We aimed to investigate the effects of the maternal plane of nutrition during gestation on the proteome profile of the skeletal muscle of the newborn. Pregnant goats were assigned to the following experimental treatments: restriction maintenance (RM) where pregnant dams were fed at 50% of their maintenance requirements from 8−84 days of gestation, and then feed of 100% of the maintenance requirements was supplied from 85—parturition (n = 6); maintenance restriction (MR) where pregnant dams were fed at 100% of their maintenance requirements from 8−84 days of gestation, and then experienced feed restriction of 50% of the maintenance requirements from 85—parturition (n = 8). At birth, newborns were euthanized and samples of the Longissimus dorsi muscle were collected and used to perform HPLC-MS/MS analysis. The network analyses were performed to identify the biological processes and KEGG pathways of the proteins identified as differentially abundant protein and were deemed significant when the adjusted p-value (FDR) < 0.05. Our results suggest that treatment RM affects the energy metabolism of newborns’ skeletal muscle by changing the energy-investment phase of glycolysis, in addition to utilizing glycogen as a carbon source. Moreover, the RM plane of nutrition may contribute to fatty acid oxidation and increases in the cytosolic α-KG and mitochondrial NADH levels in the skeletal muscle of the newborn. On the other hand, treatment MR likely affects the energy-generation phase of glycolysis, contributing to the accumulation of mitochondrial α-KG and the biosynthesis of glutamine.
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http://dx.doi.org/10.3390/ani12081011 | DOI Listing |
J Clin Invest
January 2025
Department of Biochemistry, Molecular Biology & Biophysics, University of Minnesota, Minneapolis, United States of America.
Eccentric contraction- (ECC) induced force loss is a hallmark of murine dystrophin-deficient (mdx) skeletal muscle that is used to assess efficacy of potential therapies for Duchenne muscular dystrophy. While virtually all key proteins involved in muscle contraction have been implicated in ECC force loss, a unifying mechanism that orchestrates force loss across such diverse molecular targets has not been identified. We showed that correcting defective hydrogen sulfide (H2S) signaling in mdx muscle prevented ECC force loss.
View Article and Find Full Text PDFPediatr Nephrol
January 2025
Nephrology, Children's National Hospital, 111 Michigan Avenue NW, Washington, DC, 20010, USA.
Background: Obesity and metabolic syndrome (MS) accelerate arterial stiffening, increasing cardiovascular (CV) risk after transplant. BMI is limited by inability to differentiate muscle, fat mass, and fat distribution patterns. The aim of this study was to identify the best anthropometric measure to detect arterial stiffness as assessed by pulse wave velocity (PWV) in a racially diverse pediatric transplant population.
View Article and Find Full Text PDFCell Tissue Res
January 2025
Laboratory of Anatomy and Cell Biology, Department of Health Sciences, Kyorin University, 5-4-1 Shimorenjaku, Mitaka, Tokyo, 181-8612, Japan.
Adult tissue stem cells of the anterior pituitary gland, CD9/SOX2-positive cells, are believed to exist in the marginal cell layer (MCL) bordering the residual lumen of the Rathke's pouch. These cells migrate from the intermediate lobe side of the MCL (IL-MCL) to the anterior lobe side of the MCL and may be involved in supplying hormone-producing cells. Previous studies reported that some SOX2-positive cells of the anterior lobe differentiate into skeletal muscle cells.
View Article and Find Full Text PDFTurk J Pediatr
December 2024
Division of Pediatric Rheumatology, Department of Pediatrics, University of Health Sciences, Ankara Bilkent City Hospital, Ankara, Türkiye.
Background: Anti-signal recognition protein (anti-SRP) myopathy is a rare idiopathic inflammatory myopathy in children. Herein, a 3-year-old patient with severe anti-SRP myopathy showing a rapidly progressive disease course is presented in order to increase the awareness of pediatricians about idiopathic inflammatory myopathies.
Case Presentation: A previously healthy 3-year-old girl presented with progressive symmetrical proximal muscle weakness that caused difficulty in climbing stairs for two months prior to evaluation, and a marked elevation of the serum creatine kinase levels.
Hum Mol Genet
January 2025
Division of Neurology, Cincinnati Children's Hospital, 3333 Burnet Ave, Cincinnati, OH 45229, United States.
Myotonic Dystrophy type 2 (DM2) is a multisystem disease affecting many tissues, including skeletal muscle, heart, and brain. DM2 is caused by unstable expansion of CCTG repeats in an intron 1 of a gene coding for cellular nuclear binding protein (CNBP). The expanded CCTG repeats cause DM2 pathology due to the accumulation of RNA CCUG repeats, which affect RNA processing in patients' cells.
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