Effects of Type 2 Diabetes and Insulin on Whole-Body, Splanchnic, and Leg Protein Metabolism
Identifieur interne : 002267 ( Ncbi/Merge ); précédent : 002266; suivant : 002268Effects of Type 2 Diabetes and Insulin on Whole-Body, Splanchnic, and Leg Protein Metabolism
Auteurs : Kevin R. Short ; Brian A. Irving ; Ananda Basu ; C. Michael Johnson ; K. Sreekumaran Nair ; Rita BasuSource :
- The Journal of Clinical Endocrinology and Metabolism [ 0021-972X ] ; 2012.
Abstract
Type 2 diabetes (T2D) is characterized by insulin resistance to glucose metabolism. Most studies suggest that protein metabolism is unaffected by T2D, but regional protein metabolism and response to multiple doses of insulin have not been examined.
Our objective was to determine whether insulin regulation of splanchnic and leg protein metabolism are affected by T2D during hyperglycemia and graded insulin levels.
We conducted a cross-sectional study at an academic medical center.
T2D and non-T2D adults were matched for age (62 yr) and body mass index (30 kg/m2).
Glucose was maintained at approximately 9 mmol/liter while insulin was infused at three progressively higher rates, achieving circulating concentrations of approximately 150, 350, and 700 pmol/liter, respectively.
Protein kinetics were measured using labeled phenylalanine (Phe) and tyrosine (Tyr).
Whole-body protein breakdown and synthesis rates were higher in T2D but declined with increasing insulin in both groups. Leg Phe and Tyr appearance and disappearance and estimates of protein breakdown and synthesis, respectively, were higher in T2D but did not decline significantly with insulin, resulting in similar net balance between groups. Splanchnic response to insulin was blunted in T2D, shown by a smaller reduction in rates of disappearance and net balance of Phe and Tyr as insulin increased. Splanchnic conversion of Phe to Tyr was lower in T2D and less sensitive to insulin, whereas nonsplanchnic Phe to Tyr tended to be higher in T2D.
T2D results in higher whole-body, splanchnic, and leg protein turnover and blunts the insulin-mediated suppression of splanchnic protein anabolism under hyperglycemic, hyperinsulinemic conditions.
Url:
DOI: 10.1210/jc.2012-2533
PubMed: 23032060
PubMed Central: 3591680
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Sreekumaran Nair</name></author><author><name sortKey="Basu, Rita" sort="Basu, Rita" uniqKey="Basu R" first="Rita" last="Basu">Rita Basu</name></author></titleStmt><publicationStmt><idno type="wicri:source">PMC</idno><idno type="pmid">23032060</idno><idno type="pmc">3591680</idno><idno type="url">http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3591680</idno><idno type="RBID">PMC:3591680</idno><idno type="doi">10.1210/jc.2012-2533</idno><date when="2012">2012</date><idno type="wicri:Area/Pmc/Corpus">001375</idno><idno type="wicri:Area/Pmc/Curation">001375</idno><idno type="wicri:Area/Pmc/Checkpoint">001759</idno><idno type="wicri:Area/Ncbi/Merge">002267</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a" type="main">Effects of Type 2 Diabetes and Insulin on Whole-Body, Splanchnic, and Leg Protein Metabolism</title><author><name sortKey="Short, Kevin R" sort="Short, Kevin R" uniqKey="Short K" first="Kevin R." last="Short">Kevin R. Short</name></author><author><name sortKey="Irving, Brian A" sort="Irving, Brian A" uniqKey="Irving B" first="Brian A." last="Irving">Brian A. Irving</name></author><author><name sortKey="Basu, Ananda" sort="Basu, Ananda" uniqKey="Basu A" first="Ananda" last="Basu">Ananda Basu</name></author><author><name sortKey="Johnson, C Michael" sort="Johnson, C Michael" uniqKey="Johnson C" first="C. Michael" last="Johnson">C. Michael Johnson</name></author><author><name sortKey="Nair, K Sreekumaran" sort="Nair, K Sreekumaran" uniqKey="Nair K" first="K. Sreekumaran" last="Nair">K. Sreekumaran Nair</name></author><author><name sortKey="Basu, Rita" sort="Basu, Rita" uniqKey="Basu R" first="Rita" last="Basu">Rita Basu</name></author></analytic><series><title level="j">The Journal of Clinical Endocrinology and Metabolism</title><idno type="ISSN">0021-972X</idno><idno type="eISSN">1945-7197</idno><imprint><date when="2012">2012</date></imprint></series></biblStruct></sourceDesc></fileDesc><profileDesc><textClass></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en"><sec><title>Context:</title><p>Type 2 diabetes (T2D) is characterized by insulin resistance to glucose metabolism. Most studies suggest that protein metabolism is unaffected by T2D, but regional protein metabolism and response to multiple doses of insulin have not been examined.</p></sec><sec><title>Objective:</title><p>Our objective was to determine whether insulin regulation of splanchnic and leg protein metabolism are affected by T2D during hyperglycemia and graded insulin levels.</p></sec><sec><title>Design and Setting:</title><p>We conducted a cross-sectional study at an academic medical center.</p></sec><sec><title>Participants:</title><p>T2D and non-T2D adults were matched for age (62 yr) and body mass index (30 kg/m<sup>2</sup>).</p></sec><sec><title>Interventions:</title><p>Glucose was maintained at approximately 9 mmol/liter while insulin was infused at three progressively higher rates, achieving circulating concentrations of approximately 150, 350, and 700 pmol/liter, respectively.</p></sec><sec><title>Main Outcome Measures:</title><p>Protein kinetics were measured using labeled phenylalanine (Phe) and tyrosine (Tyr).</p></sec><sec><title>Results:</title><p>Whole-body protein breakdown and synthesis rates were higher in T2D but declined with increasing insulin in both groups. Leg Phe and Tyr appearance and disappearance and estimates of protein breakdown and synthesis, respectively, were higher in T2D but did not decline significantly with insulin, resulting in similar net balance between groups. Splanchnic response to insulin was blunted in T2D, shown by a smaller reduction in rates of disappearance and net balance of Phe and Tyr as insulin increased. Splanchnic conversion of Phe to Tyr was lower in T2D and less sensitive to insulin, whereas nonsplanchnic Phe to Tyr tended to be higher in T2D.</p></sec><sec><title>Conclusions:</title><p>T2D results in higher whole-body, splanchnic, and leg protein turnover and blunts the insulin-mediated suppression of splanchnic protein anabolism under hyperglycemic, hyperinsulinemic conditions.</p></sec></div></front></TEI><pmc article-type="research-article"><pmc-comment>The publisher of this article does not allow downloading of the full text in XML form.</pmc-comment>
<front><journal-meta><journal-id journal-id-type="nlm-ta">J Clin Endocrinol Metab</journal-id><journal-id journal-id-type="iso-abbrev">J. Clin. Endocrinol. Metab</journal-id><journal-id journal-id-type="hwp">jcem</journal-id><journal-id journal-id-type="publisher-id">jceme</journal-id><journal-id journal-id-type="pmc">jcem</journal-id><journal-title-group><journal-title>The Journal of Clinical Endocrinology and Metabolism</journal-title></journal-title-group><issn pub-type="ppub">0021-972X</issn><issn pub-type="epub">1945-7197</issn><publisher><publisher-name>Endocrine Society</publisher-name><publisher-loc>Chevy Chase, MD</publisher-loc></publisher></journal-meta><article-meta><article-id pub-id-type="pmid">23032060</article-id><article-id pub-id-type="pmc">3591680</article-id><article-id pub-id-type="publisher-id">12-2533</article-id><article-id pub-id-type="doi">10.1210/jc.2012-2533</article-id><article-categories><subj-group subj-group-type="hwp-journal-coll"><subject>4</subject><subject>8</subject></subj-group><subj-group subj-group-type="heading"><subject>Endocrine Research</subject></subj-group></article-categories><title-group><article-title>Effects of Type 2 Diabetes and Insulin on Whole-Body, Splanchnic, and Leg Protein Metabolism</article-title></title-group><contrib-group><contrib contrib-type="author"><name><surname>Short</surname><given-names>Kevin R.</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref></contrib><contrib contrib-type="author"><name><surname>Irving</surname><given-names>Brian A.</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref></contrib><contrib contrib-type="author"><name><surname>Basu</surname><given-names>Ananda</given-names></name></contrib><contrib contrib-type="author"><name><surname>Johnson</surname><given-names>C. Michael</given-names></name></contrib><contrib contrib-type="author"><name><surname>Nair</surname><given-names>K. Sreekumaran</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref></contrib><contrib contrib-type="author" corresp="yes"><name><surname>Basu</surname><given-names>Rita</given-names></name><xref ref-type="author-notes" rid="FN1">*</xref></contrib><aff>Endocrinology Research Unit (K.R.S., B.A.I., A.B., K.S.N., R.B.), Mayo Clinic School of Medicine, and Department of Vascular and Interventional Radiology (C.M.J.), Mayo Clinic, Rochester, Minnesota 55905</aff></contrib-group><author-notes><corresp>Address all correspondence and requests for reprints to: Rita Basu, M.D., Mayo College of Medicine, Endocrinology Research Unit, 5-194 Joseph, 200 First Street SW, Rochester, Minnesota 55905. E-mail: <email>basu.rita@mayo.edu</email>.</corresp><fn fn-type="equal" id="FN1"><label>*</label><p>K.R.S. and B.A.I. contributed equally; K.S.N. and R.B. also contributed equally.</p></fn></author-notes><pub-date pub-type="ppub"><month>12</month><year>2012</year></pub-date><pub-date pub-type="epub"><day>2</day><month>10</month><year>2012</year></pub-date><pub-date pub-type="pmc-release"><day>1</day><month>12</month><year>2013</year></pub-date><pmc-comment> PMC Release delay is 12 months and 0 days and was based on the
<volume>97</volume><issue>12</issue><fpage>4733</fpage><lpage>4741</lpage><history><date date-type="received"><day>18</day><month>6</month><year>2012</year></date><date date-type="accepted"><day>12</day><month>9</month><year>2012</year></date></history><permissions><copyright-statement>Copyright © 2012 by The Endocrine Society</copyright-statement><copyright-year>2012</copyright-year></permissions><self-uri xlink:title="pdf" xlink:type="simple" xlink:href="zeg01212004733.pdf"></self-uri><abstract><sec><title>Context:</title><p>Type 2 diabetes (T2D) is characterized by insulin resistance to glucose metabolism. Most studies suggest that protein metabolism is unaffected by T2D, but regional protein metabolism and response to multiple doses of insulin have not been examined.</p></sec><sec><title>Objective:</title><p>Our objective was to determine whether insulin regulation of splanchnic and leg protein metabolism are affected by T2D during hyperglycemia and graded insulin levels.</p></sec><sec><title>Design and Setting:</title><p>We conducted a cross-sectional study at an academic medical center.</p></sec><sec><title>Participants:</title><p>T2D and non-T2D adults were matched for age (62 yr) and body mass index (30 kg/m<sup>2</sup>).</p></sec><sec><title>Interventions:</title><p>Glucose was maintained at approximately 9 mmol/liter while insulin was infused at three progressively higher rates, achieving circulating concentrations of approximately 150, 350, and 700 pmol/liter, respectively.</p></sec><sec><title>Main Outcome Measures:</title><p>Protein kinetics were measured using labeled phenylalanine (Phe) and tyrosine (Tyr).</p></sec><sec><title>Results:</title><p>Whole-body protein breakdown and synthesis rates were higher in T2D but declined with increasing insulin in both groups. Leg Phe and Tyr appearance and disappearance and estimates of protein breakdown and synthesis, respectively, were higher in T2D but did not decline significantly with insulin, resulting in similar net balance between groups. Splanchnic response to insulin was blunted in T2D, shown by a smaller reduction in rates of disappearance and net balance of Phe and Tyr as insulin increased. Splanchnic conversion of Phe to Tyr was lower in T2D and less sensitive to insulin, whereas nonsplanchnic Phe to Tyr tended to be higher in T2D.</p></sec><sec><title>Conclusions:</title><p>T2D results in higher whole-body, splanchnic, and leg protein turnover and blunts the insulin-mediated suppression of splanchnic protein anabolism under hyperglycemic, hyperinsulinemic conditions.</p></sec></abstract></article-meta></front></pmc><affiliations><list></list><tree><noCountry><name sortKey="Basu, Ananda" sort="Basu, Ananda" uniqKey="Basu A" first="Ananda" last="Basu">Ananda Basu</name><name sortKey="Basu, Rita" sort="Basu, Rita" uniqKey="Basu R" first="Rita" last="Basu">Rita Basu</name><name sortKey="Irving, Brian A" sort="Irving, Brian A" uniqKey="Irving B" first="Brian A." last="Irving">Brian A. Irving</name><name sortKey="Johnson, C Michael" sort="Johnson, C Michael" uniqKey="Johnson C" first="C. Michael" last="Johnson">C. Michael Johnson</name><name sortKey="Nair, K Sreekumaran" sort="Nair, K Sreekumaran" uniqKey="Nair K" first="K. Sreekumaran" last="Nair">K. Sreekumaran Nair</name><name sortKey="Short, Kevin R" sort="Short, Kevin R" uniqKey="Short K" first="Kevin R." last="Short">Kevin R. Short</name></noCountry></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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