0
views
0
recommends
+1 Recommend
0 collections
    0
    shares
      • Record: found
      • Abstract: found
      • Article: found
      Is Open Access

      Effectiveness of date seed on glycemia and advanced glycation end-products in type 2 diabetes: a randomized placebo-controlled trial

      research-article

      Read this article at

      Bookmark
          There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

          Abstract

          Background

          Type 2 diabetes mellitus (T2DM) is a chronic medical condition affecting more than 95% of people with diabetes. Traditionally, some medicinal plants have been considered as an effective approach in management of T2DM. This trial evaluated the effects of date seed powder (DSP) on glycemia indices and oxidative stress in T2DM patients.

          Methods

          In this trail, 43 patients with T2DM were randomized to two groups: either 5 g/d of the DSP or placebo for 8 weeks. Levels of glycemic indices, lipolpolysaccharide (LPS), and soluble receptor for advanced glycation end products (s-RAGE), as well as other parameters associated with oxidative stress were assessed at baseline and after 8 weeks. Independent t-test and analysis of covariance (ANCOVA) were used for between-groups comparisons at baseline and the post-intervention phase, respectively.

          Results

          The results showed that supplementation with DSP significantly decreased HbA1c (−0.30 ± 0.48%), insulin (−1.70 ± 2.21 μU/ml), HOMA-IR (−1.05 ± 0.21), HOMA-B (−0.76 ± 21.21), lipopolysaccharide (LPS) (−3.68 ± 6.05 EU/mL), and pentosidine (118.99 ± 21.67 pg/mL) ( P < 0.05, ANCOVA adjusted for baseline and confounding factors). On the other hand, DSP supplementation significantly increased total antioxidant capacity (TAC) (0.50 ± 0.26 mmol/L), superoxide dismutase (SOD) (0.69 ± 0.32 U/ml), and s-RAGE (240.13 ± 54.25 pg/mL) compared to the placebo group. FPG, hs-CRP, GPx, CML, and uric acid had no significant within- or between-group changes.

          Conclusion

          Supplementation of DSP could be considered an effective strategy to improve glycemic control and oxidative stress in T2DM patients (Registration ID at www.irct.ir: IRCT20150205020965N10).

          Related collections

          Most cited references47

          • Record: found
          • Abstract: found
          • Article: not found

          Oxidative stress and reactive oxygen species in endothelial dysfunction associated with cardiovascular and metabolic diseases.

          Reactive oxygen species (ROS) are reactive intermediates of molecular oxygen that act as important second messengers within the cells; however, an imbalance between generation of reactive ROS and antioxidant defense systems represents the primary cause of endothelial dysfunction, leading to vascular damage in both metabolic and atherosclerotic diseases. Endothelial activation is the first alteration observed, and is characterized by an abnormal pro-inflammatory and pro-thrombotic phenotype of the endothelial cells lining the lumen of blood vessels. This ultimately leads to reduced nitric oxide (NO) bioavailability, impairment of the vascular tone and other endothelial phenotypic changes collectively termed endothelial dysfunction(s). This review will focus on the main mechanisms involved in the onset of endothelial dysfunction, with particular focus on inflammation and aberrant ROS production and on their relationship with classical and non-classical cardiovascular risk factors, such as hypertension, metabolic disorders, and aging. Furthermore, new mediators of vascular damage, such as microRNAs, will be discussed. Understanding mechanisms underlying the development of endothelial dysfunction is an important base of knowledge to prevent vascular damage in metabolic and cardiovascular diseases.
            Bookmark
            • Record: found
            • Abstract: found
            • Article: not found

            Short chain fatty acids in human gut and metabolic health

            Evidence is accumulating that short chain fatty acids (SCFA) play an important role in the maintenance of gut and metabolic health. The SCFA acetate, propionate and butyrate are produced from the microbial fermentation of indigestible carbohydrates and appear to be key mediators of the beneficial effects elicited by the gut microbiome. Microbial SCFA production is essential for gut integrity by regulating the luminal pH, mucus production, providing fuel for epithelial cells and effects on mucosal immune function. SCFA also directly modulate host metabolic health through a range of tissue-specific mechanisms related to appetite regulation, energy expenditure, glucose homeostasis and immunomodulation. Therefore, an increased microbial SCFA production can be considered as a health benefit, but data are mainly based on animal studies, whereas well-controlled human studies are limited. In this review an expert group by ILSI Europe’s Prebiotics Task Force discussed the current scientific knowledge on SCFA to consider the relationship between SCFA and gut and metabolic health with a particular focus on human evidence. Overall, the available mechanistic data and limited human data on the metabolic consequences of elevated gut-derived SCFA production strongly suggest that increasing SCFA production could be a valuable strategy in the preventing gastro-intestinal dysfunction, obesity and type 2 diabetes mellitus. Nevertheless, there is an urgent need for well controlled longer term human SCFA intervention studies, including measurement of SCFA fluxes and kinetics, the heterogeneity in response based on metabolic phenotype, the type of dietary fibre and fermentation site in fibre intervention studies and the control for factors that could shape the microbiome like diet, physical activity and use of medication.
              Bookmark
              • Record: found
              • Abstract: found
              • Article: found
              Is Open Access

              Advanced Glycation End Products and Oxidative Stress in Type 2 Diabetes Mellitus

              Type 2 diabetes mellitus (T2DM) is a very complex and multifactorial metabolic disease characterized by insulin resistance and β cell failure leading to elevated blood glucose levels. Hyperglycemia is suggested to be the main cause of diabetic complications, which not only decrease life quality and expectancy, but are also becoming a problem regarding the financial burden for health care systems. Therefore, and to counteract the continually increasing prevalence of diabetes, understanding the pathogenesis, the main risk factors, and the underlying molecular mechanisms may establish a basis for prevention and therapy. In this regard, research was performed revealing further evidence that oxidative stress has an important role in hyperglycemia-induced tissue injury as well as in early events relevant for the development of T2DM. The formation of advanced glycation end products (AGEs), a group of modified proteins and/or lipids with damaging potential, is one contributing factor. On the one hand it has been reported that AGEs increase reactive oxygen species formation and impair antioxidant systems, on the other hand the formation of some AGEs is induced per se under oxidative conditions. Thus, AGEs contribute at least partly to chronic stress conditions in diabetes. As AGEs are not only formed endogenously, but also derive from exogenous sources, i.e., food, they have been assumed as risk factors for T2DM. However, the role of AGEs in the pathogenesis of T2DM and diabetic complications—if they are causal or simply an effect—is only partly understood. This review will highlight the involvement of AGEs in the development and progression of T2DM and their role in diabetic complications.
                Bookmark

                Author and article information

                Contributors
                dehghan.nut@gmail.com
                azizi.s@arakmu.ac.ir
                Journal
                Nutr Diabetes
                Nutr Diabetes
                Nutrition & Diabetes
                Nature Publishing Group UK (London )
                2044-4052
                1 June 2024
                1 June 2024
                2024
                : 14
                : 37
                Affiliations
                [1 ]GRID grid.412888.f, ISNI 0000 0001 2174 8913, Student Research Committee, Faculty of Nutrition and Food Science, , Tabriz University of Medical Sciences, ; Tabriz, Iran
                [2 ]Department of Biochemistry and Diet Therapy, Nutrition Research Center, Faculty of Nutrition and Food Science, Tabriz University of Medical Sciences, ( https://ror.org/04krpx645) Tabriz, Iran
                [3 ]Department of Nutrition, School of Health, Arak University of Medical Sciences, ( https://ror.org/056mgfb42) Arak, Iran
                Author information
                http://orcid.org/0000-0001-8929-3302
                Article
                287
                10.1038/s41387-024-00287-1
                11144252
                38824123
                866a63f4-4c20-4c58-ac8d-ebb6c7232602
                © The Author(s) 2024

                Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

                History
                : 13 August 2023
                : 28 April 2024
                : 30 April 2024
                Funding
                Funded by: FundRef https://doi.org/10.13039/501100004366, Tabriz University of Medical Sciences (TUOMS);
                Award ID: 68035
                Award ID: 68035
                Award ID: 68035
                Award Recipient :
                Categories
                Article
                Custom metadata
                © Springer Nature Limited 2024

                Endocrinology & Diabetes
                nutrition,health care,endocrinology
                Endocrinology & Diabetes
                nutrition, health care, endocrinology

                Comments

                Comment on this article