No abstract

The side effects of soft drinks are still an important challenge especially for the expressed genes of foetuses that regulate ossification. For that purpose, we investigate the expression of R-spending2 (RSPO2), Hydroxyacid Oxidase 1 (HAO1), and runt related transcription factor 2 (RUNX2) genes and the foetuses skeletal malformation due to maternal Pepsi consumption. Pregnant rats were divided into control group that was administrated orally with distilled water, group1 from day 1 to day 7 was orally administrated with 2.5 ml/day of Pepsi, group2 from day 1 to day 7 was administrated orally with 5ml/day of Pepsi, group 3 from day 8 to day 20 was orally administrated with 2.5 ml/day of Pepsi, and group 4 from day 8 to day 20 was orally administrated with 5 ml/day of Pepsi. Gene expression analysis revealed that the RSPO2 gene is significantly decreased with increasing the dosage of soft drinks during the 1 st stage of pregnancy. Conversely, there is a significant increase in the HAO1 gene in 1 st stage group relative to the control group. RUNX2 gene is significantly decreased in group1 and group 2 while it was significantly increased in groups 3 and 4 regarding the control group. Pepsi administration caused retarded body length and weight, ossification and lengths of some bones, and shortness of others. Different bones are seriously affected by Pepsi. Therefore, our findings reveal the effect of soft drink consumption on skeletal malformation and the RSPO2, HAO1, and RUNX2 genes that can be used as biomarkers for skeletal modulation.

Calpains are a class of calcium-dependent, non-lysosomal proteins. Two main calpain isoforms are expressed in skeletal muscle, m-calpain, and mu-calpain, which exert critical proteolytic activities related to muscle functions, muscle atrophy, and myogenesis. Cathepsins are lysosomal acid proteases. The main cathepsin isoforms implicated in muscle aging and atrophy are cathepsins B, L, and H. This study characterized calpain1, calpain2, cathepsin L, cathepsin B, and cathepsin H genes in the tilapia genome. In addition, the expressions of these genes were examined in the muscle tissues of starved versus fed; and refed versus control tilapia, Oreochromis niloticus. qPCR expression data showed that Calpain1 and 2 catalytic subunits and the regulatory subunit were significantly higher in starved compared to the fed tilapia. Similarly, cathepsin L, B, and H showed significant upregulation in the starved compared to the fed fish. Besides, calpain and cathepsin L enzymatic catalytic activity increased in the starved fish relative to the fed fish. The results indicate that the studied genes are involved in atrophying muscle and are considered to have a potential role as markers of tilapia muscle accretion.

Improvements in growth-related traits reduce fish time and production costs to reach market size. Feed deprivation and refeeding cycles have been introduced to maximize aquaculture profits through compensatory growth. However, the molecular compensatory growth signature is still uncertain in Nile tilapia. In this study, fish were subjected to two weeks of fasting followed by two weeks of refeeding. The growth curve in refed tilapia was suggestive of a partial compensatory response. Transcriptome profiling of starved and refed fish was conducted to identify genes regulating muscle atrophy and compensatory growth. Pairwise comparisons revealed 5,009 and 478 differentially expressed (DE) transcripts during muscle atrophy and recovery, respectively. Muscle atrophy appears to be mediated by the ubiquitin-proteasome and autophagy/lysosome systems. Autophagy-related 2A, F-box and WD repeat domain containing 7, F-box only protein 32, miR-137, and miR-153 showed exceptional high expression suggesting them as master regulators of muscle atrophy. On the other hand, the muscle compensatory growth response appears to be mediated by the continuous stimulation of muscle hypertrophy which exceeded normal levels found in control fish. For instance, genes promoting ribosome biogenesis or enhancing the efficiency of translational machinery were upregulated in compensatory muscle growth. Additionally, myogenic microRNAs (e.g., miR-1 and miR-206), and hypertrophy-associated microRNAs (e.g., miR-27a-3p, miR-29c, and miR-29c) were reciprocally expressed to favor hypertrophy during muscle recovery. Overall, the present study provided insights into the molecular mechanisms regulating muscle mass in fish. The study pinpoints extensive growth-related gene networks that could be used to inform breeding programs and also serve as valuable genomic resources for future mechanistic studies.