Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects

Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects Helen Karakelides 1 , Yan W. Asmann 1 , Maureen L. Bigelow 1 , Kevin R. Short 1 , Ketan Dhatariya 1 , Jill Coenen-Schimke 1 , Jane Kahl 1 , Debabrata Mukhopadhyay 2 and K. Sree...

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Bibliographic Details
Published inDiabetes (New York, N.Y.) Vol. 56; no. 11; pp. 2683 - 2689
Main Authors Karakelides, Helen, Asmann, Yan W., Bigelow, Maureen L., Short, Kevin R., Dhatariya, Ketan, Coenen-Schimke, Jill, Kahl, Jane, Mukhopadhyay, Debabrata, Nair, K. Sreekumaran
Format Journal Article
LanguageEnglish
Published Alexandria, VA American Diabetes Association 01.11.2007
Subjects
Adenosine Triphosphate - metabolism
Adult
Amino acids
Biological and medical sciences
Blood Glucose - metabolism
Body Mass Index
Cardiovascular disease
Catheters
Cytochrome
Diabetes
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - metabolism
Diabetes. Impaired glucose tolerance
Diabetics
DNA Primers
Dosage and administration
Drug therapy
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Evaluation
Fatty Acids, Nonesterified - blood
Genes
Genetic aspects
Genetic transcription
Glucose
Health aspects
Humans
Hypotheses
Insulin
Insulin - deficiency
Insulin resistance
Medical sciences
Mitochondria, Muscle - metabolism
Mitochondrial DNA
Muscle, Skeletal - metabolism
Oligonucleotide Array Sequence Analysis
Oxidative Phosphorylation
Peptides
Phosphorylation
Plasma
Polymerase Chain Reaction
Protons
Research design
Transcription (Genetics)
Transcription, Genetic
Type 1 diabetes
Vascular endothelial growth factor
United States
Endocrinopathy
Human
Immunopathology
Pancreatic hormone
Mitochondria
Gene
Type 1 diabetes
Autoimmune disease
Muscle
ATP
Insulin
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Abstract Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects Helen Karakelides 1 , Yan W. Asmann 1 , Maureen L. Bigelow 1 , Kevin R. Short 1 , Ketan Dhatariya 1 , Jill Coenen-Schimke 1 , Jane Kahl 1 , Debabrata Mukhopadhyay 2 and K. Sreekumaran Nair 1 1 Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 2 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota Address correspondence and reprint requests to K. Sreekumaran Nair, MD, PhD, Mayo Clinic, 200 First St. SW, Joseph 5-194, Rochester, MN 55905. E-mail: nair.sree{at}mayo.edu Abstract OBJECTIVE—Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. RESEARCH DESIGN AND METHODS—We withdrew insulin for 8.6 ± 0.6 h in nine C-peptide–negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. RESULTS—Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, β-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. CONCLUSIONS—Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred. COX5B, cytochrome c oxidase subunit 5 CRU, Clinical Research Unit HIF, hypoxia-inducible factor IPA, ingenuity pathway analysis MAPR, mitochondrial ATP production rate NIH, National Institutes of Health SDH, succinate dehydrogenase TCA, tricarboxylic acid TFAM, mitochondrial transcription factor A UCP, uncoupling protein UQCR, ubiquinol cytochrome c reductase VEGF, vascular endothelial growth factor Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 27 July 2007. DOI: 10.2337/db07-0378. Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-0378 . The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Received March 20, 2007. Accepted July 23, 2007. DIABETES
AbstractList OBJECTIVE—Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. RESEARCH DESIGN AND METHODS—We withdrew insulin for 8.6 ± 0.6 h in nine C-peptide–negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. RESULTS—Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, β-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. CONCLUSIONS—Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.
Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. We withdrew insulin for 8.6 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.
Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects Helen Karakelides 1 , Yan W. Asmann 1 , Maureen L. Bigelow 1 , Kevin R. Short 1 , Ketan Dhatariya 1 , Jill Coenen-Schimke 1 , Jane Kahl 1 , Debabrata Mukhopadhyay 2 and K. Sreekumaran Nair 1 1 Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota 2 Department of Biochemistry and Molecular Biology, Mayo Clinic, Rochester, Minnesota Address correspondence and reprint requests to K. Sreekumaran Nair, MD, PhD, Mayo Clinic, 200 First St. SW, Joseph 5-194, Rochester, MN 55905. E-mail: nair.sree{at}mayo.edu Abstract OBJECTIVE—Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. RESEARCH DESIGN AND METHODS—We withdrew insulin for 8.6 ± 0.6 h in nine C-peptide–negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. RESULTS—Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, β-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. CONCLUSIONS—Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred. COX5B, cytochrome c oxidase subunit 5 CRU, Clinical Research Unit HIF, hypoxia-inducible factor IPA, ingenuity pathway analysis MAPR, mitochondrial ATP production rate NIH, National Institutes of Health SDH, succinate dehydrogenase TCA, tricarboxylic acid TFAM, mitochondrial transcription factor A UCP, uncoupling protein UQCR, ubiquinol cytochrome c reductase VEGF, vascular endothelial growth factor Footnotes Published ahead of print at http://diabetes.diabetesjournals.org on 27 July 2007. DOI: 10.2337/db07-0378. Additional information for this article can be found in an online appendix at http://dx.doi.org/10.2337/db07-0378 . The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked “advertisement” in accordance with 18 U.S.C. Section 1734 solely to indicate this fact. Received March 20, 2007. Accepted July 23, 2007. DIABETES
Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment.OBJECTIVEMuscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment.We withdrew insulin for 8.6 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen.RESEARCH DESIGN AND METHODSWe withdrew insulin for 8.6 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen.Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased.RESULTSWithdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased.Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.CONCLUSIONSInsulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.
Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. We withdrew insulin for 8.6 +/- 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, beta-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.
OBJECTIVE-Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may cause insulin resistance. We determined the impact of insulin deficiency on muscle mitochondrial ATP production by temporarily depriving type 1 diabetic patients of insulin treatment. RESEARCH DESIGN AND METHODS-We withdrew insulin for 8.6 plus or minus 0.6 h in nine C-peptide-negative type 1 diabetic subjects and measured muscle mitochondrial ATP production and gene transcript levels (gene array and real-time quantitative PCR) and compared with insulin-treated state. We also measured oxygen consumption (indirect calorimetry); plasma levels of glucagon, bicarbonate, and other substrates; and urinary nitrogen. RESULTS-Withdrawal of insulin resulted in increased plasma glucose, branched chain amino acids, nonesterified fatty acids, {szligbeta}-hydroxybutyrate, and urinary nitrogen but no change in bicarbonate. Insulin deprivation decreased muscle mitochondrial ATP production rate (MAPR) despite an increase in whole-body oxygen consumption and altered expression of many muscle mitochondrial gene transcripts. Transcript levels of genes involved in oxidative phosphorylation were decreased, whereas those involved in vascular endothelial growth factor (VEGF) signaling, inflammation, cytoskeleton signaling, and integrin signaling pathways were increased. CONCLUSIONS-Insulin deficiency and associated metabolic changes reduce muscle MAPR and expression of oxidative phosphorylation genes in type 1 diabetes despite an increase in whole-body oxygen consumption. Increase in transcript levels of genes involved in VEGF, inflammation, cytoskeleton, and integrin signaling pathways suggest that vascular factors and cell proliferation that may interact with mitochondrial changes occurred.
Audience Professional
Author K. Sreekumaran Nair
Helen Karakelides
Kevin R. Short
Yan W. Asmann
Debabrata Mukhopadhyay
Maureen L. Bigelow
Jill Coenen-Schimke
Jane Kahl
Ketan Dhatariya
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  givenname: Maureen L.
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  fullname: Bigelow, Maureen L.
  organization: Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
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  givenname: Kevin R.
  surname: Short
  fullname: Short, Kevin R.
  organization: Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
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  fullname: Dhatariya, Ketan
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  surname: Coenen-Schimke
  fullname: Coenen-Schimke, Jill
  organization: Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
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  surname: Kahl
  fullname: Kahl, Jane
  organization: Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
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  surname: Mukhopadhyay
  fullname: Mukhopadhyay, Debabrata
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  givenname: K. Sreekumaran
  surname: Nair
  fullname: Nair, K. Sreekumaran
  organization: Division of Endocrinology and Metabolism and Endocrine Research Unit, Mayo Clinic, Rochester, Minnesota
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ClassificationCodes 2834
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Copyright 2008 INIST-CNRS
COPYRIGHT 2007 American Diabetes Association
Copyright American Diabetes Association Nov 2007
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Issue 11
Keywords Endocrinopathy
Human
Immunopathology
Pancreatic hormone
Mitochondria
Gene
Type 1 diabetes
Autoimmune disease
Muscle
ATP
Insulin
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Snippet Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects Helen Karakelides 1 , Yan W. Asmann...
OBJECTIVE—Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial...
Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial dysfunction may...
OBJECTIVE-Muscle mitochondrial dysfunction occurs in many insulin-resistant states, such as type 2 diabetes, prompting a hypothesis that mitochondrial...
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SubjectTerms Adenosine Triphosphate - metabolism
Adult
Amino acids
Biological and medical sciences
Blood Glucose - metabolism
Body Mass Index
Cardiovascular disease
Catheters
Cytochrome
Diabetes
Diabetes Mellitus, Type 1 - blood
Diabetes Mellitus, Type 1 - genetics
Diabetes Mellitus, Type 1 - metabolism
Diabetes. Impaired glucose tolerance
Diabetics
DNA Primers
Dosage and administration
Drug therapy
Endocrine pancreas. Apud cells (diseases)
Endocrinopathies
Etiopathogenesis. Screening. Investigations. Target tissue resistance
Evaluation
Fatty Acids, Nonesterified - blood
Genes
Genetic aspects
Genetic transcription
Glucose
Health aspects
Humans
Hypotheses
Insulin
Insulin - deficiency
Insulin resistance
Medical sciences
Mitochondria, Muscle - metabolism
Mitochondrial DNA
Muscle, Skeletal - metabolism
Oligonucleotide Array Sequence Analysis
Oxidative Phosphorylation
Peptides
Phosphorylation
Plasma
Polymerase Chain Reaction
Protons
Research design
Transcription (Genetics)
Transcription, Genetic
Type 1 diabetes
Vascular endothelial growth factor
Title Effect of Insulin Deprivation on Muscle Mitochondrial ATP Production and Gene Transcript Levels in Type 1 Diabetic Subjects
URI http://diabetes.diabetesjournals.org/content/56/11/2683.abstract
https://www.ncbi.nlm.nih.gov/pubmed/17660267
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