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      Aerobic exercise improves cognitive impairment in mice with type 2 diabetes by regulating the MALAT1/miR-382-3p/BDNF signaling pathway in serum-exosomes

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          Abstract

          Background

          It has been documented that aerobic exercise (AE) has a positive effect on improving cognitive function in type 2 diabetes (T2DM) patients. Here, we tried to explore how AE regulates the expression of long non-coding RNA in serum-exosomes (Exos), thereby affecting cognitive impairment in T2DM mice as well as its potential molecular mechanism.

          Methods

          T2DM mouse models were constructed, and serum-Exos were isolated for whole transcriptome sequencing to screen differentially expressed lncRNA and mRNA, followed by prediction of downstream target genes. The binding ability of miR-382-3p with a long non-coding RNA MALAT1 and brain-derived neurotrophic factor (BDNF) was explored. Then, primary mouse hippocampal neurons were collected for in vitro mechanism verification, as evidenced by the detection of hippocampal neurons' vitality, proliferation, and apoptosis capabilities, and insulin resistance. Finally, in vivo mechanism verification was performed to assess the effect of AE on insulin resistance and cognitive disorder.

          Results

          Transcriptome sequencing analysis showed that MALAT1 was lowly expressed and miR-382-3p was highly expressed in serum-Exos samples of T2DM mice. There were targeted binding sites between MALAT1 and miR-382-3p and between miR-382-3p and BDNF. In vitro experiments showed that MALAT1 upregulated BDNF expression by inhibiting miR-382-3p. Silencing MALAT1 or overexpressing miR-382-3p could reduce the expression of INSR, IRS-1, IRS-2, PI3K/AKT, and Ras/MAPK, inhibit neuronal proliferation, and promote apoptosis. In vivo experiments further confirmed that AE could increase the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thereby improving cognitive impairment in T2DM mice.

          Conclusion

          AE may upregulate the expression of MALAT1 in serum-Exos to competitively inhibit miR-382-3p and upregulate BDNF expression, thus improving cognitive impairment in T2DM mice.

          Supplementary Information

          The online version contains supplementary material available at 10.1186/s10020-023-00727-1.

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          The biology, function, and biomedical applications of exosomes

          Raghu Kalluri, Valerie LeBleu (2020)
          The study of extracellular vesicles (EVs) has the potential to identify unknown cellular and molecular mechanisms in intercellular communication and in organ homeostasis and disease. Exosomes, with an average diameter of ~100 nanometers, are a subset of EVs. The biogenesis of exosomes involves their origin in endosomes, and subsequent interactions with other intracellular vesicles and organelles generate the final content of the exosomes. Their diverse constituents include nucleic acids, proteins, lipids, amino acids, and metabolites, which can reflect their cell of origin. In various diseases, exosomes offer a window into altered cellular or tissue states, and their detection in biological fluids potentially offers a multicomponent diagnostic readout. The efficient exchange of cellular components through exosomes can inform their applied use in designing exosome-based therapeutics.
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            Brain insulin resistance in type 2 diabetes and Alzheimer disease: concepts and conundrums

            Aaron M Koenig, Shannon L. Macauley-Rambach, Zoe Arvanitakis … (2018)
            Considerable overlap has been identified in the risk factors, comorbidities and putative pathophysiological mechanisms of Alzheimer disease and related dementias (ADRDs) and type 2 diabetes mellitus (T2DM), two of the most pressing epidemics of our time. Much is known about the biology of each condition, but whether T2DM and ADRDs are parallel phenomena arising from coincidental roots in ageing or synergistic diseases linked by vicious pathophysiological cycles remains unclear. Insulin resistance is a core feature of T2DM and is emerging as a potentially important feature of ADRDs. Here, we review key observations and experimental data on insulin signalling in the brain, highlighting its actions in neurons and glia. In addition, we define the concept of 'brain insulin resistance' and review the growing, although still inconsistent, literature concerning cognitive impairment and neuropathological abnormalities in T2DM, obesity and insulin resistance. Lastly, we review evidence of intrinsic brain insulin resistance in ADRDs. By expanding our understanding of the overlapping mechanisms of these conditions, we hope to accelerate the rational development of preventive, disease-modifying and symptomatic treatments for cognitive dysfunction in T2DM and ADRDs alike.
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              Inflammation in obesity, diabetes, and related disorders.

              Theresa Rohm, Daniel Meier, Jerrold Olefsky … (2022)
              Obesity leads to chronic, systemic inflammation and can lead to insulin resistance (IR), β-cell dysfunction, and ultimately type 2 diabetes (T2D). This chronic inflammatory state contributes to long-term complications of diabetes, including non-alcoholic fatty liver disease (NAFLD), retinopathy, cardiovascular disease, and nephropathy, and may underlie the association of type 2 diabetes with other conditions such as Alzheimer's disease, polycystic ovarian syndrome, gout, and rheumatoid arthritis. Here, we review the current understanding of the mechanisms underlying inflammation in obesity, T2D, and related disorders. We discuss how chronic tissue inflammation results in IR, impaired insulin secretion, glucose intolerance, and T2D and review the effect of inflammation on diabetic complications and on the relationship between T2D and other pathologies. In this context, we discuss current therapeutic options for the treatment of metabolic disease, advances in the clinic and the potential of immune-modulatory approaches.
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                Author and article information

                Contributors
                Ying Cai:
                ORCID: http://orcid.org/0000-0002-6284-8416
                403991@csu.edu.cn
                Journal
                Journal ID (nlm-ta): Mol Med
                Journal ID (iso-abbrev): Mol Med
                Title: Molecular Medicine
                Publisher: BioMed Central (London )
                ISSN (Print): 1076-1551
                ISSN (Electronic): 1528-3658
                Publication date (Electronic): 22 September 2023
                Publication date PMC-release: 22 September 2023
                Publication date Collection: 2023
                Volume: 29
                Electronic Location Identifier: 130
                Affiliations
                [1 ]National Clinical Research Center for Geriatric Disorders, Department of Rehabilitation, Xiangya Hospital Central South University, ( https://ror.org/05c1yfj14) Changsha, 410008 Hunan China
                [2 ]National Clinical Research Center for Geriatric Disorders, Department of Neurology, Xiangya Hospital Central South University, ( https://ror.org/05c1yfj14) Changsha, 410008 China
                Author information
                http://orcid.org/0000-0002-6284-8416
                Article
                Publisher ID: 727
                DOI: 10.1186/s10020-023-00727-1
                PMC ID: 10517522
                PubMed ID: 37740187
                SO-VID: de963314-dd78-45fd-8e05-018d2edb15d1
                Copyright © © The Feinstein Institute for Medical Research 2023
                License:

                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
                Date received : 1 June 2023
                Date accepted : 11 September 2023
                Funding
                Funded by: General program of the National Natural Science Foundation of China
                Award ID: 82072554
                Award Recipient :
                Funded by: National Natural Science Foundation of China Youth Fund
                Award ID: 82002404
                Award Recipient :
                Funded by: Key Research and Development Program in Hunan Province
                Award ID: 2020SK2069
                Award Recipient :
                Categories
                Subject: Research Article
                Custom metadata
                issue-copyright-statement © The Feinstein Institute for Medical Research 2023

                Keywords: aerobic exercise,serum-exosomes,non-coding rna,type 2 diabetes,hippocampal neurons,malat1,mir-382-3p,bdnf
                Data availability:
                Keywords: aerobic exercise, serum-exosomes, non-coding rna, type 2 diabetes, hippocampal neurons, malat1, mir-382-3p, bdnf

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