Organophosphorus pesticides (OPs) can be metabolized to diethyl phosphate (DEP) in the gut environment, which may affect the immune and endocrine systems and the microbiota. Correlations between OPs and diseases have been established by epidemiological studies, mainly based on the contents of their metabolites, including DEP, in the serum or urine. However, the effects of DEP require further study. Therefore, in this study, adult male rats were exposed to 0.08 or 0.13 mg/kg DEP for 20 weeks. Serum levels of hormones, lipids, and inflammatory cytokines as well as gut microbiota were measured. DEP significantly enriched opportunistic pathogens, including Paraprevotella, Parabacteroides, Alloprevotella, and Helicobacter, leading to a decrease in interleukin-6 (IL-6). Exposure to the high dose of DEP enriched the butyrate-producing genera, Alloprevotella and Intestinimonas, leading to an increase in estradiol and a resulting decrease in total triglycerides (TGs) and low-density lipoprotein cholesterol (LDL-C); meanwhile, DEP-induced increases in peptide tyrosine‒tyrosine (PYY) and ghrelin were attributed to the enrichment of short-chain fatty acid-producing Clostridium sensu stricto 1 and Lactobacillus. These findings indicate that measuring the effects of DEP is not a proxy for measuring the effects of its parent compounds.

Nonalcoholic fatty liver disease (NAFLD) is characterized by lipotoxicity and ectopic lipid deposition within hepatocytes. Sulforaphane (SFA), an active compound used for inhibiting tumors, was found to have the potency to improve lipid metabolism. However, its molecular mechanisms on ameliorating NAFLD are still incompletely understood. This research evaluated if SFA could inhibit hepatic steatosis and apoptosis. The effects of SFA on cell viability, lipid accumulation, triglyceride (TG) contents, apoptosis, ceramide contents, and reactive oxygen species (ROS) levels were analyzed in palmitic acid (PA)-treated HepG2 cells and high-fat diet (HFD)-fed mice. The related molecular mechanisms were further explored in hepatocytes. The results showed SFA alleviated lipid accumulation and regulated AMPK/SREBP1c/FAS signaling pathway in PA-stressed HepG2 cells. In addition, SFA alleviated PA-mediated apoptosis, downregulated the expressions of cleaved caspase 3, as well as reduced ceramide contents and ROS levels. Moreover, SFA treatment reduced HFD-induced body weight gain, alleviated insulin resistance, decreased serum TG, total cholesterol (TC), and alanine aminotransferase (ALT) levels, and prevented lipid deposition and apoptosis in the liver. This study showed SFA suppressed lipid deposition and apoptosis both in vitro and in vivo, indicating that SFA may be a potential candidate for preventing and treating NAFLD.

Fatty acid β-oxidation (FAO) is confirmed to be impaired in obesity, especially in adipose tissues. We previously proved that Bifidobacterium animalis subsp. lactis A6 (BAA6) had protective effects against diet-induced obesity. However, whether BAA6 enhances FAO to ameliorate the development of obesity has not been explored. After being fed with high-fat diet (HFD) for 9 weeks, male C57BL/6J mice were fed HFD or BAA6 for 8 weeks. In vitro study was carried out using 3T3-L1 adipocytes to determine the effect of BAA6 culture supernatant (BAA6-CM). Here, we showed that administration of BAA6 to mice fed with HFD decreased body weight gain (by 5.03 g) and significantly up-regulated FAO in epididymal adipose tissues. In parallel, FAO in 3T3-L1 cells was increased after BAA6-CM treatment. Acetate was identified as a constituent of BAA6-CM that showed a similar effect to BAA6-CM. Furthermore, acetate treatment activated the GPR43-PPARα signaling, thereby promoting FAO in 3T3-L1 cells. The levels of acetate were also elevated in serum and feces (by 1.92- and 2.27-fold) of HFD-fed mice following BAA6 administration. The expression levels of GPR43 and PPARα were increased by 55.45% and 69.84% after BAA6 supplement in the epididymal fat of mice. Together, these data reveal that BAA6 promotes FAO of adipose tissues through the GPR43-PPARα signaling, mainly by increasing acetate levels, leading to alleviating the development of obesity.

Sulforaphane (SFN) was generated by the hydrolysis of glucoraphanin under the action of myrosinase. However, due to the instability of SFN, the bioavailability of SFN was limited. Meanwhile, the gut flora obtained the ability to synthesize myrosinase and glucoraphanin, which could be converted into SFN in the intestine. However, the ability of microorganisms to synthesize myrosinase in the gut was limited. Therefore, microorganisms with myrosinase synthesis ability need to be supplemented. With the development of research, microorganisms with high levels of myrosinase synthesis could be obtained by artificial selection and gene modification. Researchers found the SFN production rate of the transformed microorganisms could be significantly improved. However, despite applying transformation technology and regulating nutrients to microorganisms, it still could not provide the best efficiency during generating SFN and could not accomplish colonization in the intestine. Due to the great effect of microencapsulation on improving the colonization ability of microorganisms, microencapsulation is currently an important way to deliver microorganisms into the gut. This article mainly analyzed the possibility of obtaining SFN-producing microorganisms through gene modification and delivering them to the gut via microencapsulation to improve the utilization rate of SFN. It could provide a theoretical basis for expanding the application scope of SFN.

Background: Acrylamide is formed during food heating and is neurotoxic to animals and potentially carcinogenic to humans. It is important to reduce acrylamide content during food processing. Researchers have suggested that garlic powder could reduce acrylamide content, but the key substance and acrylamide reduction pathway of garlic powder was unclear. Methods: The inhibitory effect of garlic powder on acrylamide in asparagine/glucose solution and a fried potato model system were firstly evaluated. Furthermore, the effect of allicin on the amount of produced acrylamide in the asparagine/glucose solution model system and fried potatoes was studied with kinetic analysis. Results: The freeze-dried garlic powder had a higher inhibition rate (41.0%) than oven-dried garlic powder (maximum inhibition rate was 37.3%), and allicin had a 71.3% attribution to the reduction of acrylamide content. Moreover, the inhibition rate of allicin had a nonlinear relationship with the addition level increase. The kinetic analysis indicated that garlic powder and allicin could reduce acrylamide content through the AA formation stage, but not the decomposition stage. Conclusions: Allicin was the key component of garlic powder in reducing acrylamide content during acrylamide formation stage. This research could provide a new method to reduce acrylamide content during food processing and expand the application area of garlic.