Richard J Millstein1, Laura L Pyle2, Bryan C Bergman3, Robert H Eckel4, David M Maahs5, Marian J Rewers6, Irene E Schauer7, Janet K Snell-Bergeon8. 1. Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, University of Colorado Denver Anschutz Medical Campus, Aurora, CO, United States; Division of Endocrinology, VA Eastern Colorado Health Care System, Denver, CO, United States. Electronic address: Richard.millstein@ucdenver.edu. 2. Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Biostatistics and Informatics, Colorado School of Public Health, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: laura.pyle@ucdenver.edu. 3. Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, University of Colorado Denver Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Bryan.bergman@ucdenver.edu. 4. Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, University of Colorado Denver Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Robert.Eckel@ucdenver.edu. 5. Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, United States; Department of Pediatrics, Division of Pediatric Endocrinology and Diabetes, Stanford University School of Medicine, Stanford, CA, United States.. Electronic address: dmaahs@stanford.edu. 6. Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Marian.rewers@ucdenver.edu. 7. Division of Endocrinology, Metabolism, and Diabetes, Department of Medicine, University of Colorado Denver Anschutz Medical Campus, Aurora, CO, United States; Division of Endocrinology, VA Eastern Colorado Health Care System, Denver, CO, United States; Eastern Colorado Geriatric Research, Education, and Clinical Center, United States. Electronic address: Irene.schauer@ucdenver.edu. 8. Barbara Davis Center for Childhood Diabetes, University of Colorado Anschutz Medical Campus, Aurora, CO, United States. Electronic address: Janet.snell-bergeon@ucdenver.edu.
Abstract
OBJECTIVE: To test the hypothesis that multitissue deficits in insulin sensitivity are greater among women than men with type 1 diabetes compared to respective controls. RESEARCH DESIGN AND METHODS: Three-stage hyperinsulinemic-euglycemic clamps (4, 8, 40 mU/m2/min) were performed on 41 people with type 1 diabetes and 47 adults without diabetes (mean ± SD age 46 ± 8). Infusions of [1-13C]palmitate, [1,1,2,3,3-2H2]glycerol, and [6,6-2H2]glucose isotope tracers were used to determine free fatty acid (FFA), glycerol, and glucose kinetics in 52 of these participants (25 M and 27 W). RESULTS: There was no difference in age or BMI by type 1 diabetes status in either sex. Free fatty acid rate of appearance (FFA Ra) was higher in both sexes with type 1 diabetes compared to those without diabetes during stages 1 and 2. The same was seen with glycerol for stages 1 and 2. During stage 3 glucose rate of disappearance (Rd) was lower in those with type 1 diabetes among both sexes. All had sex by type 1 diabetes interactions with greater deficits in insulin sensitivity in women. While there was no sex by diabetes interaction in regards to glucose rate of appearance (Ra), those with type 1 diabetes had a higher glucose Ra than those without diabetes. CONCLUSIONS: We found that type 1 diabetes affected adipose and skeletal muscle insulin sensitivity to a greater extent in women than in men, perhaps contributing to the greater relative increase in cardiovascular risk in women with type 1 diabetes.
OBJECTIVE: To test the hypothesis that multitissue deficits in insulin sensitivity are greater among women than men with type 1 diabetes compared to respective controls. RESEARCH DESIGN AND METHODS: Three-stage hyperinsulinemic-euglycemic clamps (4, 8, 40 mU/m2/min) were performed on 41 people with type 1 diabetes and 47 adults without diabetes (mean ± SD age 46 ± 8). Infusions of [1-13C]palmitate, [1,1,2,3,3-2H2]glycerol, and [6,6-2H2]glucose isotope tracers were used to determine free fatty acid (FFA), glycerol, and glucose kinetics in 52 of these participants (25 M and 27 W). RESULTS: There was no difference in age or BMI by type 1 diabetes status in either sex. Free fatty acid rate of appearance (FFARa) was higher in both sexes with type 1 diabetes compared to those without diabetes during stages 1 and 2. The same was seen with glycerol for stages 1 and 2. During stage 3 glucose rate of disappearance (Rd) was lower in those with type 1 diabetes among both sexes. All had sex by type 1 diabetes interactions with greater deficits in insulin sensitivity in women. While there was no sex by diabetes interaction in regards to glucose rate of appearance (Ra), those with type 1 diabetes had a higher glucose Ra than those without diabetes. CONCLUSIONS: We found that type 1 diabetes affected adipose and skeletal muscle insulin sensitivity to a greater extent in women than in men, perhaps contributing to the greater relative increase in cardiovascular risk in women with type 1 diabetes.
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