Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus
Objective The underlying causes of type 2 diabetes (T2DM) remain poorly understood. Adipose tissue dysfunction with high leptin, inflammation, and increased oxidative stress may play a pivotal role in T2DM development in obese patients. Little is known about the changes in the adipose tissue after R...
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creator | Billeter, Adrian T. Vittas, Spiros Israel, Barbara Scheurlen, Katharina M. Hidmark, Asa Fleming, Thomas H. Kopf, Stefan Büchler, Markus W. Müller-Stich, Beat P. |
description | Objective
The underlying causes of type 2 diabetes (T2DM) remain poorly understood. Adipose tissue dysfunction with high leptin, inflammation, and increased oxidative stress may play a pivotal role in T2DM development in obese patients. Little is known about the changes in the adipose tissue after Roux-Y gastric bypass (RYGB) in non-severely obese patients (BMI |
doi_str_mv | 10.1007/s00423-017-1601-x |
format | Article |
fullrecord | <record><control><sourceid>proquest_cross</sourceid><recordid>TN_cdi_proquest_miscellaneous_1917664744</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><sourcerecordid>1917664744</sourcerecordid><originalsourceid>FETCH-LOGICAL-c344t-7fbab0a6dc460b332f61550bea043ade51b67114df69b94dae30405d9125efc13</originalsourceid><addsrcrecordid>eNp9kMFu1jAQhC0EouWHB-CCfOQS2I0dhxxRRQtSJS5wtux4g1wlTsjaqP_b4yqlR0670s6MZj8h3iJ8QID-IwPoVjWAfYMGsLl_Ji5Rq65pdYfPn3atLsQr5jsAMP2gX4qL9pMZEHV_KZYbx3mPo_TnzTFLjkuZs0u0Fp7PMi7bvv4hli7EbWWSOTIXklNJY45rki4FGROXOaYm0EYpUMoynzeSrQzRecrVvdA8x1z4tXgxuZnpzeM8iZ_XX35cfW1uv998u_p824xK69z0k3cenAmjNuCVaieDXQeeHGjlAnXoTV_7h8kMftDBkQINXRiw7WgaUZ3E-yO3tv9diLNdIo-1xPGYxQF7Y3Rf0ZwEHtJxX5l3muy2x8XtZ4tgHyjbg7KtlO0DZXtfPe8e44tfKDw5_mGtgvYQcD2lX7Tbu7Xsqb78n9S_8ACK8A</addsrcrecordid><sourcetype>Aggregation Database</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1917664744</pqid></control><display><type>article</type><title>Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus</title><source>MEDLINE</source><source>SpringerNature Journals</source><creator>Billeter, Adrian T. ; Vittas, Spiros ; Israel, Barbara ; Scheurlen, Katharina M. ; Hidmark, Asa ; Fleming, Thomas H. ; Kopf, Stefan ; Büchler, Markus W. ; Müller-Stich, Beat P.</creator><creatorcontrib>Billeter, Adrian T. ; Vittas, Spiros ; Israel, Barbara ; Scheurlen, Katharina M. ; Hidmark, Asa ; Fleming, Thomas H. ; Kopf, Stefan ; Büchler, Markus W. ; Müller-Stich, Beat P.</creatorcontrib><description>Objective
The underlying causes of type 2 diabetes (T2DM) remain poorly understood. Adipose tissue dysfunction with high leptin, inflammation, and increased oxidative stress may play a pivotal role in T2DM development in obese patients. Little is known about the changes in the adipose tissue after Roux-Y gastric bypass (RYGB) in non-severely obese patients (BMI < 35 kg/m
2
) and since these patients have more T2DM-associated complications than obese patients (“obesity paradox”), we investigated changes in adipose tissue function in a cohort of BMI <35 kg/m
2
with insulin-dependent T2DM after RYGB surgery which resolves T2DM.
Methods
Twenty patients with insulin-dependent T2DM and BMI <35 kg/m
2
underwent RYGB. Insulin-resistance, leptin, oxidative stress, and cytokines were determined over 24 months. Expression of cytokines and NF-kappaB pathway genes were measured in leukocytes (PBMC). Adipose tissue inflammation was examined histologically preoperatively and 24 months after RGYB in subcutaneous adipose tissue.
Results
Insulin-resistance, leptin, oxidative stress as well as adipose tissue inflammation decreased significantly after RYGB. Similarly, systemic inflammation was reduced and peripheral blood mononuclear cells (PBMCs) were reprogrammed towards an M2-type inflammation. Loss of BMI correlated with leptin levels (
r
= 0.891,
p
< 0.0001), insulin resistance (
r
= 0.527,
p
= 0.003), and oxidative stress (
r
= 0.592,
p
= 0.016). Leptin correlated with improved insulin resistance (
r
= 0.449,
p
= 0.032) while reduced leptin showed a strong association with improved oxidative stress (
r
= 0.809,
p
= 0.001). Lastly, reduced oxidative stress correlated strongly with improved insulin-resistance (
r
= 0.776,
p
= 0.001).
Conclusions
RYGB improves adipose tissue function and inflammation. Leptin as marker for adipose tissue dysfunction may be the mediating factor between insulin resistance and oxidative stress and thereby likely improving T2DM.</description><identifier>ISSN: 1435-2443</identifier><identifier>EISSN: 1435-2451</identifier><identifier>DOI: 10.1007/s00423-017-1601-x</identifier><identifier>PMID: 28691147</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>Abdominal Surgery ; Adipose Tissue - metabolism ; Adult ; Body Mass Index ; Cardiac Surgery ; Cohort Studies ; Comorbidity ; Diabetes Mellitus, Type 2 - diagnosis ; Diabetes Mellitus, Type 2 - drug therapy ; Diabetes Mellitus, Type 2 - epidemiology ; Female ; Follow-Up Studies ; Gastric Bypass - methods ; General Surgery ; Humans ; Insulin - therapeutic use ; Insulin Resistance ; Male ; Medicine ; Medicine & Public Health ; Middle Aged ; Obesity, Morbid - diagnosis ; Obesity, Morbid - epidemiology ; Obesity, Morbid - surgery ; Original Article ; Oxidative Stress - physiology ; Prospective Studies ; Risk Assessment ; Thoracic Surgery ; Traumatic Surgery ; Treatment Outcome ; Vascular Surgery ; Weight Loss - physiology</subject><ispartof>Langenbeck's archives of surgery, 2017-09, Vol.402 (6), p.901-910</ispartof><rights>Springer-Verlag GmbH Germany 2017</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c344t-7fbab0a6dc460b332f61550bea043ade51b67114df69b94dae30405d9125efc13</citedby><cites>FETCH-LOGICAL-c344t-7fbab0a6dc460b332f61550bea043ade51b67114df69b94dae30405d9125efc13</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00423-017-1601-x$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00423-017-1601-x$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>315,781,785,27929,27930,41493,42562,51324</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28691147$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Billeter, Adrian T.</creatorcontrib><creatorcontrib>Vittas, Spiros</creatorcontrib><creatorcontrib>Israel, Barbara</creatorcontrib><creatorcontrib>Scheurlen, Katharina M.</creatorcontrib><creatorcontrib>Hidmark, Asa</creatorcontrib><creatorcontrib>Fleming, Thomas H.</creatorcontrib><creatorcontrib>Kopf, Stefan</creatorcontrib><creatorcontrib>Büchler, Markus W.</creatorcontrib><creatorcontrib>Müller-Stich, Beat P.</creatorcontrib><title>Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus</title><title>Langenbeck's archives of surgery</title><addtitle>Langenbecks Arch Surg</addtitle><addtitle>Langenbecks Arch Surg</addtitle><description>Objective
The underlying causes of type 2 diabetes (T2DM) remain poorly understood. Adipose tissue dysfunction with high leptin, inflammation, and increased oxidative stress may play a pivotal role in T2DM development in obese patients. Little is known about the changes in the adipose tissue after Roux-Y gastric bypass (RYGB) in non-severely obese patients (BMI < 35 kg/m
2
) and since these patients have more T2DM-associated complications than obese patients (“obesity paradox”), we investigated changes in adipose tissue function in a cohort of BMI <35 kg/m
2
with insulin-dependent T2DM after RYGB surgery which resolves T2DM.
Methods
Twenty patients with insulin-dependent T2DM and BMI <35 kg/m
2
underwent RYGB. Insulin-resistance, leptin, oxidative stress, and cytokines were determined over 24 months. Expression of cytokines and NF-kappaB pathway genes were measured in leukocytes (PBMC). Adipose tissue inflammation was examined histologically preoperatively and 24 months after RGYB in subcutaneous adipose tissue.
Results
Insulin-resistance, leptin, oxidative stress as well as adipose tissue inflammation decreased significantly after RYGB. Similarly, systemic inflammation was reduced and peripheral blood mononuclear cells (PBMCs) were reprogrammed towards an M2-type inflammation. Loss of BMI correlated with leptin levels (
r
= 0.891,
p
< 0.0001), insulin resistance (
r
= 0.527,
p
= 0.003), and oxidative stress (
r
= 0.592,
p
= 0.016). Leptin correlated with improved insulin resistance (
r
= 0.449,
p
= 0.032) while reduced leptin showed a strong association with improved oxidative stress (
r
= 0.809,
p
= 0.001). Lastly, reduced oxidative stress correlated strongly with improved insulin-resistance (
r
= 0.776,
p
= 0.001).
Conclusions
RYGB improves adipose tissue function and inflammation. Leptin as marker for adipose tissue dysfunction may be the mediating factor between insulin resistance and oxidative stress and thereby likely improving T2DM.</description><subject>Abdominal Surgery</subject><subject>Adipose Tissue - metabolism</subject><subject>Adult</subject><subject>Body Mass Index</subject><subject>Cardiac Surgery</subject><subject>Cohort Studies</subject><subject>Comorbidity</subject><subject>Diabetes Mellitus, Type 2 - diagnosis</subject><subject>Diabetes Mellitus, Type 2 - drug therapy</subject><subject>Diabetes Mellitus, Type 2 - epidemiology</subject><subject>Female</subject><subject>Follow-Up Studies</subject><subject>Gastric Bypass - methods</subject><subject>General Surgery</subject><subject>Humans</subject><subject>Insulin - therapeutic use</subject><subject>Insulin Resistance</subject><subject>Male</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Middle Aged</subject><subject>Obesity, Morbid - diagnosis</subject><subject>Obesity, Morbid - epidemiology</subject><subject>Obesity, Morbid - surgery</subject><subject>Original Article</subject><subject>Oxidative Stress - physiology</subject><subject>Prospective Studies</subject><subject>Risk Assessment</subject><subject>Thoracic Surgery</subject><subject>Traumatic Surgery</subject><subject>Treatment Outcome</subject><subject>Vascular Surgery</subject><subject>Weight Loss - physiology</subject><issn>1435-2443</issn><issn>1435-2451</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kMFu1jAQhC0EouWHB-CCfOQS2I0dhxxRRQtSJS5wtux4g1wlTsjaqP_b4yqlR0670s6MZj8h3iJ8QID-IwPoVjWAfYMGsLl_Ji5Rq65pdYfPn3atLsQr5jsAMP2gX4qL9pMZEHV_KZYbx3mPo_TnzTFLjkuZs0u0Fp7PMi7bvv4hli7EbWWSOTIXklNJY45rki4FGROXOaYm0EYpUMoynzeSrQzRecrVvdA8x1z4tXgxuZnpzeM8iZ_XX35cfW1uv998u_p824xK69z0k3cenAmjNuCVaieDXQeeHGjlAnXoTV_7h8kMftDBkQINXRiw7WgaUZ3E-yO3tv9diLNdIo-1xPGYxQF7Y3Rf0ZwEHtJxX5l3muy2x8XtZ4tgHyjbg7KtlO0DZXtfPe8e44tfKDw5_mGtgvYQcD2lX7Tbu7Xsqb78n9S_8ACK8A</recordid><startdate>20170901</startdate><enddate>20170901</enddate><creator>Billeter, Adrian T.</creator><creator>Vittas, Spiros</creator><creator>Israel, Barbara</creator><creator>Scheurlen, Katharina M.</creator><creator>Hidmark, Asa</creator><creator>Fleming, Thomas H.</creator><creator>Kopf, Stefan</creator><creator>Büchler, Markus W.</creator><creator>Müller-Stich, Beat P.</creator><general>Springer Berlin Heidelberg</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope></search><sort><creationdate>20170901</creationdate><title>Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus</title><author>Billeter, Adrian T. ; Vittas, Spiros ; Israel, Barbara ; Scheurlen, Katharina M. ; Hidmark, Asa ; Fleming, Thomas H. ; Kopf, Stefan ; Büchler, Markus W. ; Müller-Stich, Beat P.</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c344t-7fbab0a6dc460b332f61550bea043ade51b67114df69b94dae30405d9125efc13</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Abdominal Surgery</topic><topic>Adipose Tissue - metabolism</topic><topic>Adult</topic><topic>Body Mass Index</topic><topic>Cardiac Surgery</topic><topic>Cohort Studies</topic><topic>Comorbidity</topic><topic>Diabetes Mellitus, Type 2 - diagnosis</topic><topic>Diabetes Mellitus, Type 2 - drug therapy</topic><topic>Diabetes Mellitus, Type 2 - epidemiology</topic><topic>Female</topic><topic>Follow-Up Studies</topic><topic>Gastric Bypass - methods</topic><topic>General Surgery</topic><topic>Humans</topic><topic>Insulin - therapeutic use</topic><topic>Insulin Resistance</topic><topic>Male</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Middle Aged</topic><topic>Obesity, Morbid - diagnosis</topic><topic>Obesity, Morbid - epidemiology</topic><topic>Obesity, Morbid - surgery</topic><topic>Original Article</topic><topic>Oxidative Stress - physiology</topic><topic>Prospective Studies</topic><topic>Risk Assessment</topic><topic>Thoracic Surgery</topic><topic>Traumatic Surgery</topic><topic>Treatment Outcome</topic><topic>Vascular Surgery</topic><topic>Weight Loss - physiology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Billeter, Adrian T.</creatorcontrib><creatorcontrib>Vittas, Spiros</creatorcontrib><creatorcontrib>Israel, Barbara</creatorcontrib><creatorcontrib>Scheurlen, Katharina M.</creatorcontrib><creatorcontrib>Hidmark, Asa</creatorcontrib><creatorcontrib>Fleming, Thomas H.</creatorcontrib><creatorcontrib>Kopf, Stefan</creatorcontrib><creatorcontrib>Büchler, Markus W.</creatorcontrib><creatorcontrib>Müller-Stich, Beat P.</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><jtitle>Langenbeck's archives of surgery</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Billeter, Adrian T.</au><au>Vittas, Spiros</au><au>Israel, Barbara</au><au>Scheurlen, Katharina M.</au><au>Hidmark, Asa</au><au>Fleming, Thomas H.</au><au>Kopf, Stefan</au><au>Büchler, Markus W.</au><au>Müller-Stich, Beat P.</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus</atitle><jtitle>Langenbeck's archives of surgery</jtitle><stitle>Langenbecks Arch Surg</stitle><addtitle>Langenbecks Arch Surg</addtitle><date>2017-09-01</date><risdate>2017</risdate><volume>402</volume><issue>6</issue><spage>901</spage><epage>910</epage><pages>901-910</pages><issn>1435-2443</issn><eissn>1435-2451</eissn><abstract>Objective
The underlying causes of type 2 diabetes (T2DM) remain poorly understood. Adipose tissue dysfunction with high leptin, inflammation, and increased oxidative stress may play a pivotal role in T2DM development in obese patients. Little is known about the changes in the adipose tissue after Roux-Y gastric bypass (RYGB) in non-severely obese patients (BMI < 35 kg/m
2
) and since these patients have more T2DM-associated complications than obese patients (“obesity paradox”), we investigated changes in adipose tissue function in a cohort of BMI <35 kg/m
2
with insulin-dependent T2DM after RYGB surgery which resolves T2DM.
Methods
Twenty patients with insulin-dependent T2DM and BMI <35 kg/m
2
underwent RYGB. Insulin-resistance, leptin, oxidative stress, and cytokines were determined over 24 months. Expression of cytokines and NF-kappaB pathway genes were measured in leukocytes (PBMC). Adipose tissue inflammation was examined histologically preoperatively and 24 months after RGYB in subcutaneous adipose tissue.
Results
Insulin-resistance, leptin, oxidative stress as well as adipose tissue inflammation decreased significantly after RYGB. Similarly, systemic inflammation was reduced and peripheral blood mononuclear cells (PBMCs) were reprogrammed towards an M2-type inflammation. Loss of BMI correlated with leptin levels (
r
= 0.891,
p
< 0.0001), insulin resistance (
r
= 0.527,
p
= 0.003), and oxidative stress (
r
= 0.592,
p
= 0.016). Leptin correlated with improved insulin resistance (
r
= 0.449,
p
= 0.032) while reduced leptin showed a strong association with improved oxidative stress (
r
= 0.809,
p
= 0.001). Lastly, reduced oxidative stress correlated strongly with improved insulin-resistance (
r
= 0.776,
p
= 0.001).
Conclusions
RYGB improves adipose tissue function and inflammation. Leptin as marker for adipose tissue dysfunction may be the mediating factor between insulin resistance and oxidative stress and thereby likely improving T2DM.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>28691147</pmid><doi>10.1007/s00423-017-1601-x</doi><tpages>10</tpages></addata></record> |
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source | MEDLINE; SpringerNature Journals |
subjects | Abdominal Surgery Adipose Tissue - metabolism Adult Body Mass Index Cardiac Surgery Cohort Studies Comorbidity Diabetes Mellitus, Type 2 - diagnosis Diabetes Mellitus, Type 2 - drug therapy Diabetes Mellitus, Type 2 - epidemiology Female Follow-Up Studies Gastric Bypass - methods General Surgery Humans Insulin - therapeutic use Insulin Resistance Male Medicine Medicine & Public Health Middle Aged Obesity, Morbid - diagnosis Obesity, Morbid - epidemiology Obesity, Morbid - surgery Original Article Oxidative Stress - physiology Prospective Studies Risk Assessment Thoracic Surgery Traumatic Surgery Treatment Outcome Vascular Surgery Weight Loss - physiology |
title | Gastric bypass simultaneously improves adipose tissue function and insulin-dependent type 2 diabetes mellitus |
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