Dietary saponins of sea cucumber alleviate orotic acid-induced fatty liver in rats via PPARα and SREBP-1c signaling

<p>Abstract</p> <p>Background</p> <p>Nonalcoholic fatty liver disease is the most common chronic liver disease in the world, and is becoming increasingly prevalent. Saponins of sea cucumber (SSC) are proven to exhibit various biological activities. Therefore, the present study was undertaken to examine the effect of saponins extracted from sea cucumber (Pearsonothuria graeffei) on the preventive activity of fatty liver in rats.</p> <p>Methods</p> <p>Male Wistar rats were randomly divided into five groups, including normal control group, fatty liver model group, SSC-treated group with SSC at levels of 0.01%, 0.03% and 0.05%. Model rats were established by administration with 1% orotic acid (OA). After the experiment period, serum total cholesterol (TC), triglyceride (TG), and hepatic lipid concentrations were determined. To search for a possible mechanism, we examined the changes of key enzymes and transcriptional factors involved in hepatic lipids biosynthesis, fatty acid β-oxidation.</p> <p>Results</p> <p>Both 0.03% and 0.05% SSC treatment alleviated hepatic steatosis and reduced serum TG and TC concentration significantly in OA fed rats. Hepatic lipogenic enzymes, such as fatty acid synthase (FAS), malic enzyme (ME), and glucose-6-phosphate dehydrogenase (G6PDH) activities were inhibited by SSC treatment. SSC also decreased the gene expression of FAS, ME, G6PDH and sterol-regulatory element binding protein (SREBP-1c). Otherwise, the rats feeding with SSC showed increased carnitine palmitoyl transferase (CPT) activity in the liver. Hepatic peroxisome proliferator-activated receptor (PPARα), together with its target gene CPT and acyl-CoA oxidase (ACO) mRNA expression were also upregulated by SSC.</p> <p>Conclusions</p> <p>According to our study, the lipids-lowering effect of dietary SSC may be partly associated with the enhancement of β-oxidation via PPARα activation. In addition, the inhibited SREBP-1c- mediated lipogenesis caused by SSC may also contribute to alleviating fatty liver.</p

The mechanism of dietary cholesterol effects on lipids metabolism in rats

<p>Abstract</p> <p>Background</p> <p>Cholesterol administration has been reported to influence hepatic lipid metabolism in rats. In the present study, the effect of dietary cholesterol on hepatic activity and mRNA expression of the enzymes involved in lipid metabolism were investigated. Fourteen male Wistar rats were randomly divided into 2 groups and fed 1% cholesterol or cholesterol free AIN76 diets for 4 weeks.</p> <p>Results</p> <p>The serum triglyceride and high density lipoprotein cholesterol levels were significantly decreased but the total cholesterol and non high density lipoprotein cholesterol levels were significantly increased in the cholesterol-fed rats compared with the control rats. And the concentrations of the hepatic total cholesterol and triglyceride increased about 4-fold and 20-fold separately by dietary cholesterol. The activities of hepatic malic enzyme, glucose-6-phosphate dehydrogenase, fatty acid synthase, phosphatidate phophatase and carnitine palmitoyl transferase were depressed by the cholesterol feeding (40%, 70%, 50%, 15% and 25% respectively). The results of mRNA expression showed that fatty acid synthase, carnitine palmitoyl transferase 1, carnitine palmitoyl transferase 2, and HMG-CoA reductase were down-regulated (35%, 30%, 50% and 25% respectively) and acyl-CoA: cholesterol acyltransferase and cholesterol 7α-hydroxylase were up regulated (1.6 and 6.5 folds) in liver by the cholesterol administration.</p> <p>Conclusions</p> <p>The dietary cholesterol increased the triglyceride accumulation in liver, but did not stimulate the activity and the gene expression of hepatic enzymes related to triglyceride and fatty acid biosynthesis.</p

1-Benzoyl-3-(5-quinol­yl)thio­urea

The title compound, C17H13N3OS, was obtained by the reaction of benzoyl chloride, ammonium thio­cyanate and 5-amino­quinoline in the presence of polyethyl­eneglycol-400 (PEG-400) as a phase-transfer catalyst. The compound crystallized as discrete mol­ecules linked by N—H⋯N and C—H⋯N hydrogen bonds involving all the potential donors, generating sheets parallel to (100). An intramolecular N—H⋯O bond is also present

A Duty to Forget, a Right to be Assured? Exposing Vulnerabilities in Machine Unlearning Services

The right to be forgotten requires the removal or "unlearning" of a user's data from machine learning models. However, in the context of Machine Learning as a Service (MLaaS), retraining a model from scratch to fulfill the unlearning request is impractical due to the lack of training data on the service provider's side (the server). Furthermore, approximate unlearning further embraces a complex trade-off between utility (model performance) and privacy (unlearning performance). In this paper, we try to explore the potential threats posed by unlearning services in MLaaS, specifically over-unlearning, where more information is unlearned than expected. We propose two strategies that leverage over-unlearning to measure the impact on the trade-off balancing, under black-box access settings, in which the existing machine unlearning attacks are not applicable. The effectiveness of these strategies is evaluated through extensive experiments on benchmark datasets, across various model architectures and representative unlearning approaches. Results indicate significant potential for both strategies to undermine model efficacy in unlearning scenarios. This study uncovers an underexplored gap between unlearning and contemporary MLaaS, highlighting the need for careful considerations in balancing data unlearning, model utility, and security.Comment: To Appear in the Network and Distributed System Security Symposium (NDSS) 2024, San Diego, CA, US

Short term effects of different omega-3 fatty acid formulation on lipid metabolism in mice fed high or low fat diet

BACKGROUND: Bioactivities of Docosahexaenoic acid (DHA) and Eicosapentaenoic acid (EPA) depend on their chemical forms. The present study was to investigate short term effects of triglyceride (TG), ethyl ester (EE), free fatty acid (FFA) and phospholipid (PL) forms of omega-3 fatty acid (FA) on lipid metabolism in mice, fed high fat or low fat diet. METHOD: Male Balb/c mice were fed with 0.7% different Omega-3 fatty acid formulation: DHA bound free fatty acid (DHA-FFA), DHA bound triglyceride (DHA-TG), DHA bound ethyl ester (DHA-EE) and DHA bound phospholipid (DHA-PL) for 1 week, with dietary fat levels at 5% and 22.5%. Serum and hepatic lipid concentrations were analyzed, as well as the fatty acid composition of liver and brain. RESULT: At low fat level, serum total cholesterol (TC) level in mice fed diets with DHA-FFA, DHA-EE and DHA-PL were significantly lower than that in the control group (P < 0.05). Hepatic TG level decreased significantly in mice fed diets with DHA-TG (P < 0.05), DHA-EE (P < 0.05) and DHA-PL (P < 0.05), while TC level in liver was significantly lower in mice fed diets with TG and EE compared with the control group (P < 0.05). At high fat level, mice fed diets with DHA-EE and DHA-PL had significantly lower hepatic TC level compared with the control diet (P < 0.05). Hepatic PL concentration experienced a significant increase in mice fed the diet with PL at high fat level (P < 0.05). Furthermore, both at low and high fat levels, hepatic DHA level significantly increased and AA level significantly decreased in all forms of DHA groups (P < 0.05), compared to control groups at two different fat levels, respectively. Additionally, cerebral DHA level in mice fed diets with DHA-FFA, DHA-EE and DHA-PL significantly increased compared with the control at high fat level (P < 0.05), but no significant differences were observed among dietary treatments for mice fed diets with low fat level. CONCLUSION: The present study suggested that not only total dietary fat content but also the molecular forms of omega-3 fatty acids contributed to lipid metabolism in mice. DHA-PL showed effective bioactivity in decreasing hepatic and serum TC, TG levels and increasing omega-3 concentration in liver and brain

A new stripe rust resistance gene transferred from Thinopyrum intermedium to hexaploid wheat (Triticum aestivum)

Wheat stripe rust (Puccinia striiforis f. sp. tritici) races CYR31 and CYR32, prevalent in China, are virulent to many wheat stripe rust resistance genes (Yr genes). To expand the availability of effective resistance to CYR31 and CYR32, stripe rust resistance was transferred from intermediate wheatgrass (Thinopyrum intermedium) to common wheat (Triticum aestivum). The susceptible wheat cultivar CM107 was crossed with amphiploid TAI7047, derived from the wide cross Taiyuan768/Thinopyrum intermedium//76(64). Two wheat lines originating from the cross, YU24 and YU25, were resistant to CYR31 and CYR32. Pedigree analysis showed that the resistance to stripe rust in YU24 and YU25 originated from intermediate wheatgrass. Genetic analyses indicated that the resistance to stripe rust is controlled by a single dominant gene. Allelic tests determined that the resistance gene(s) in YU24 and YU25 are identical. The new gene has temporarily been designated as YrYU25. SSR and RAPD analyses showed that YrYU25 was introduced by cryptic translocation into common wheat.Les races CYR31 et CYR32 de la rouille jaune du blé (Puccinia striiforis f. sp. tritici), très répandues en Chine, sont virulentes pour plusieurs gènes de résistance à cette maladie (gènes Yr). Afin d'accroître la disponibilité d'une résistance efficace aux races CYR31 et CYR32, la résistance à la rouille jaune du blé a été transférée de l'agropyre intermédiaire (Thinopyrum intermedium) au blé tendre (Triticum aestivum). CM107, un cultivar de blé sensible, a été croisé avec l'amphiploïde AI7047 dérivé du croisement éloigné Taiyuan768/Thinopyrum intermedium//76(64). Deux lignées de blé provenant de ce croisement, soit YU24 et YU25, étaient résistantes aux races CYR31 et CYR32. Une analyse généalogique a démontré que la résistance à la rouille jaune du blé chez les lignées YU24 et YU25 provenait de l'agropyre intermédiaire. Des analyses génétiques ont indiqué que cette résistance était contrôlée par un seul gène dominant. Des tests d'allélisme ont révélé que le(s) gène(s) de résistance dans les lignées YU24 et YU25 étaient identiques. Le nouveau gène a temporairement été nommé YrYU25. Des analyses SSR et RAPD ont démontré que le gène YrYU25 avait été introduit dans le blé tendre par translocation cryptique