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Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers

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Langdahl, JH, Frederiksen, AL, Vissing, J, Nielsen, MF, Yderstræde, KB & Andersen, PH 2019, 'Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers' Endocrine Connections, bind 8, nr. 7, s. 829-837. https://doi.org/10.1530/EC-19-0118

APA

Langdahl, J. H., Frederiksen, A. L., Vissing, J., Nielsen, M. F., Yderstræde, K. B., & Andersen, P. H. (2019). Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers. Endocrine Connections, 8(7), 829-837. https://doi.org/10.1530/EC-19-0118

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Author

Langdahl, Jakob Høgild ; Frederiksen, Anja Lisbeth ; Vissing, John ; Nielsen, Morten Frost ; Yderstræde, Knud Bonnet ; Andersen, Per Heden. / Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers. I: Endocrine Connections. 2019 ; Bind 8, Nr. 7. s. 829-837.

Bibtex

@article{c5a054294e8c40f185148dc832893074,
title = "Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers",
abstract = "AIM: This case-control study aimed to examine impairments in glucose metabolism in non-diabetic carriers of the mitochondrial mutation m.3243A>G by evaluating insulin secretion capacity and sensitivity.METHODS: Glucose metabolism was investigated in 23 non-diabetic m.3243A>G carriers and matched healthy controls with an extended 4-hour oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on basis of the OGTT. This was accompanied by examination of body composition by Dual-energy X-ray Absorptiometry (DXA), maximum aerobic capacity, and a Recent Physical Activity Questionnaire (RPAQ).RESULTS: Fasting p-glucose, s-insulin and s-c-peptide levels did not differ between m.3243A>G carriers and controls. Insulin sensitivity index (BIGTT-S1) was significantly lower in the m.3243A>G carriers, but there was no difference in the acute insulin response between groups. P-lactate levels were higher in carriers throughout the OGTT. VO2max, but not BMI, waist and hip circumferences, lean and fat body mass {\%}, MET or grip strength, was lower in mutation carriers. BIGTT-S1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO2max in regression analyses.CONCLUSIONS: Glucose metabolism in m.3243A>G carriers was characterized by reduced insulin sensitivity, which could represent the earliest phase in the pathogenesis of m.3243A>G-associated diabetes.",
keywords = "Insulin resistance, Mitochondrial DNA point mutation m.3243A>G, Mitochondrial dysfunction, Monogenic diabetes",
author = "Langdahl, {Jakob H{\o}gild} and Frederiksen, {Anja Lisbeth} and John Vissing and Nielsen, {Morten Frost} and Yderstr{\ae}de, {Knud Bonnet} and Andersen, {Per Heden}",
year = "2019",
month = "5",
day = "1",
doi = "10.1530/EC-19-0118",
language = "English",
volume = "8",
pages = "829--837",
journal = "Endocrine Connections",
issn = "2049-3614",
publisher = "BioScientifica Ltd",
number = "7",

}

RIS

TY - JOUR

T1 - Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers

AU - Langdahl, Jakob Høgild

AU - Frederiksen, Anja Lisbeth

AU - Vissing, John

AU - Nielsen, Morten Frost

AU - Yderstræde, Knud Bonnet

AU - Andersen, Per Heden

PY - 2019/5/1

Y1 - 2019/5/1

N2 - AIM: This case-control study aimed to examine impairments in glucose metabolism in non-diabetic carriers of the mitochondrial mutation m.3243A>G by evaluating insulin secretion capacity and sensitivity.METHODS: Glucose metabolism was investigated in 23 non-diabetic m.3243A>G carriers and matched healthy controls with an extended 4-hour oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on basis of the OGTT. This was accompanied by examination of body composition by Dual-energy X-ray Absorptiometry (DXA), maximum aerobic capacity, and a Recent Physical Activity Questionnaire (RPAQ).RESULTS: Fasting p-glucose, s-insulin and s-c-peptide levels did not differ between m.3243A>G carriers and controls. Insulin sensitivity index (BIGTT-S1) was significantly lower in the m.3243A>G carriers, but there was no difference in the acute insulin response between groups. P-lactate levels were higher in carriers throughout the OGTT. VO2max, but not BMI, waist and hip circumferences, lean and fat body mass %, MET or grip strength, was lower in mutation carriers. BIGTT-S1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO2max in regression analyses.CONCLUSIONS: Glucose metabolism in m.3243A>G carriers was characterized by reduced insulin sensitivity, which could represent the earliest phase in the pathogenesis of m.3243A>G-associated diabetes.

AB - AIM: This case-control study aimed to examine impairments in glucose metabolism in non-diabetic carriers of the mitochondrial mutation m.3243A>G by evaluating insulin secretion capacity and sensitivity.METHODS: Glucose metabolism was investigated in 23 non-diabetic m.3243A>G carriers and matched healthy controls with an extended 4-hour oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on basis of the OGTT. This was accompanied by examination of body composition by Dual-energy X-ray Absorptiometry (DXA), maximum aerobic capacity, and a Recent Physical Activity Questionnaire (RPAQ).RESULTS: Fasting p-glucose, s-insulin and s-c-peptide levels did not differ between m.3243A>G carriers and controls. Insulin sensitivity index (BIGTT-S1) was significantly lower in the m.3243A>G carriers, but there was no difference in the acute insulin response between groups. P-lactate levels were higher in carriers throughout the OGTT. VO2max, but not BMI, waist and hip circumferences, lean and fat body mass %, MET or grip strength, was lower in mutation carriers. BIGTT-S1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO2max in regression analyses.CONCLUSIONS: Glucose metabolism in m.3243A>G carriers was characterized by reduced insulin sensitivity, which could represent the earliest phase in the pathogenesis of m.3243A>G-associated diabetes.

KW - Insulin resistance

KW - Mitochondrial DNA point mutation m.3243A>G

KW - Mitochondrial dysfunction

KW - Monogenic diabetes

UR - http://www.scopus.com/inward/record.url?scp=85069721076&partnerID=8YFLogxK

U2 - 10.1530/EC-19-0118

DO - 10.1530/EC-19-0118

M3 - Journal article

VL - 8

SP - 829

EP - 837

JO - Endocrine Connections

JF - Endocrine Connections

SN - 2049-3614

IS - 7

ER -

ID: 58155781