Dataset Information

Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

ABSTRACT: Short-term intrauterine hyperglycaemia significantly reduced lean mass in male offspring at 8 weeks, resulting in decreased exercise endurance and metabolic disorders. Disrupted organization and function of the mitochondria in skeletal muscle were also observed among them. Foetal exposure to hyperglycaemia decreased phosphorylated CREB and reduced the transcription of Ppargc1a.

INSTRUMENT(S): Q Exactive HF

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Skeletal Muscle

SUBMITTER: Yi-Shang Yan

LAB HEAD: Yi-Shang Yan

PROVIDER: PXD049987 | Pride | 2024-08-09

REPOSITORIES: Pride

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Intrauterine hyperglycaemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling.

Yan Yi-Shang YS Mo Jia-Ying JY Huang Yu-Tong YT Zhu Hong H Wu Hai-Yan HY Lin Zhong-Liang ZL Liu Rui R Liu Xuan-Qi XQ Lv Ping-Ping PP Feng Chun C Sheng Jian-Zhong JZ Jin Min M Huang He-Feng HF

Nutrition & diabetes 20240723 1

<h4>Background</h4>Maternal diabetes mellitus can influence the development of offspring. Gestational diabetes mellitus (GDM) creates a short-term intrauterine hyperglycaemic environment in offspring, leading to glucose intolerance in later life, but the long-term effects and specific mechanism involved in skeletal muscle dysfunction in offspring remain to be clarified.<h4>Methods</h4>Pregnant mice were divided into two groups: The GDM group was intraperitoneally injected with 100 mg/kg streptoz ...[more]

PMID: 39043630

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Project description:Purpose: Exploring the alteration in CREB/CRTC binding related to long-term memory Methods: The nuclei of Drosophila mushroom bodies were purified and the histone acetylation and CREB/CRTC binding were examined by ChIP-seq using specific antibodies. The sequencing was performed using Miseq, and aligned to dm3 using CLCbio. The sequence reads that passed quality filters were analyzed by peak calling using PICS and ERD equipped on Strand NGS software. This method using two algorisms excludes false-positive calling of peaks. The PICS and ERD were run using a default setting except for the following parameters; for PICS, 120 bp as an average fragment length, 10 bp as a minimum distance between forward and reverse reads, 200 bp as a minimum distance between forward and reverse reads, 100 bp as a window width, with 5% false discovery rate; for ERD, 1.5 as an enrichment factor, 100 bp as a window size, 10 bp as a window slide size, 100 bp as a minimum region size. The peaks obtained by ERD analysis were filtered by an enrichment factor of 2, and a density of reads at 0.12 for CREB and 0.2 for CRTC. The CREB and the CRTC binding sites were determined as the peak-called region in at least 2 samples out of the three replicates. The CREB and the CRTC binding sites located 200 bp vicinity to each other were defined as the CREB/CRTC binding sites. In parallel, the read counts were obtained in the 1 kb window covering entire genome and analyzed by DESeq2, to determine the region enriched with CREB/CRTC in a specific group of samples. The region with increased or decreased CREB/CRTC binding were determined if the region were defined by the CREB/CRTC binding sites in the above criteria. Results: Using an optimized data analysis workflow, the filtered reads amounted to 8-11million reads for CREB in each of 3 replicates, 8-17 million reads for CRTC in each of 3 replicates, and 4.4 million reads for input. Using anti-CREB antibody, we found 239 significant increases in CREB binding out of 4995 CREB/CRTC binding sites 1 day after training. Using anti-CRTC antibody, we found 4989 significant increases in CRTC binding out of 4995 CREB/CRTC binding sites 1 day after spaced training. Conclusions: Our study shows that, although CREB binding is mostly unchanged, CRTC binding is significantly increased after long-term memory formation in Drosophila mushroom bodies.

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Dataset Information

Intrauterine hyperglycemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling

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Publications

Intrauterine hyperglycaemia during late gestation caused mitochondrial dysfunction in skeletal muscle of male offspring through CREB/PGC1A signaling.

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