Journal
WORLD JOURNAL OF DIABETES
Volume 6, Issue 1, Pages 8-16Publisher
BAISHIDENG PUBLISHING GROUP INC
DOI: 10.4239/wjd.v6.i1.8
Keywords
Type 1 diabetes; Insulin sensitivity; Vascular complications; Hyperfiltration; Cystatin C; Creatinine; Glomerular filtration rate
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Funding
- NCATS NIH HHS [UL1 TR001082] Funding Source: Medline
- NHLBI NIH HHS [R01 HL113029] Funding Source: Medline
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Despite improvements in glucose, lipids and blood pressure control, vascular complications remain the most important cause of morbidity and mortality in patients with type 1 diabetes. For that reason, there is a need to identify additional risk factors to utilize in clinical practice or translate to novel therapies to prevent vascular complications. Reduced insulin sensitivity is an increasingly recognized component of type 1 diabetes that has been linked with the development and progression of both micro- and macrovascular complications. Adolescents and adults with type 1 diabetes have reduced insulin sensitivity, even when compared to their non-diabetic counterparts of similar adiposity, serum triglycerides, high-density lipoprotein cholesterol, level of habitual physical activity, and in adolescents, pubertal stage. Reduced insulin sensitivity is thought to contribute both to the initiation and progression of macro-and microvascular complications in type 1 diabetes. There are currently clinical trials underway examining the benefits of improving insulin sensitivity with regards to vascular complications in type 1 diabetes. Reduced insulin sensitivity is an increasingly recognized component of type 1 diabetes, is implicated in the pathogenesis of vascular complications and is potentially an important therapeutic target to prevent vascular complications. In this review, we will focus on the pathophysiologic contribution of insulin sensitivity to vascular complications and summarize related ongoing clinical trials.
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