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

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

55 Downloads (Pure)

Resumé

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 age-, sex-and BMI-matched healthy controls with an extended 4-h oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on the 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-S 1) 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. VO 2max, but not BMI, waist and hip circumferences, lean and fat body mass%, MET or grip strength, was lower in mutation carriers. BIGTT-S 1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO 2max 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.

OriginalsprogEngelsk
TidsskriftEndocrine Connections
Vol/bind8
Udgave nummer7
Sider (fra-til)829–837
ISSN2049-3614
DOI
StatusUdgivet - jun. 2019

Fingeraftryk

Insulin Resistance
Glucose Tolerance Test
Insulin
Mutation
Fat Body
Photon Absorptiometry
Hip
Lactic Acid
Fasting
Regression Analysis
Peptides

Emneord

  • Mitochondrial Diseases/genetics
  • Diabetes

Citer dette

@article{86cd7fcdef2142dbb4dea5c8e6950084,
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 age-, sex-and BMI-matched healthy controls with an extended 4-h oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on the 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-S 1) 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. VO 2max, but not BMI, waist and hip circumferences, lean and fat body mass{\%}, MET or grip strength, was lower in mutation carriers. BIGTT-S 1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO 2max 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 = "Mitochondrial Diseases/genetics, Diabetes, 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 Morten Frost and Yderstr{\ae}de, {Knud Bonnet} and Andersen, {Per Heden}",
year = "2019",
month = "6",
doi = "10.1530/EC-19-0118",
language = "English",
volume = "8",
pages = "829–837",
journal = "Endocrine Connections",
issn = "2049-3614",
publisher = "BioScientifica Ltd.",
number = "7",

}

Mitochondrial mutation m.3243A>G associates with insulin resistance in non-diabetic carriers. / Langdahl, Jakob Høgild; Frederiksen, Anja Lisbeth; Vissing, John; Frost, Morten; Yderstræde, Knud Bonnet; Andersen, Per Heden.

I: Endocrine Connections, Bind 8, Nr. 7, 06.2019, s. 829–837.

Publikation: Bidrag til tidsskriftTidsskriftartikelForskningpeer review

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 - Frost, Morten

AU - Yderstræde, Knud Bonnet

AU - Andersen, Per Heden

PY - 2019/6

Y1 - 2019/6

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 age-, sex-and BMI-matched healthy controls with an extended 4-h oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on the 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-S 1) 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. VO 2max, but not BMI, waist and hip circumferences, lean and fat body mass%, MET or grip strength, was lower in mutation carriers. BIGTT-S 1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO 2max 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 age-, sex-and BMI-matched healthy controls with an extended 4-h oral glucose tolerance test (OGTT). Insulin sensitivity index and acute insulin response were estimated on the 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-S 1) 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. VO 2max, but not BMI, waist and hip circumferences, lean and fat body mass%, MET or grip strength, was lower in mutation carriers. BIGTT-S 1 remained lower in mutation carriers after adjustment for multiple confounding factors including VO 2max 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 - Mitochondrial Diseases/genetics

KW - Diabetes

KW - Insulin resistance

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

KW - Mitochondrial dysfunction

KW - Monogenic diabetes

U2 - 10.1530/EC-19-0118

DO - 10.1530/EC-19-0118

M3 - Journal article

C2 - 31146262

VL - 8

SP - 829

EP - 837

JO - Endocrine Connections

JF - Endocrine Connections

SN - 2049-3614

IS - 7

ER -