ArticleMolecular neurobiology2023
Role of Bmal1 in Type 2 Diabetes Mellitus-Related Glycolipid Metabolic Disorder and Neuropsychiatric Injury: Involved in the Regulation of Synaptic Plasticity and Circadian Rhythms.
Article in Molecular neurobiology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- lncRNAInternational journal of molecular medicine · 2026Article
- Peripheral metabolic dysfunction is associated with cognitive frailty in a mouse model of type 2 diabetes.Metabolic brain disease · 2026Article
- Bmal1 overexpression in suprachiasmatic nucleus protects from retinal neurovascular deficits in a mouse model of diabetes.Diabetologia · 2026Article
- Celecoxib Ameliorates Chronic Restraint Stress-Induced Depression-Like Behavior in Sprague-Dawley Rats.Neuropsychiatric disease and treatment · 2026Article
- Core Circadian Protein BMAL1: Implication for Nervous System Functioning and Its Diseases.Brain sciences · 2025Review
- Mechanisms underlying cognitive impairment and management strategies in type 2 diabetes.Frontiers in endocrinology · 2025Review
- Article
- Targeting the circadian modulation: novel therapeutic approaches in the management of ASD.Frontiers in psychiatry · 2024Review
- ED-71 Ameliorates Bone Loss in Type 2 Diabetes Mellitus by Enhancing Osteogenesis Through Upregulation of the Circadian Rhythm Coregulator BMAL1.Drug design, development and therapy · 2024Article
- The contribution of circadian clock to the biological processes.Frontiers in molecular biosciences · 2024Review
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Authors and funding
9 authors at 3 institutions in 2 countries.
Funding
Abstract
Increasing data suggest a crucial role of circadian rhythm in regulating metabolic and neurological diseases, and Bmal1 is regarded as a key regulator of circadian transcription. The aim of this study is to investigate the role of Bmal1 in the disruption of circadian rhythm and neuropsychiatric injuries in type 2 diabetes mellitus (T2DM). A T2DM model was induced by the combination of high-fat-diet (HFD) and streptozotocin (STZ) in vivo or HT-22 cells challenged with palmitic-acid (PA) in vitro. The glucolipid metabolism indicators, behavioral performance, and expression of synaptic plasticity proteins and circadian rhythm-related proteins were detected. These changes were also observed after interference of Bmal1 expression via overexpressed plasmid or small interfering RNAs in vitro. The results showed that HFD/STZ could induce T2DM-like glycolipid metabolic turmoil and abnormal neuropsychiatric behaviors in mice, as indicated by the increased concentrations of fasting blood-glucose (FBG), HbA1c and lipids, the impaired glucose tolerance, and the decreased preference index of novel object or novel arm in the novel object recognition test (NOR) and Y-maze test (Y-maze). Consistently, the protein expression of synaptic plasticity proteins and circadian rhythm-related proteins and the positive fluorescence intensity of MT1B and Bmal1 were decreased in the hippocampus of HFD/STZ-induced mice or PA-challenged HT-22 cells. Furthermore, overexpression of Bmal1 could improve the PA-induced lipid metabolic dysfunction and increase the decreased expressions of synaptic plasticity proteins and circadian rhythm-related proteins, and vice versa. These results suggested a crucial role of Bmal1 in T2DM-related glycolipid metabolic disorder and neuropsychiatric injury, which mechanism might be involved in the regulation of synaptic plasticity and circadian rhythms.
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