Protective effects of butyric acid during heat stress on the survival, immune response, histopathology, and gene expression in the hepatopancreas of juvenile pacific shrimp (L. Vannamei).

This study looked at the effects of adding butyric acid (BA) to the diets of juvenile Pacific shrimp and how it affected their response to survival, immunity, histopathological, and gene expression profiles under heat stress. The shrimp were divided into groups: a control group with no BA supplementation and groups with BA inclusion levels of 0.5 %, 1 %, 1.5 %, 2 %, and 2.5 %. Following the 8-week feeding trial period, the shrimp endured a heat stress test lasting 1 h at a temperature of 38 °C. The results showed that the control group had a lower survival rate than those given BA. Interestingly, no mortality was observed in the group receiving 1.5 % BA supplementation. Heat stress had a negative impact on the activities of alkaline phosphatase (AKP) and acid phosphatase (ACP) in the control group. Still, these activities were increased in shrimp fed the BA diet. Similar variations were observed in AST and ALT fluctuations among the different groups. The levels of triglycerides (TG) and cholesterol (CHO) increased with high temperatures but were reduced in shrimp-supplemented BA. The activity of an antioxidant enzyme superoxide dismutase (SOD) increased with higher BA levels (P < 0.05). Moreover, the groups supplemented with 1.5 % BA exhibited a significant reduction in malondialdehyde (MDA) content (P < 0.05), suggesting the potential antioxidant properties of BA. The histology of the shrimp's hepatopancreas showed improvements in the groups given BA. Conversely, the BA significantly down-regulated the HSPs and up-regulated MnSOD transcript level in response to heat stress. The measured parameters determine the essential dietary requirement of BA for shrimp. Based on the results, the optimal level of BA for survival, antioxidant function, and immunity for shrimp under heat stress is 1.5 %.

Glycerol monolaurate (GML), a medium-chain fatty acid derivative, ameliorate growth performance, immune function, disease resistance and intestinal microbiota in juvenile hybrid grouper (Epinephelus fuscoguttatus♀ × Epinephelus lanceolatus♂).

In order to evaluate the effects of glycerol monolaurate (GML) on the growth performance, immunology function, disease resistance and intestinal microbiota for hybrid groupers. Seven levels of GML (0, 600, 1200, 1800, 2400, 3000 and 3600 mg/kg) were added to diets and were noted as the G1 (control group), G2, G3, G4, G5, G6 and G7, respectively. Each experimental diet was fed to triplicate groups of 30 juvenile groupers for 8 weeks. The FBW, WGR and SGR were significantly higher and FCR was significantly lower in the G4 group compared to the G1 group (P < 0.05). Serum immune enzyme activities (ACP, AKP and LZM) rose and then fell and had the highest values in the G4 group (P < 0.05). The expression of TNF-α and IL6 in head kidney was significantly inhibited (P < 0.05), while the expression of TLR22 was increased (P < 0.05). After the Vibrio parahaemolyticus challenge test, ACP and AKP activities were increased in the G4 and G5 groups, while mortality was lower than in the G1 group (P < 0.05). GML significantly modulated the abundance of intestinal microbiota, with the G4 and G5 groups increasing the relative abundance of the Firmicutes and Bacillus, respectively (P < 0.05). The alpha diversity of the G5 group (Sob, Chao1 and ACE) was significantly higher than that of the G1 group (P < 0.05). In summary, the optimal level of GML was 1700 mg/kg according to the regression equation model fitted by the WGR index.

Comprehensive analysis of butyric acid impact on immunology, histopathology, gene expression, and metabolomic responses in pacific shrimp experiencing cold stress.

In this study, our objective was to investigate the impact of dietary butyric acid (BA) on the homeostasis mechanism of Pacific shrimp under cold stress. Specifically, we analyzed its effects on immunity, antioxidant capacity, gene expression, and metabolomics response. To carry out this research, Litopenaeus vannamei were fed a diet supplemented with BA for 8 weeks. Following this feeding period, a total of 180 shrimp, with an average weight of 12.76 ± 0.38 g, were exposed to cold conditions, with the temperature decreasing from 28 °C to 14 °C within an hour. The results of our study revealed survival rates ranging from 90 % to 100 %. Shrimp that were fed a diet containing 1.5 % BA exhibited a significant increase in acid phosphatase (ACP) and alkaline phosphatase (AKP) activity. Conversely, the control groups showed an increase in aspartate aminotransferase (AST) and alanine transaminase (ALT) activity. Shrimp that consumed diets containing 1.5 % BA displayed the lowest malondialdehyde (MDA) levels with the highest superoxide dismutase (SOD) content. The shrimp fed the BA diet exhibited tightly organized hepatic tubules with a star-shaped lumen filled with numerous B and R cells. Furthermore, shrimp fed the BA diet demonstrated a significant increase in caspase 3 (CASP) expression. There were no significant variations in the expression levels of prophenoloxidase (ProPO), manganese superoxide dismutase (MnSOD), and glutathione S-transferase (GST) The metabolites of Dl-carnitine, acetyl-l-carnitine, propionylcarnitine, hexanoylcarnitine, palmitoylcarnitine, decanoylcarnitine, and Dl-carnitine exhibited significantly increased expression in shrimp that were fed BA, suggesting their role in the lipolysis process. Based on the findings, adding 2 % BA to the diet of Pacific shrimp helps reduce inflammation and oxidative stress when they are under cold stress.

Genetic and inflammatory factors underlying gestational diabetes mellitus: a review.

Gestational diabetes mellitus (GDM) poses a significant global health concern, impacting both maternal and fetal well-being. Early detection and treatment are imperative to mitigate adverse outcomes during pregnancy. This review delves into the pivotal role of insulin function and the influence of genetic variants, including SLC30A8, CDKAL1, TCF7L2, IRS1, and GCK, in GDM development. These genetic variations affect beta-cell function and insulin activity in crucial tissues, such as muscle, disrupting glucose regulation during pregnancy. We propose a hypothesis that this variation may disrupt zinc transport, consequently impairing insulin production and secretion, thereby contributing to GDM onset. Furthermore, we discussed the involvement of inflammatory pathways, such as TNF-alpha and IL-6, in predisposing individuals to GDM. Genetic modulation of these pathways may exacerbate glucose metabolism dysregulation observed in GDM patients. We also discussed how GDM affects cardiovascular disease (CVD) through a direct correlation between pregnancy and cardiometabolic function, increasing atherosclerosis, decreased vascular function, dyslipidemia, and hypertension in women with GDM history. However, further research is imperative to unravel the intricate interplay between inflammatory pathways, genetics, and GDM. This understanding is pivotal for devising targeted gene therapies and pharmacological interventions to rectify genetic variations in SLC30A8, CDKAL1, TCF7L2, IRS1, GCK, and other pertinent genes. Ultimately, this review offers insights into the pathophysiological mechanisms of GDM, providing a foundation for developing strategies to mitigate its impact.