Diabetic Microvascular Disease: An Endocrine Society Scientific Statement

Eugene J. Barrett; Zhenqi Liu; Mogher Khamaisi; George L. King; Ronald Klein; Barbara E. K. Klein; Timothy M. Hughes; Suzanne Craft; Barry I. Freedman; Donald W. Bowden; Aaron I. Vinik; Carolina M. Casellini

Disclosures

J Clin Endocrinol Metab. 2017;102(12):4343-4410. 

In This Article

Abstract and Introduction

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.

Introduction

The cellular elements of the microvasculature appear to be particularly sensitive to injury from sustained hyperglycemia. This injury (and responses by the body directed toward its repair) cause tissue/organ dysfunction that affects the quality and duration of life for persons with either type 1 diabetes mellitus (T1DM) or type 2 diabetes mellitus (T2DM). Despite the disparate pathogenesis of these two common forms of diabetes, they (along with secondary forms of diabetes resulting from genetic mutations or pharmaceutical or surgical interventions) all share microvascular injury/dysfunction as a chronic outcome. This scientific statement provides an up-to-date overview of the general pathogenesis of microvascular disease in diabetes, as well as its impact on specific tissues. As such, this statement provides readers with a clear understanding of how microvascular injury adversely affects the normal physiologic function of multiple tissues within the body. This statement does not attempt to provide a compendium of all of the organspecific treatments for limiting microvascular damage that are in use or in development. Nor do we attempt to review/critique the more general systemic approaches to treatment designed to control glycemia, blood pressure (BP), lipids, or oxidative stress.

At the outset, we are reminded that the very diagnosis of diabetes rests on identifying the level of blood glucose that associates with microvascular injury to the eye. In addition, much of the impetus for developing effective glycemic therapy arises from clinical trials that demonstrate that improved glycemic control decreases the incidence and progression of microvascular injury.

The body's microvasculature is a diffuse target whose properties differ considerably between different tissues and organs. The response of the microvasculature to injury/repair likewise differs across tissues and organs. For this reason we chose to use an organbased organizational structure for this scientific statement. However, although we discuss the microvascular complications of diabetes on an organ-by-organ basis, we recognize that in the individual patient all organs are affected simultaneously to a greater or lesser degree (i.e., evident microvascular dysfunction found in one organ is a sentinel of systemic injury, which may be preclinical).

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