Biology subjects

Patel, D. K.

Publications and source records attributed to Patel, D. K..

3 recordsLinked to original sources

bioRxiv2025

Metabolic modulation in liver by glucan from Enterococcus hirae (OL616073) via gut-liver axis culture model of steatosis

Metabolic dysfunction associated fatty liver disease (MAFLD) starts with increased fat deposition called steatosis progressing towards steatohepatitis, fibrosis, cirrhosis and end stage liver disease. Dysfunctional metabolism in type-2 diabetes or obesity is associated with gut dysbiosis, causing release of gut microbial endotoxins like lipopolysaccharides (LPS) into the liver via portal circulation also known as gut-liver axis. Endotoxins or LPS signals metabolic changes in the liver initiating steatosis via gut-liver axis. Various pre-clinical models have been studied to evaluate the role of fermented food derived bioactive compounds preventing the process of steatosis. Among them exopolysaccharides (EPS), as a part of fermented foods have been reported to produce metabolites by the gut microbial fermentation, providing liver with health benefits. In the present study, we have evaluated the role of a noble EPS or G (glucan) in the condition of liver steatosis by using cell culture model of gut-liver axis by co-culturing Caco-2 and HepG2 cells in transwell culture dishes. LPS was used to mimic gut dysbiosis, with or without pre-treatment of G to caco-2 cells in the upper chamber, wherease, HepG2 cells in lower chamber were extracted for metabolites to be analyzed by LC-Q-TOF. The global metabolomic profiles of LPS+G+ and LPS+ treated cells were compared. The primary target of G showed its role in cholesterol and primary bile acid metabolism along with changes in nucleotide, vitamins and branched chain aminoacid metabolites helpful in reducing fatty liver. Future studies with this glucan using targeted metabolomics could confirm biomarkers of therapeutic intervention of steatosis and could be translated into healthy food products.

biochemistry↗

bioRxiv2025

Modular Assembly of Biohybrid Machines Using Force-Enhanced Skeletal Muscle Actuators

Muscle-based biohybrid systems integrate living muscle with engineered structures to create soft robots, biological models, and regenerative platforms. However, current actuators often lack strength and are difficult to assemble into complex devices. This study presents a suspended compliant skeleton that enhances muscle maturation by providing passive resistance, enabling high-stroke self-exercise without external stimulation. Using immortalized C2C12 cells, the resulting actuators achieved millimeter-scale strokes and millinewton-scale forces, surpassing previous benchmarks. Magnetic interfaces embedded in the skeleton allowed modular assembly into multi-degree-of-freedom devices such as grippers, arms, and positioning stages. These interfaces also support actuator replacement and repair, improving resilience and scalability. This approach significantly boosts engineered muscle performance and offers a robust, modular platform for building high-functioning, repairable biohybrid machines.

bioengineering↗

bioRxiv2019

CGGBP1 regulates chromatin barrier activity and CTCF occupancy at repeats

CGGBP1 is a repeat-binding protein with diverse functions in regulation of gene expression, cytosine methylation, repeat silencing and genomic integrity. CGGBP1 has also been identified as a cooperator factor in histone modifying complexes and as a component of protein complexes that form the enhancer-promoter loops. Here we report that the occupancy of CTCF at repeats and the chromatin barrier function of these repeat sequences depends on CGGBP1. Using ChIP-sequencing for CTC we describe CTCF binding on repetitive DNA. Our results show that CGGBP1 determines the CTCF occupancy preference for repeats over canonical CTCF-motif. By combining CTCF ChIP-sequencing results with ChIP-sequencing for three different kinds of histone modifications (H3K4me3, H3K9me3 and H3K27me3) we uncover insulator-like chromatin barrier activities of the repeat-rich CTCF-binding sites. This work shows that CGGBP1 is a regulator of CTCF occupancy and posits it as a regulator of barrier functions of CTCF-binding sites.

genomics↗