Dietary Beta-Hydroxy-Beta-Methyl Butyrate Supplementation Inhibits Hepatic Fat Deposition via Regulating Gut Microbiota in Broiler Chickens

The present study is aimed to explore the effects of different dietary beta-hydroxy-beta-methyl butyrate (HMB) levels (0, 0.05%, 0.10%, or 0.15%) on liver lipid metabolism on Wenshi broiler chickens. Results showed that HMB reduced the liver weight as well as liver concentrations of triacylglycerol (TG) and total cholesterol (TC) (quadratically, p < 0.05), and the lowest values were observed in the 0.10% HMB group. Meanwhile, HMB supplementation significantly altered the expression levels of key genes related to lipid metabolism in the liver of broiler chickens (p < 0.05). Furthermore, 16S rRNA gene sequencing revealed that HMB supplementation could greatly change the richness, diversity, and composition of the broiler gut microbiota, and the Bacteroidetes relative abundance at the phylum level and the Alistipes relative abundance at the genus level were affected (p < 0.05). Correlation analysis further suggested a strong association between Bacteroidetes relative abundance and lipid metabolism-related parameters (p < 0.05). Together, these data suggest that 0.10% HMB supplementation could inhibit hepatic fat deposition via regulating gut microbiota in broilers.

Dietary supplementation with inosine-5′-monophosphate improves the functional, energetic, and antioxidant status of liver and muscle growth in pigs

Inosine 5′-monophosphate (5′-IMP) is an essential nucleotide for de novo nucleotide biosynthesis and metabolism of energy, proteins, and antioxidants. Nucleotides are conditionally essential, as they cannot be produced sufficiently rapidly to meet the needs of the body in situations of oxidative stress or rapid muscle growth. A deficient intake of nucleotides can result in decreased ATP and GTP synthesis and impaired metabolism. We demonstrated that supplementation of finishing pig diets with 5′-IMP reduces the relative weight of the liver, and increases oxygen consumption during mitochondrial respiration without changing the ADP/O ratio, indicating an increase in the respiratory efficiency of liver mitochondria. We also observed a reduction in liver lipid peroxidation and an increase in muscle creatine. Moreover, 5′IMP supplementation increases slaughter weight, lean meat yield, sarcomere length, and backfat thickness in finishing barrows, demonstrating influence on protein metabolism. We suggest that 5′-IMP supplementation increase the mitochondrial respiratory capacity when the liver metabolic activity is stimulated, enhances antioxidant defense, and promotes muscle growth in finishing barrows.

Effect of Dietary Marula Nut Meal on Liver Lipid Content and Surrogate Markers of Liver and Kidney Function of Broiler and Layer Japanese Quail

Marula nut meal (MNM) can substitute soyabean meal (SBM) as a dietary protein source in Japanese quail diets without compromising growth performance and egg production. However, MNM has a high residual oil content which may impact metabolic health. The effects of MNM on hepatic lipid content and general, liver and kidney health have not been determined in both broilers and layers. Accordingly, two studies were run. In the broiler study two hundred 9-days old Japanese quail were randomly allocated to five diets wherein MNM replaced SBM on a crude protein (CP) basis at 0%, 25%, 50%, 75% and 100%, respectively, in both grower and finisher diets. In the layer study, sixty 5-weeks old Japanese maiden hens, individually housed, were randomly allocated to five-layer diets where MNM replaced SBM on a graded CP basis as for the broilers and fed for 8 weeks. At study termination the birds were slaughtered, blood collected and plasma harvested. Livers were excised, weighed and liver lipid content determined. Plasma surrogate markers of general health, liver and kidney function were determined. Dietary MNM had no effect (P > 0.05) on liver lipid content as well plasma surrogate markers of general health, liver and kidney function of the broiler quail. Dietary MNM at 75% of SBM CP significantly increased plasma phosphorus concentration of quail hens compared to that of counterparts fed control. Dietary MNM can be used in broiler and layer Japanese quail diets without risking development of fatty livers and compromising liver and kidney function.

Effects of hookah smoking on liver functions, lipid profile, and adult blood count

Introduction and Aim: Smoking is the most common habit and the largest health risk among people who have an impact on the human body. The goal of our study was to examine the effects of hookah (Shisha) on the liver, lipid profile, and blood content in adult smokers to adult non-smokers. Materials and Methods: A total of 50 men between the ages of 30 and 60 years took part in the study. These samples were divided into two groups: 30 smokers and 20 non-smokers. Every male is subjected to a complete medical history survey as well as frequent tests to rule out any underlying illnesses or diseases. Blood samples were taken in quantities of 10 mL to examine the blood. Blood samples were placed on the red roof when blood samples were used with anticoagulant factor. The identification of biological parameters was done using enzyme methods and a Random kit. Results: The results showed that Hb, PCV, WBC, ESR, platelets, and RBC were all elevated, whereas ALP and transaminase enzymes were not. Although not significantly, TC and TG increased the lipid profile findings. Our analysis yielded a wide range of outcomes. Various factors could be to blame for these disparities. Conclusion: We describe how future research will focus on the relationship between organ functions and their working tests for smoking effects based on our findings. Age, sex, nutrition, and hereditary behavior must all be included in future studies.

Lipidomic Profiling Reveals the Reducing Lipid Accumulation Effect of Dietary Taurine in Groupers (Epinephelus coioides)

A lipidomic analysis was conducted to provide the first detailed overview of lipid molecule profiles in response to dietary lipid and taurine and associations of liver lipid-lowering effects of dietary taurine with lipid molecular species and the positional distributions of fatty acids in the liver of juvenile orange-spotted groupers (Epinephelus coioides). The results indicated that the liver was more sensitive to varied dietary lipid and taurine contents than the muscle with regard to lipid molecules. A total of 131 differential lipid molecules (DLMs) were observed in the liver of groupers when dietary taurine was increased from 0 to 1% at 15% lipid, among which all the up and down-regulated DLMs are phospholipids (PLs) and triglycerides (TGs), respectively. The liver content of TGs containing 18:2n-6 attached at the sn-2 and sn-3 positions on the glycerol backbone increased with increasing dietary lipid from 10 to 15% but decreased with increasing dietary taurine from 0 to 1%. Therefore, dietary taurine can not only reduce lipid accumulation through decreasing the contents of TGs containing 18:2n-6 at the sn-2 and sn-3 positions but also enhance the anti-inflammatory capacity and health status of groupers. This study will also provide a new insight into the function of taurine in farmed fish.

Transcriptomic Analysis Reveals the Protective Effects of Empagliflozin on Lipid Metabolism in Nonalcoholic Fatty Liver Disease

Empagliflozin is a novel type of sodium-glucose cotransporter two inhibitor with diverse beneficial effects in the treatment of nonalcoholic fatty liver disease (NAFLD). Although empagliflozin impacts NAFLD by regulating lipid metabolism, the underlying mechanism has not been fully elucidated. In this study, we investigated transcriptional regulation pathways affected by empagliflozin in a mouse model of NAFLD. In this study, NAFLD was established in male C57BL/6J mice by administration of a high-fat diet; it was then treated with empagliflozin and whole transcriptome analysis was conducted. Gene expression levels detected by transcriptome analysis were then verified by quantitative real-time polymerase chain reaction, protein levels detected by Western Blot. Differential expression genes screened from RNA-Seq data were enriched in lipid metabolism and synthesis. The Gene Set Enrichment Analysis (GSEA) results showed decreased lipid synthesis and improved lipid metabolism. Empagliflozin improved NAFLD through enhanced triglyceride transfer, triglyceride lipolysis and microsomal mitochondrial β-oxidation. This study provides new insights concerning the mechanisms by which sodium-glucose cotransporter two inhibitors impact NAFLD, particularly in terms of liver lipid metabolism. The lipid metabolism-related genes identified in this experiment provide robust evidence for further analyses of the mechanism by which empagliflozin impacts NAFLD.

Hepatocyte-specific activity of TSC22D4 triggers progressive NAFLD by impairing mitochondrial function

Objective: Fibrotic organ responses have recently been identified as long-term complication in diabetes. Indeed, insulin resistance and aberrant hepatic lipid accumulation represent driving features of progressive non-alcoholic fatty liver disease (NAFLD), ranging from simple steatosis and non-alcoholic steatohepatitis (NASH) to fibrosis. Effective pharmacological regimens to stop progressive liver disease are still lacking to-date. Methods: Based on our previous discovery of transforming growth factor beta-like stimulated clone (TSC)22D4 as a key driver of insulin resistance and glucose intolerance in obesity and type diabetes, we generated a TSC22D4-hepatocyte specific knockout line (TSC22D4-HepaKO) and exposed mice to control or NASH diet models. Mechanistic insights were generated by metabolic phenotyping and single cell liver sequencing. Results: Hepatic TSC22D4 expression was significantly correlated with markers of liver disease progression and fibrosis in both murine and human livers. Indeed, hepatic TSC22D4 levels were elevated in human NASH patients as well as in several murine NASH models. Specific genetic deletion of TSC22D4 in hepatocytes led to reduced liver lipid accumulation, improvements in steatosis and inflammation scores and decreased apoptosis in mice. Single cell RNA sequencing revealed a distinct gene signature identifying an upregulation of mitochondrial-related processes. An enrichment of genes involved in the TCA cycle, mitochondrial organization, and triglyceride metabolism underscored the hepatocyte-protective phenotype and overall decreased liver damage as seen in mouse models. Conclusions: Together, our data uncover a new connection between targeted depletion of TSC22D4 and intrinsic metabolic processes in progressive liver disease. Cell-specific reduction of TSC22D4 improves hepatic steatosis, inflammation and promotes hepatocyte survival thus paving the way for further preclinical therapy developments.

Comparison of Visceral Fat Lipolysis Adaptation to High-Intensity Interval Training in Obesity-Prone and Obesity-Resistant Rats

Background/objectives: Visceral obesity is one of the key features of metabolic syndrome. High-intensity interval training (HIIT) could effectively reduce visceral fat but its effects show strong heterogeneity in populations with different obesity degree. The mechanism may be related to the differential adaptation to training between obesity phenotypes, namely obesity prone (OP) and obesity resistant (OR). The aim of the present study was to compare adaptive changes of visceral adipose lipolysis adaptation to HIIT between OP and OR animals and further explore the upstream pathway.Methods: OP and OR Sprague Dawley rats were established after feeding a high-fat diet for 6 weeks; they were then divided into HIIT (H-OP and H-OR) and control (C-OP and C-OR) groups. After 12 weeks of HIIT or a sedentary lifestyle, animals were fasted for 12 h and then sacrificed for histology as well as gene and protein analysis. Visceral adipocytes were isolated without fasting for catecholamine stimulation and β3-adrenergic receptor (β3-AR) blockade in vitro to evaluate the role of upstream pathways.Results: After training, there were no differences in weight loss or food intake between OP and OR rats (P > 0.05). However, the visceral fat mass, adipocyte volume and liver lipid of OP rats decreased more than that of OR rats (P < 0.05). Meanwhile, the cell lipolytic capacity and the increase in the expression of β3-AR was higher in the OP compared with OR groups (P < 0.05). Although training did not increase sympathetic nervous system activity (P > 0.05), the cell sensitivity to catecholamine increased significantly in the OP compared with OR groups (P < 0.05). After blocking β3-AR, the increased sensitivity disappeared.Conclusion: With HIIT, OP rats lost more visceral fat than OR rats, which was related to stronger adaptive changes in lipolysis. Increased β3-AR expression, rather than altered sympathetic nerve activity, mediated this adaption.