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Effect of Vitamin D Supplementation ...
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Moreira-Lucas, Tracy Sousa.
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Effect of Vitamin D Supplementation on Oral Glucose Tolerance in Individuals at Risk for Developing Type 2 Diabetes.
Record Type:
Electronic resources : Monograph/item
Title/Author:
Effect of Vitamin D Supplementation on Oral Glucose Tolerance in Individuals at Risk for Developing Type 2 Diabetes./
Author:
Moreira-Lucas, Tracy Sousa.
Published:
Ann Arbor : ProQuest Dissertations & Theses, : 2018,
Description:
225 p.
Notes:
Source: Dissertations Abstracts International, Volume: 80-02, Section: B.
Contained By:
Dissertations Abstracts International80-02B.
Subject:
Endocrinology. -
Online resource:
http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10787248
ISBN:
9780438187894
Effect of Vitamin D Supplementation on Oral Glucose Tolerance in Individuals at Risk for Developing Type 2 Diabetes.
Moreira-Lucas, Tracy Sousa.
Effect of Vitamin D Supplementation on Oral Glucose Tolerance in Individuals at Risk for Developing Type 2 Diabetes.
- Ann Arbor : ProQuest Dissertations & Theses, 2018 - 225 p.
Source: Dissertations Abstracts International, Volume: 80-02, Section: B.
Thesis (Ph.D.)--University of Toronto (Canada), 2018.
This item must not be sold to any third party vendors.
Vitamin D status is inversely associated with insulin resistance, β-cell dysfunction, and an increased risk for type 2 diabetes (T2D). Clinical trials examining the effect of vitamin D supplementation on various glycemic outcomes and incident T2D have been equivocal. The objectives of this thesis were to determine the effect of weekly vitamin D3 supplementation on oral glucose tolerance, indices of insulin resistance/sensitivity and β-cell function and inflammatory markers in individuals at an increased risk for T2D. We conducted a 24-week, double-blind, randomized, placebo-controlled trial to examine the effect of 28,000 IU of vitamin D3 once weekly on plasma glucose 2 hours after a 75g oral glucose tolerance test (2hPC glucose) and additional glucose-related outcome measures. Seventy-one participants with serum 25-hydroxyvitamin-D [25(OH)D] ≤65 nmol/L, impaired fasting glucose, and/or elevated glycated haemoglobin (HbA1c) were randomly assigned to receive 28,000 IU of vitamin D3 (vitD, n=35) or placebo (n=36) cheese once weekly. The primary outcome was the change in 2hPC glucose. Additional outcomes of interest included fasting glucose, fasting and postprandial insulin, insulin resistance/sensitivity and β-cell function, HbA1c, fasting lipids and inflammatory biomarkers. Participants underwent an oral glucose tolerance test at baseline and week-24. Mean±SD baseline 25(OH)D was 48.1±14.3 and 47.6±14.3 nmol/L in the vitD and placebo groups, respectively; vitamin D3 supplementation increased 25(OH)D to 98.7±36.8 nmol/L (p<0.0001). No effects on 2hPC glucose (0.04, vitD vs 0.03 mmol/L, placebo; p=0.55) or other glycemic-related measures including HbA1c (p=0.60) were observed. Subgroup analyses of individuals with 25(OH)D <50 nmol/L and prediabetes (n=14, vitD; n=14, placebo) did not alter these results. LDL-cholesterol was significantly reduced in the vitD group compared to placebo (-0.27 vs. 0.01 mmol/L; p=0.03) with no significant differences in LDL response to supplementation between males and females (-0.137 and -0.165; p=0.85). No effect on markers of inflammation including CRP (p=0.72), IL-6 (p=0.59), leptin (p=0.48) and TNFα (p=0.10), or anti-inflammatory adiponectin (p=0.95). Vitamin D supplementation did not improve oral glucose tolerance, glycemic markers or inflammation, but significantly reduced LDL-cholesterol. Future work should examine the effect of long-term vitamin D supplementation in individuals with 25(OH)D <50 nmol/L and who are at high-risk for T2D.
ISBN: 9780438187894Subjects--Topical Terms:
610914
Endocrinology.
Subjects--Index Terms:
Beta-cell function
Effect of Vitamin D Supplementation on Oral Glucose Tolerance in Individuals at Risk for Developing Type 2 Diabetes.
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Vitamin D status is inversely associated with insulin resistance, β-cell dysfunction, and an increased risk for type 2 diabetes (T2D). Clinical trials examining the effect of vitamin D supplementation on various glycemic outcomes and incident T2D have been equivocal. The objectives of this thesis were to determine the effect of weekly vitamin D3 supplementation on oral glucose tolerance, indices of insulin resistance/sensitivity and β-cell function and inflammatory markers in individuals at an increased risk for T2D. We conducted a 24-week, double-blind, randomized, placebo-controlled trial to examine the effect of 28,000 IU of vitamin D3 once weekly on plasma glucose 2 hours after a 75g oral glucose tolerance test (2hPC glucose) and additional glucose-related outcome measures. Seventy-one participants with serum 25-hydroxyvitamin-D [25(OH)D] ≤65 nmol/L, impaired fasting glucose, and/or elevated glycated haemoglobin (HbA1c) were randomly assigned to receive 28,000 IU of vitamin D3 (vitD, n=35) or placebo (n=36) cheese once weekly. The primary outcome was the change in 2hPC glucose. Additional outcomes of interest included fasting glucose, fasting and postprandial insulin, insulin resistance/sensitivity and β-cell function, HbA1c, fasting lipids and inflammatory biomarkers. Participants underwent an oral glucose tolerance test at baseline and week-24. Mean±SD baseline 25(OH)D was 48.1±14.3 and 47.6±14.3 nmol/L in the vitD and placebo groups, respectively; vitamin D3 supplementation increased 25(OH)D to 98.7±36.8 nmol/L (p<0.0001). No effects on 2hPC glucose (0.04, vitD vs 0.03 mmol/L, placebo; p=0.55) or other glycemic-related measures including HbA1c (p=0.60) were observed. Subgroup analyses of individuals with 25(OH)D <50 nmol/L and prediabetes (n=14, vitD; n=14, placebo) did not alter these results. LDL-cholesterol was significantly reduced in the vitD group compared to placebo (-0.27 vs. 0.01 mmol/L; p=0.03) with no significant differences in LDL response to supplementation between males and females (-0.137 and -0.165; p=0.85). No effect on markers of inflammation including CRP (p=0.72), IL-6 (p=0.59), leptin (p=0.48) and TNFα (p=0.10), or anti-inflammatory adiponectin (p=0.95). Vitamin D supplementation did not improve oral glucose tolerance, glycemic markers or inflammation, but significantly reduced LDL-cholesterol. Future work should examine the effect of long-term vitamin D supplementation in individuals with 25(OH)D <50 nmol/L and who are at high-risk for T2D.
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http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=10787248
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