PMID- 36370225 OWN - NLM STAT- MEDLINE DCOM- 20230113 LR - 20230202 IS - 1573-7365 (Electronic) IS - 0885-7490 (Linking) VI - 38 IP - 1 DP - 2023 Jan TI - Light-intensity exercise improves memory dysfunction with the restoration of hippocampal MCT2 and miRNAs in type 2 diabetic mice. PG - 245-254 LID - 10.1007/s11011-022-01117-y [doi] AB - Cognitive decline associated with type 2 diabetes mellitus (T2DM) is a risk factor to impair human health. Although light-intensity exercise prevents hippocampal memory dysfunction in pre-symptomatic T2DM animals by altering hippocampal lactate transport and neurotrophic factors, the effects of light-intensity exercise in an advanced stage of T2DM animals remain unclear. Here, ob/ob mice, an animal model of T2DM, were subjected to light-intensity exercise (5.0 m/min) for 30 min/day, five days/week for four weeks. The effects of light-intensity exercise on hippocampal complications, mRNA expressions of monocarboxylate transporter (MCT), and miRNA levels were assessed. The light-intensity exercise improved hippocampal memory retention in ob/ob mice. Downregulated hippocampal Mct2 mRNA levels in T2DM were improved with light-intensity exercise. Hippocampal mRNA levels of Mct1 and Mct4 were unchanged within groups. Based on miRNA sequencing, sedentary ob/ob mice exhibited that 71 miRNAs were upregulated, and 77 miRNAs were downregulated in the hippocampus. In addition, the exercise significantly increased 24 miRNAs and decreased 4 miRNAs in the T2DM hippocampus. The exercise reversed T2DM-induced alterations of hippocampal 9 miRNAs, including miR-200a-3p. Our findings imply that miR-200a-3p/Mct2 in the hippocampus would be a possible clinical target for treating T2DM-induced memory dysfunction. CI - (c) 2022. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature. FAU - Shima, Takeru AU - Shima T AUID- ORCID: 0000-0003-4209-1564 AD - Department of Health and Physical Education, Cooperative Faculty of Education, Gunma University, 4-2 Aramaki-machi, Gunma, 371-8510, Maebashi, Japan. ta-shima@gunma-u.ac.jp. FAU - Kawabata-Iwakawa, Reika AU - Kawabata-Iwakawa R AUID- ORCID: 0000-0002-3504-1393 AD - Division of Integrated Oncology Research, Gunma University Initiative for Advanced Research, 3-39-22, Showa-machi, Maebashi, Gunma, 371-8511, Japan. FAU - Onishi, Hayate AU - Onishi H AD - Department of Health and Physical Education, Cooperative Faculty of Education, Gunma University, 4-2 Aramaki-machi, Gunma, 371-8510, Maebashi, Japan. FAU - Jesmin, Subrina AU - Jesmin S AUID- ORCID: 0000-0003-0165-827X AD - Faculty of Medicine, Toho University Graduate School of Medicine, 5-21-16 Omorinishi, Ota-ku, 143-0015, Tokyo, Japan. FAU - Yoshikawa, Tomonori AU - Yoshikawa T AD - Department of Health and Physical Education, Cooperative Faculty of Education, Gunma University, 4-2 Aramaki-machi, Gunma, 371-8510, Maebashi, Japan. LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't DEP - 20221112 PL - United States TA - Metab Brain Dis JT - Metabolic brain disease JID - 8610370 RN - 0 (MicroRNAs) SB - IM MH - Humans MH - Mice MH - Animals MH - *Diabetes Mellitus, Type 2/complications/therapy/metabolism MH - *MicroRNAs/genetics/metabolism MH - *Diabetes Mellitus, Experimental/metabolism MH - Hippocampus/metabolism MH - Memory OTO - NOTNLM OT - Light-intensity exercise OT - Memory function OT - Monocarboxylate transporter OT - Type 2 diabetes OT - miR-Seq EDAT- 2022/11/13 06:00 MHDA- 2023/01/14 06:00 CRDT- 2022/11/12 11:16 PHST- 2022/06/15 00:00 [received] PHST- 2022/10/28 00:00 [accepted] PHST- 2022/11/13 06:00 [pubmed] PHST- 2023/01/14 06:00 [medline] PHST- 2022/11/12 11:16 [entrez] AID - 10.1007/s11011-022-01117-y [pii] AID - 10.1007/s11011-022-01117-y [doi] PST - ppublish SO - Metab Brain Dis. 2023 Jan;38(1):245-254. doi: 10.1007/s11011-022-01117-y. Epub 2022 Nov 12.