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Integrated transcriptome and single-cell sequencing analysis identify blood-pancreas shared lncRNA biomarkers in new-onset T2DM

ABSTRACT: Type 2 diabetes mellitus (T2DM) is characterized by beta-cell dysfunction and insulin resistance, but the early molecular drivers remain elusive. The aim of this study was to identify blood long non-coding RNAs (lncRNAs) as a potential systemic biomarkers in patients with new-onset, unmedicated T2DM. We performed transcriptome sequencing of peripheral blood from eight T2DM patients and eight healthy individuals. The intersection of three differential expression analysis methods (Limma, DESeq2 and EdgeR) identified 1,709 lncRNAs with dysregulated expression in peripheral blood, of which , 853 lncRNAs were up-regulated and 856 lncRNAs were down-regulated. Weighted gene co-expression network analysis (WGCNA) identified two modules comprising a total of 1,617 lncRNAs that were significantly negatively associated with T2DM. By integrating differential expression analysis and WGCNA, we screened a total of 257 lncRNAs that were highly correlated with T2DM and exhibited significant changes in expression levels.Our findings provide valuable transcriptomic data for further studies of T2DM, and the screened blood lncRNAs may reflect systemic dysregulation as early biomarkers.

ORGANISM(S): Homo sapiens

PROVIDER: GSE298690 | GEO | 2025/06/04

REPOSITORIES: GEO

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Project description:Skeletal muscle mitochondrial dysfunction is secondary to T2DM and can be improved by long-term regular exercise training Mitochondrial dysfunction has long been implicated to play a causative role in development of type 2 diabetes (T2DM). However, a growing number of recent studies provide data that mitochondrial dysfunction is a consequence of T2DM development. The aim of our study is to clarify in further detail the causal role of mitochondrial dysfunction in T2DM by a comprehensive ex vivo analysis of mitochondrial function combined with global gene expression analysis in muscle of pre-diabetic newly diagnosed untreated T2DM subjects and long-standing insulin treated T2DM subjects compared with age- and BMI-matched controls. In addition, we assessed the impact of long-term interval exercise training on physical activity performance, mitochondrial function and glycemic control in long-standing insulin-treated T2DM subjects. Ex vivo mitochondrial density, quality and functioning was comparable between pre-diabetic subjects and matched controls, however, gene expression analysis showed a switch from carbohydrate toward lipids as energy source in pre-diabetes subjects. In contrast, long-term insulin treated T2DM subjects had slightly decreased mitochondrial density and ex vivo function. Expression of Krebs cycle and OXPHOS related genes were decreased, indicating a decreased capacity to use lipids as an energy source. The insulin-treated T2DM subjects had a lower physical activity level than pre-diabetic and normoglycemic subjects. A 52 weeks exercise training of these subjects increased submaximal oxidative efficiency, increased in vivo PCr recovery rate, as well as mildly increased in vitro mitochondrial function. Gene expression of β-oxidation, Krebs cycle and OXPHOS-related genes was increased. Our data demonstrate that mitochondrial dysfunction is rather a consequence than a causative factor in T2DM development as it was only detected in overt diabetes and not in early diabetes. Regular exercise training stabilized exogenous insulin requirement and improved mitochondrial functioning, fatty acid oxidation and general physical work load capacity in long-standing insulin-treated T2DM subjects. As such, the present study shows for the first time that long-term exercise interventions are beneficial in this group of complex diabetes patient and may prevent further metabolic deterioration.

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Integrated transcriptome and single-cell sequencing analysis identify blood-pancreas shared lncRNA biomarkers in new-onset T2DM

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