Loss of coupling between calcium influx, energy consumption and insulin secretion associated with development of hyperglycaemia in the UCD-T2DM rat model of type 2 diabetes
Identifieur interne : 000196 ( Main/Merge ); précédent : 000195; suivant : 000197Loss of coupling between calcium influx, energy consumption and insulin secretion associated with development of hyperglycaemia in the UCD-T2DM rat model of type 2 diabetes
Auteurs : A. M. Rountree [États-Unis] ; B. J. Reed [États-Unis] ; B. P. Cummings [États-Unis] ; S.-R. Jung [États-Unis] ; K. L. Stanhope [États-Unis] ; J. L. Graham [États-Unis] ; S. C. Griffen [États-Unis] ; R. L. Hull [États-Unis] ; P. J. Havel [États-Unis] ; I. R. Sweet [États-Unis]Source :
- Diabetologia : (Berlin) [ 0012-186X ] ; 2013.
Descripteurs français
- Pascal (Inist)
- Wicri :
- topic : Calcium.
English descriptors
- KwdEn :
Abstract
Aims/hypothesis Previous studies on isolated islets have demonstrated tight coupling between calcium (Ca2+) influx and oxygen consumption rate (OCR) that is correlated with insulin secretion rate (ISR). To explain these observations, we have proposed a mechanism whereby the activation of a highly energetic process (Ca2+/metabolic coupling process [CMCP]) by Ca2+ mediates the stimulation of ISR. The aim of the study was to test whether impairment of the CMCP could play a role in the development of type 2 diabetes. Methods Glucose- and Ca2+-mediated changes in OCR and ISR in isolated islets were compared with the time course of changes of plasma insulin concentrations observed during the progression to hyperglycaemia in a rat model of type-2 diabetes (the University of California at Davis type 2 diabetes mellitus [UCD-T2DM] rat). Islets were isolated from UCD-T2DM rats before, 1 week, and 3 weeks after the onset of hyperglycaemia. Results Glucose stimulation of cytosolic Ca2+ and OCR was similar for islets harvested before and 1 week after the onset of hyperglycaemia. In contrast, a loss of decrement in islet OCR and ISR in response to Ca2+ channel blockade coincided with decreased fasting plasma insulin concentrations observed in rats 3 weeks after the onset of hyperglycaemia. Conclusions/interpretation These results suggest that phenotypic impairment of diabetic islets in the UCD-T2DM rat is downstream of Ca2+ influx and involves unregulated stimulation of the CMCP. The continuously elevated levels of CMCP induced by chronic hyperglycaemia in these islets may mediate the loss of islet function.
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Hull</name><affiliation wicri:level="4"><inist:fA14 i1="04"><s1>Department of Medicine, VA Puget Sound Health Care System and University of Washington</s1><s2>Seattle, WA</s2><s3>USA</s3><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Havel, P J" sort="Havel, P J" uniqKey="Havel P" first="P. J." last="Havel">P. J. Havel</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California</s1><s2>Davis, CA</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Sweet, I R" sort="Sweet, I R" uniqKey="Sweet I" first="I. R." last="Sweet">I. R. Sweet</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Diabetes and Obesity Center of Excellence, University of Washington, 850 Republican Street</s1><s2>Seattle, WA 98109-8055</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author></titleStmt><publicationStmt><idno type="wicri:source">INIST</idno><idno type="inist">13-0246579</idno><date when="2013">2013</date><idno type="stanalyst">PASCAL 13-0246579 INIST</idno><idno type="RBID">Pascal:13-0246579</idno><idno type="wicri:Area/PascalFrancis/Corpus">000052</idno><idno type="wicri:Area/PascalFrancis/Curation">000716</idno><idno type="wicri:Area/PascalFrancis/Checkpoint">000036</idno><idno type="wicri:doubleKey">0012-186X:2013:Rountree A:loss:of:coupling</idno><idno type="wicri:Area/Main/Merge">000196</idno></publicationStmt><sourceDesc><biblStruct><analytic><title xml:lang="en" level="a">Loss of coupling between calcium influx, energy consumption and insulin secretion associated with development of hyperglycaemia in the UCD-T2DM rat model of type 2 diabetes</title><author><name sortKey="Rountree, A M" sort="Rountree, A M" uniqKey="Rountree A" first="A. M." last="Rountree">A. M. Rountree</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Diabetes and Obesity Center of Excellence, University of Washington, 850 Republican Street</s1><s2>Seattle, WA 98109-8055</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Reed, B J" sort="Reed, B J" uniqKey="Reed B" first="B. J." last="Reed">B. J. Reed</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Diabetes and Obesity Center of Excellence, University of Washington, 850 Republican Street</s1><s2>Seattle, WA 98109-8055</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Cummings, B P" sort="Cummings, B P" uniqKey="Cummings B" first="B. P." last="Cummings">B. P. Cummings</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California</s1><s2>Davis, CA</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Jung, S R" sort="Jung, S R" uniqKey="Jung S" first="S.-R." last="Jung">S.-R. Jung</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Diabetes and Obesity Center of Excellence, University of Washington, 850 Republican Street</s1><s2>Seattle, WA 98109-8055</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Stanhope, K L" sort="Stanhope, K L" uniqKey="Stanhope K" first="K. L." last="Stanhope">K. L. Stanhope</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California</s1><s2>Davis, CA</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Graham, J L" sort="Graham, J L" uniqKey="Graham J" first="J. L." last="Graham">J. L. Graham</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California</s1><s2>Davis, CA</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Griffen, S C" sort="Griffen, S C" uniqKey="Griffen S" first="S. C." last="Griffen">S. C. Griffen</name><affiliation wicri:level="2"><inist:fA14 i1="03"><s1>Bristol-Myers Squibb</s1><s2>Princeton, NJ</s2><s3>USA</s3><sZ>7 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">New Jersey</region></placeName></affiliation></author><author><name sortKey="Hull, R L" sort="Hull, R L" uniqKey="Hull R" first="R. L." last="Hull">R. L. Hull</name><affiliation wicri:level="4"><inist:fA14 i1="04"><s1>Department of Medicine, VA Puget Sound Health Care System and University of Washington</s1><s2>Seattle, WA</s2><s3>USA</s3><sZ>8 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author><author><name sortKey="Havel, P J" sort="Havel, P J" uniqKey="Havel P" first="P. J." last="Havel">P. J. Havel</name><affiliation wicri:level="2"><inist:fA14 i1="02"><s1>Department of Molecular Biosciences, School of Veterinary Medicine and Department of Nutrition, University of California</s1><s2>Davis, CA</s2><s3>USA</s3><sZ>3 aut.</sZ><sZ>5 aut.</sZ><sZ>6 aut.</sZ><sZ>9 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Californie</region></placeName></affiliation></author><author><name sortKey="Sweet, I R" sort="Sweet, I R" uniqKey="Sweet I" first="I. R." last="Sweet">I. R. Sweet</name><affiliation wicri:level="4"><inist:fA14 i1="01"><s1>Diabetes and Obesity Center of Excellence, University of Washington, 850 Republican Street</s1><s2>Seattle, WA 98109-8055</s2><s3>USA</s3><sZ>1 aut.</sZ><sZ>2 aut.</sZ><sZ>4 aut.</sZ><sZ>10 aut.</sZ></inist:fA14><country>États-Unis</country><placeName><region type="state">Washington (État)</region><settlement type="city">Seattle</settlement></placeName><orgName type="university">Université de Washington</orgName></affiliation></author></analytic><series><title level="j" type="main">Diabetologia : (Berlin)</title><title level="j" type="abbreviated">Diabetologia : (Berl.)</title><idno type="ISSN">0012-186X</idno><imprint><date when="2013">2013</date></imprint></series></biblStruct></sourceDesc><seriesStmt><title level="j" type="main">Diabetologia : (Berlin)</title><title level="j" type="abbreviated">Diabetologia : (Berl.)</title><idno type="ISSN">0012-186X</idno></seriesStmt></fileDesc><profileDesc><textClass><keywords scheme="KwdEn" xml:lang="en"><term>Animal</term><term>Animal model</term><term>Calcium</term><term>Development</term><term>Hyperglycemia</term><term>Insulin</term><term>Oxygen consumption</term><term>Rat</term><term>Secretion</term><term>Type 2 diabetes</term></keywords><keywords scheme="Pascal" xml:lang="fr"><term>Calcium</term><term>Insuline</term><term>Sécrétion</term><term>Développement</term><term>Animal</term><term>Hyperglycémie</term><term>Modèle animal</term><term>Diabète de type 2</term><term>Consommation oxygène</term><term>Rat</term></keywords><keywords scheme="Wicri" type="topic" xml:lang="fr"><term>Calcium</term></keywords></textClass></profileDesc></teiHeader><front><div type="abstract" xml:lang="en">Aims/hypothesis Previous studies on isolated islets have demonstrated tight coupling between calcium (Ca<sup>2+</sup>) influx and oxygen consumption rate (OCR) that is correlated with insulin secretion rate (ISR). To explain these observations, we have proposed a mechanism whereby the activation of a highly energetic process (Ca<sup>2+</sup>/metabolic coupling process [CMCP]) by Ca<sup>2+</sup> mediates the stimulation of ISR. The aim of the study was to test whether impairment of the CMCP could play a role in the development of type 2 diabetes. Methods Glucose- and Ca<sup>2+</sup>-mediated changes in OCR and ISR in isolated islets were compared with the time course of changes of plasma insulin concentrations observed during the progression to hyperglycaemia in a rat model of type-2 diabetes (the University of California at Davis type 2 diabetes mellitus [UCD-T2DM] rat). Islets were isolated from UCD-T2DM rats before, 1 week, and 3 weeks after the onset of hyperglycaemia. Results Glucose stimulation of cytosolic Ca<sup>2+</sup> and OCR was similar for islets harvested before and 1 week after the onset of hyperglycaemia. In contrast, a loss of decrement in islet OCR and ISR in response to Ca<sup>2+</sup> channel blockade coincided with decreased fasting plasma insulin concentrations observed in rats 3 weeks after the onset of hyperglycaemia. Conclusions/interpretation These results suggest that phenotypic impairment of diabetic islets in the UCD-T2DM rat is downstream of Ca<sup>2+</sup> influx and involves unregulated stimulation of the CMCP. The continuously elevated levels of CMCP induced by chronic hyperglycaemia in these islets may mediate the loss of islet function.</div></front></TEI><affiliations><list><country><li>États-Unis</li></country><region><li>Californie</li><li>New Jersey</li><li>Washington (État)</li></region><settlement><li>Seattle</li></settlement><orgName><li>Université de Washington</li></orgName></list><tree><country name="États-Unis"><region name="Washington (État)"><name sortKey="Rountree, A M" sort="Rountree, A M" uniqKey="Rountree A" first="A. M." last="Rountree">A. M. Rountree</name></region><name sortKey="Cummings, B P" sort="Cummings, B P" uniqKey="Cummings B" first="B. P." last="Cummings">B. P. Cummings</name><name sortKey="Graham, J L" sort="Graham, J L" uniqKey="Graham J" first="J. L." last="Graham">J. L. Graham</name><name sortKey="Griffen, S C" sort="Griffen, S C" uniqKey="Griffen S" first="S. C." last="Griffen">S. C. Griffen</name><name sortKey="Havel, P J" sort="Havel, P J" uniqKey="Havel P" first="P. J." last="Havel">P. J. Havel</name><name sortKey="Hull, R L" sort="Hull, R L" uniqKey="Hull R" first="R. L." last="Hull">R. L. Hull</name><name sortKey="Jung, S R" sort="Jung, S R" uniqKey="Jung S" first="S.-R." last="Jung">S.-R. Jung</name><name sortKey="Reed, B J" sort="Reed, B J" uniqKey="Reed B" first="B. J." last="Reed">B. J. Reed</name><name sortKey="Stanhope, K L" sort="Stanhope, K L" uniqKey="Stanhope K" first="K. L." last="Stanhope">K. L. Stanhope</name><name sortKey="Sweet, I R" sort="Sweet, I R" uniqKey="Sweet I" first="I. R." last="Sweet">I. R. Sweet</name></country></tree></affiliations></record>Pour manipuler ce document sous Unix (Dilib)
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