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Review
. 2017 Dec 1;102(12):4343-4410.
doi: 10.1210/jc.2017-01922.

Diabetic Microvascular Disease: An Endocrine Society Scientific Statement

Eugene J Barrett  1 , Zhenqi Liu  1 , Mogher Khamaisi  2 , George L King  2 , Ronald Klein  3 , Barbara E K Klein  3 , Timothy M Hughes  4 , Suzanne Craft  4 , Barry I Freedman  5 , Donald W Bowden  5 , Aaron I Vinik  6 , Carolina M Casellini  6
Affiliations
Review

Diabetic Microvascular Disease: An Endocrine Society Scientific Statement

Eugene J Barrett et al. J Clin Endocrinol Metab. .

Abstract

Both type 1 and type 2 diabetes adversely affect the microvasculature in multiple organs. Our understanding of the genesis of this injury and of potential interventions to prevent, limit, or reverse injury/dysfunction is continuously evolving. This statement reviews biochemical/cellular pathways involved in facilitating and abrogating microvascular injury. The statement summarizes the types of injury/dysfunction that occur in the three classical diabetes microvascular target tissues, the eye, the kidney, and the peripheral nervous system; the statement also reviews information on the effects of diabetes and insulin resistance on the microvasculature of skin, brain, adipose tissue, and cardiac and skeletal muscle. Despite extensive and intensive research, it is disappointing that microvascular complications of diabetes continue to compromise the quantity and quality of life for patients with diabetes. Hopefully, by understanding and building on current research findings, we will discover new approaches for prevention and treatment that will be effective for future generations.

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Figures

Figure 1.
Figure 1.
Schema of hyperglycemia’s induced pathways to microvascular complications. MAP, mitogen-activated protein.
Figure 2.
Figure 2.
Interplay of hyperglycemia’s toxic mechanisms and tissues’ endogenous protective properties. IGF, insulinlike growth factor.
Figure 3.
Figure 3.
Conceptual diagram showing the effect of hyperglycemia on different mechanisms hypothesized to be involved in the pathogenesis of diabetic retinopathy.
Figure 4.
Figure 4.
Prevalence of any retinopathy and proliferative retinopathy in persons with diabetes by type/onset and duration in the Wisconsin Epidemiologic Study of Diabetic Retinopathy. (A) T1DM diagnosed at age <30 years. (B) T2DM diagnosed at age ≥30 years, taking and not taking insulin.
Figure 5.
Figure 5.
Test of trend P < 0.001 for both groups.
Figure 6.
Figure 6.
Neuroimaging measures related to cerebral small vessel disease and concomitant pathologies.
Figure 7.
Figure 7.
Modified diabetic neuropathy classification first proposed by Thomas. N, normal. Reference: Jirousek et al. (25).
See this image and copyright information in PMC

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