Biology subjects

Trinh, D.

Publications and source records attributed to Trinh, D..

3 recordsLinked to original sources

bioRxiv2026

Waste oil substrates reshape the black soldier fly larval gut microbiome and biomass composition during bioconversion

Black soldier fly larvae (BSFL) are generalist decomposers with promise for converting agricultural and food-processing by-products into value-added bioproducts, but BSFL performance on lipid-rich waste oil streams and the role of the gut microbiome in this process remains unclear. Here, we evaluated BSFL bioconversion of a standard chicken feed diet supplemented with three chemically distinct waste oils: acidulated vegetable oil (AVO), pork grease (PG), and used cooking oil (UCO). Larval performance, bioconversion rate, gut microbiome composition, total protein and fat content, and fatty-acid profiles were measured across bioconversion. Larval age was a major driver of gut microbiome structure, but waste oil supplementation further reshaped community membership and structure, with the strongest diet-associated effects occurring during early-to-intermediate bioconversion. Most differentially abundant taxa were members of the baseline core gut community, suggesting that oil supplementation primarily altered dominance patterns among resident taxa. PG and UCO supported larval growth and bioconversion performance comparable to the chicken feed control, whereas AVO reduced bioconversion rate and showed weaker growth outcomes. Oil supplementation also increased larval fat content, reduced protein content, and shifted fatty-acid profiles toward the corresponding oil feedstocks, although larval biomass composition remained shaped by basal diet and host or microbial metabolism. These findings show that selected lipid-rich waste streams can support efficient BSFL bioconversion while restructuring resident gut microbiome members that may tolerate, metabolize, or indirectly respond to oil-associated conditions, contributing to substrate-dependent changes in larval lipid accumulation and fatty-acid composition. IMPORTANCEAgricultural and food-processing systems generate large amounts of lipid-rich by-products that are difficult to manage using conventional waste-valorization approaches. Black soldier fly larvae (BSFL) offer a biological route for recovering nutrients from these materials, but efficient conversion depends on interactions among substrate chemistry, larval physiology, and the gut microbiome. This study shows that selected waste oil streams can support larval growth while restructuring resident gut microbial communities and altering larval fatty-acid composition. These findings are important for agricultural biotechnology because they frame BSFL production as a host-microbiome bioconversion system rather than simply an insect-based waste-reduction process. Understanding how gut microbes respond to chemically distinct lipid wastes can guide substrate selection, pretreatment, and microbiome-informed optimization strategies for converting underutilized agricultural and food-processing residues into value-added bioproducts for circular agricultural systems.

microbiology↗

bioRxiv2025

Toll-like Receptor 4 Contributes to PCOS-like Metabolic and Reproductive Pathogenesis

Polycystic ovary syndrome (PCOS) is a reproductive disorder with heterogeneous symptoms and severity. Despite extensive research documenting chronic immune dysfunction as a hallmark of PCOS, the specific molecular mechanisms driving immune activation and its connection to the syndromes diverse symptoms remain poorly understood. Emerging evidence suggests that gut-derived bacterial endotoxins, particularly lipopolysaccharide (LPS), may breach the intestinal barriers in PCOS patients and trigger systemic inflammation through Toll-like receptor 4 (TLR4), a pattern recognition receptor of the innate immune system. This study investigated whether TLR4 serves as a critical mechanistic driver of PCOS pathogenesis by examining the effect of genetic TLR4 knockout (TLR4-/-) in a letrozole (LET)-induced mouse model of PCOS. Our results demonstrate that TLR4 deficiency reduces many PCOS-like symptoms, including elevated luteinizing hormone, anovulation, and metabolic dysfunction. TLR4 knockout also preserved estrous cycling and fertility, improved glucose tolerance, maintained gut barrier integrity, and reduced inflammatory markers in LET-treated females. These findings establish TLR4 as a key mediator orchestrating PCOSs multi-system pathology, positioning TLR4 as a critical convergence point rather than affecting individual symptoms in isolation. This novel work reveals that TLR4-mediated inflammation drives multiple PCOS pathologies, opening avenues for targeted anti-inflammatory treatments in women with this disorder. Significance StatementPolycystic ovary syndrome (PCOS) affects up to 15% of reproductive-age women worldwide. This study reveals that TLR4, an innate immune receptor, is key to the pathophysiology of PCOS-like symptoms in female mice. When TLR4 was genetically deleted, mice treated with letrozole to induce PCOS-like symptoms maintained normal weight, glucose regulation, estrous cycling, and fertility. The improvements coincided with preserved gut barrier breakdown and reduced inflammation. These findings identify TLR4 as a key mediator between gut health, immune activation, and PCOS pathophysiology, suggesting that targeting TLR4 could offer new therapeutic approaches for this common but poorly understood syndrome affecting millions of women.

immunology↗

bioRxiv2023

Parkinsons Disease Pathology is Directly Correlated to SIRT3 in Human Subjects and Animal Models: Implications for AAV.SIRT3-myc as a Disease-Modifying Therapy.

Degeneration of the dopaminergic nigro-striatal pathway and presence of Lewy bodies are pathological hallmarks of Parkinsons disease (PD). Postmortem studies in human tissue have also demonstrated that a decline in mitochondrial number and function is also central to PD pathology. Sirtuin 3 (SIRT3) is a mitochondrial protein deacetylase which has been linked with longevity and cytoprotective effects. SIRT3 serves as a metabolic sensor and regulates mitochondrial homeostasis and oxidative stress, which likely stabilises telomere integrity, delaying senescence. Previously, we have shown that over-expression of SIRT3 rescues motor function and prevents degeneration of dopaminergic neurons in a virally over-expressing mutant (A53T)--synuclein model of PD. In the present study, we show that in the substantia nigra pars compacta (SNc) of human subjects, SIRT3 levels are negatively correlated with age (p<0.05, R=0.6539). In the hippocampus, there was no correlation between SIRT3 levels and age. In human subjects with PD, SIRT3 was reduced by 56.8{+/-}15.5% and 34.0{+/-}5.6% in the SNc and hippocampus respectively regardless of age. Given that age is the primary risk factor for PD, this finding suggests that reduced SIRT3 may be a causative factor contributing to PD pathology. Next in human subjects with PD, we measured whether there was a correlation between the amount of aggregated -synuclein and SIRT3 levels by measuring immunofluorescence of phosphorylated -synuclein (p-syn), which is a marker for Lewy bodies. Interestingly, in the hippocampus, but not SNc, there was a positive correlation between SIRT3 and p-syn levels, despite p-syn being reduced compared to control. Next using an -synuclein seeding rat model of PD, we assessed the disease-modifying effects of viral-mediated SIRT3 infusion. Six months following infusion of -synuclein pre-formed fibrils (PFF) into the SNc, there was 38.8{+/-}4.5% loss of TH-positive neurons, impaired striatal dopamine metabolism and pathological -synuclein throughout the brain. Phosphorylated--synuclein immunoreactivity was present in the SNc, olfactory tubercle, striatum, amygdala, hippocampus and motor cortex. In PD subjects, synuclein positive aggregates have also been reported in these brain regions. In PFF rats, infusion of rAAV1.SIRT3-myc in the SNc reduced abundance of -synuclein inclusions in the SNc by 30.1{+/-}18.5% which was not seen when deacetylation deficient SIRT3H248Y was transduced. This demonstrates the importance of SIRT3deacetylation in reducing -synuclein aggregation. However, while SIRT3 transduction reduced aggregation in the SNc, it had no significant effect on phosphorylated--synuclein levels in other brain regions. These studies confirm that SIRT3 is directly correlated with senescence and aging in humans. We also provide evidence that reduced SIRT3 contributes to the pathology of clinical PD. Finally, by showing that over-expression of SIRT3 prevents -synuclein aggregation through de-acetylation-dependent mechanisms, we further validate AAV1.SIRT3-myc as a potential disease-modifying therapy for PD.

neuroscience↗