Insulin secretion and insulin sensitivity are normal in non‐diabetic subjects from maternal inheritance diabetes and deafness families

Holmes-Walker, D Jane; Ward, Glenn; Boyages, Steven

doi:10.1046/j.1464-5491.2001.00472.x

Cited by 5 publications

(4 citation statements)

References 41 publications

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“…It demonstrated that the IGI was decreased in seven m.3243AϾG carriers with normal glucose tolerance. However, in other studies, defects in insulin secretion have not been found (22,23). We found an inverse relationship between ␤-cell responses and the m.3243AϾG mutation heteroplasmy.…”

Section: M3243a>g Mutation: Insulin Secretion and Actionsupporting

confidence: 40%

m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

et al. 2009

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OBJECTIVE-To study insulin sensitivity and perfusion in skeletal muscle together with the ␤-cell function in subjects with the m.3243AϾG mutation in mitochondrial DNA, the most common cause of mitochondrial diabetes. These patients included five subjects with no diabetes as defined by the oral glucose tolerance test (OGTT) (group 1), three with GHb Ͻ6.1% and newly found diabetes by OGTT (group 2), and seven with a previously diagnosed diabetes (group 3). Control subjects consisted of 13 healthy individuals who were similar to the carriers of m.3243AϾG with respect to age and physical activity. ␤-Cell function was assessed using the OGTT and subsequent mathematical modeling. RESEARCH DESIGN AND METHODS-WeRESULTS-Skeletal muscle glucose uptake was significantly lower in groups 1, 2, and 3 than in the control subjects. The glucose sensitivity of ␤-cells in group 1 patients was similar to that of the control subjects, whereas in group 2 and 3 patients, the glucose sensitivity was significantly lower. The insulin secretion parameters correlated strongly with the proportion of m.3243AϾG mutation in muscle.CONCLUSIONS-Our findings show that subjects with m.3243A ϾG are insulin resistant in skeletal muscle even when ␤-cell function is not markedly impaired or glucose control compromised. We suggest that both the skeletal muscle insulin sensitivity and the ␤-cell function are affected before the onset of the mitochondrial diabetes caused by the m.3243AϾG mutation.

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Section: M3243a>g Mutation: Insulin Secretion and Actionsupporting

confidence: 40%

m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

et al. 2009

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“…In 11 non-diabetic m.3243A>g carriers, the main finding was isolated higher p-glucose levels in an OGTT, while insulin levels were similar to the control group (2). A study of 10 NGT and 2 IGT mutation carriers demonstrated elevated glucose and insulin levels in an OGTT similar to the present study (18). Additionally, there was a non-significant trend toward reduced insulin sensitivity that was compensated by increased glucose effectiveness in an IVGTT (18).…”

Section: Discussionsupporting

confidence: 89%

“…A study of 10 NGT and 2 IGT mutation carriers demonstrated elevated glucose and insulin levels in an OGTT similar to the present study (18). Additionally, there was a non-significant trend toward reduced insulin sensitivity that was compensated by increased glucose effectiveness in an IVGTT (18). Insulin secretion defect has been demonstrated in non-DM m.3243A>G carriers with a progressive pattern from subjects with NGT toward subjects with manifest DM (17).…”

Section: Discussionsupporting

confidence: 89%

“…The insulin secretion defect progressed from carriers with normal glucose tolerance (NGT) over carriers with IGT to carriers with DM (17). Two studies of 25 and 12 non-diabetic m.3243A>G carriers reported none or only subtle impairments of insulin response to an OGTT (7, 18). First- and second-phase insulin secretion was reduced in hyperglycemic clamp studies of two and seven m.3243A>G carriers (7, 19).…”

Section: Introductionmentioning

confidence: 99%

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

Langdahl

Frederiksen

Vissing

et al. 2019

Endocrine Connections

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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-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.

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Current Awareness

2001

Diabetes Metabolism Res

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In order to keep subscribers up‐to‐date with the latest developments in their field, John Wiley & Sons are providing a current awareness service in each issue of the journal. The bibliography contains newly published material in the field of diabetes/metabolism. Each bibliography is divided into 17 sections: 1 Books, Reviews & Symposia; 2 General; 3 Genetics; 4 Epidemiology; 5 Immunology; 6 Prediction; 7 Prevention; 8 Intervention: a) General; b) Pharmacology; 9 Pathology: a) General; b) Cardiovascular; c) Neurological; d) Renal; 10 Endocrinology & Metabolism; 11 Nutrition; 12 Animal Studies; 13 Techniques. Within each section, articles are listed in alphabetical order with respect to author (12 Weeks journals ‐ Search completed at 24th Oct 2001)

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Insulin secretion and insulin sensitivity are normal in non‐diabetic subjects from maternal inheritance diabetes and deafness families

Abstract: While there appear to be subtle defects of glucose handling in non-diabetic subjects with the 3243 mutation, these could not be explained by differences in insulin sensitivity or secretion.

Cited by 5 publications

References 41 publications

m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

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

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Insulin secretion and insulin sensitivity are normal in non‐diabetic subjects from maternal inheritance diabetes and deafness families

Abstract: While there appear to be subtle defects of glucose handling in non-diabetic subjects with the 3243 mutation, these could not be explained by differences in insulin sensitivity or secretion.

Cited by 5 publications

References 41 publications

m.3243A&gt;G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

m.3243A&gt;G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

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

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m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction

m.3243A>G Mutation in Mitochondrial DNA Leads to Decreased Insulin Sensitivity in Skeletal Muscle and to Progressive β-Cell Dysfunction