our work rules out the assumption that the inflammation should be increased in obese people with type 2 diabetes compared to high IR obese. These findings indicate that some mechanisms, other than systemic and VAT inflammation must be involved in the development of type 2 diabetes in obesity | ||
650 | 4 | |a Journal Article | |
650 | 4 | |a Research Support, Non-U.S. Gov't | |
650 | 7 | |a Interleukin-1beta |2 NLM | |
650 | 7 | |a Interleukin-6 |2 NLM | |
650 | 7 | |a NF-kappa B |2 NLM | |
650 | 7 | |a STAT3 Transcription Factor |2 NLM | |
650 | 7 | |a STAT3 protein, human |2 NLM | |
650 | 7 | |a Tumor Necrosis Factor-alpha |2 NLM | |
650 | 7 | |a JNK Mitogen-Activated Protein Kinases |2 NLM | |
650 | 7 | |a EC 2.7.11.24 |2 NLM | |
650 | 7 | |a Mitogen-Activated Protein Kinase 1 |2 NLM | |
650 | 7 | |a EC 2.7.11.24 |2 NLM | |
650 | 7 | |a Mitogen-Activated Protein Kinase 3 |2 NLM | |
650 | 7 | |a EC 2.7.11.24 |2 NLM | |
700 | 1 | |a Lopez-Pedrera, Chary |e verfasserin |4 aut | |
700 | 1 | |a Garrido-Sanchez, Lourdes |e verfasserin |4 aut | |
700 | 1 | |a Mayas, Maria Dolores |e verfasserin |4 aut | |
700 | 1 | |a Oliva-Olivera, Wilfredo |e verfasserin |4 aut | |
700 | 1 | |a Bernal-Lopez, Maria Rosa |e verfasserin |4 aut | |
700 | 1 | |a El Bekay, Rajaa |e verfasserin |4 aut | |
700 | 1 | |a Tinahones, Francisco Jose |e verfasserin |4 aut | |
773 | 0 | 8 | |i Enthalten in |t PloS one |d 2006 |g 7(2012), 10 vom: 01., Seite e48155 |w (DE-627)NLM167327399 |x 1932-6203 |7 nnns |
773 | 1 | 8 | |g volume:7 |g year:2012 |g number:10 |g day:01 |g pages:e48155 |
856 | 4 | 0 | |u http://dx.doi.org/10.1371/journal.pone.0048155 |3 Volltext |
912 | |a GBV_USEFLAG_A | ||
912 | |a GBV_NLM | ||
951 | |a AR | ||
952 | |d 7 |j 2012 |e 10 |b 01 |h e48155 |