Year-end Sale % OFF 
Abstract
Diabetes remains one of the leading causes of deaths and co-morbidities in the world, with tremendous human, social and economic costs. Therefore, despite therapeutics and technological advancements, improved strategies to tackle diabetes management are still needed. One of the suggested strategies is the consumption of (poly)phenols. Positive outcomes of dietary (poly)phenols have been pointed out towards different features in diabetes. This is the case of ellagitannins, which are present in numerous foodstuffs such as pomegranate, berries, and nuts. Ellagitannins have been reported to have a multitude of effects on metabolic diseases. However, these compounds have high molecular weight and do not reach circulation at effective concentrations, being metabolized in smaller compounds. After being metabolized into ellagic acid in the small intestine, the colonic microbiota hydrolyzes and metabolizes ellagic acid into dibenzopyran-6-one derivatives, known as urolithins. These low molecular weight compounds reach circulation in considerable concentrations ranging until micromolar levels, capable of reaching target tissues. Different urolithins are formed throughout the metabolization process, but urolithin A, isourolithin A, and urolithin B, and their phase-II metabolites are the most frequent ones. In recent years, urolithins have been the focus of attention in regard to their effects on a multiplicity of chronic diseases, including cancer and diabetes. In this review, we will discuss the latest advances about the protective effects of urolithins on diabetes.
Highlights
The capacity of the human body to metabolize ellagic acid (EA) into different urolithins can be stratified into metabotypes and the classifications have changed over time
Several reports on the role of urolithins against diabetes suggest their activity as antiinflammatory, anti-obesity, and cytoprotective agents, among others
Such compounds with protective effects towards different processes associated with diabetes may be a powerful weapon to tackle such a complex disease
Summary
Since 1965, the World Health Organization (WHO) has occasionally updated guidance on how to classify diabetes mellitus (DM). Insulin resistance is the earliest detectable alteration in individuals who are likely to develop diabetes, preceding the clinical diagnosis of the disease by up to 15 years [2,8] It can occur in multiple organs and tissues, such as muscle, liver, adipose tissue, kidney, gastrointestinal tract, vasculature/brain tissues, and pancreatic β-cells [9,10,11,12]. People with diabetes have an increased risk to develop other pathologies including heart, peripheral arterial, and cerebrovascular disease, obesity, erectile dysfunction, and nonalcoholic fatty liver disease [1] Another consequence of chronic high blood glucose is the production and accumulation of advanced glycation end-products (AGE). Multiple factors have been pointed out as potential contributors for β-cell dysfunction in diabetes, including aging, glucolipotoxicity, islet cholesterol accumulation, islet inflammation, genetic defects in insulin secretion, endocrine disorders, islet amyloid polypeptide (IAPP or amylin) aggregation, among others [23,24,25,26]
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
