Abstract
Hundreds of millions of people around the globe are afflicted by diabetes mellitus. The alteration in glucose fixation process might result into hyperglycaemia and could affect the circulating plasma proteins to undergo nonenzymatic glycation reaction. If it is unchecked, it may lead to diabetes with increase in advanced glycation end products (AGEs). Therefore, the present study was designed to inhibit the diabetes and glycation by using natural antioxidant “ellagic acid” (EA). In this study, we explored the antidiabetes and antiglycation potential of EA in both in vitro (EA at micromolar concentration) and in vivo systems. The EA concentrations of 10 and 20 mg kg−1B.W./day were administered orally for 25 days to alloxan-induced diabetic rats, a week after confirmation of stable diabetes in animals. Intriguingly, EA supplementation in diabetic rats reversed the increase in fasting blood sugar (FBS) and hemoglobin A1c (HbA1c) level. EA also showed an inhibitory role against glycation intermediates including dicarbonyls, as well as AGEs, investigated in a glycation mixture with in vitro and in vivo animal plasma samples. Additionally, EA treatment resulted in inhibition of lipid peroxidation-mediated malondialdehyde (MDA) and conjugated dienes (CD). Furthermore, EA exhibited an antioxidant property, increased the level of plasma glutathione (GSH), and also helped to decrease histological changes evaluated by histoimmunostaining of animal kidney tissues. The results from our investigation clearly indicates the antiglycative property of EA, suggesting EA as an adequate inhibitor of glycation and diabetes, which can be investigated further in preclinical settings for the treatment and management of diabetes-associated complications.
Highlights
The worldwide prevalence of type 2 diabetes mellitus (T2DM) and its associated complications resulting from insufficiency of insulin secretion and resistance have increased noticeably and tremendously contribute to the global burden of disability and mortality [1]
We evaluate the low concentration of ellagic acid (EA) as an antiglycating compound to scavenge and inhibit glycating agents such as MG and glycation products in the glycation model in vitro as well as in vivo animal model
Our results suggested that ellagic acid may exert its protective effect against alloxan-induced diabetes by decreasing lipid peroxidation and by inhibition of early, intermediate products and advanced glycation end products (AGEs) formation from glycation
Summary
The worldwide prevalence of type 2 diabetes mellitus (T2DM) and its associated complications resulting from insufficiency of insulin secretion and resistance have increased noticeably and tremendously contribute to the global burden of disability and mortality [1]. Subsequent irreversible reactions leads to the formation of highly reactive glycation intermediates known as reactive carbonyl compounds mainly glyoxal (GO), methylglyoxal (MG), and 3-deoxyglucosone (3-DG). These reactive carbonyl compounds can induce more stable heterogeneous advanced glycation end products called AGEs. diabetes accelerates AGE formation and its gradual build-up in circulation and body tissues [4]. Diabetes accelerates AGE formation and its gradual build-up in circulation and body tissues [4] This phenomenon is strongly associated with renal afflictions [5], osteoarthritis [6], and atherosclerosis [7] with diabetes
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