Potential for Biomass Production and Remediation by Cultivation of the Marine Model Diatom Phaeodactylum tricornutum in Oil Field Produced Wastewater Media

While oilfield produced water (PW) is one of the largest, unclaimed wastewater streams of the oil industry, it could potentially be used as a cultivation medium for microalgae. Microalgae could help with the remediation of this water while also delivering biomass that can be transformed into valuable byproducts such as biofuels. The coupling of these two purposes is expected to cut production costs of biofuels while aiding environmental protection. In this study, we compared the cultivation capacity of the marine model diatom Phaeodactylum tricornutum in media at varying salinities and in media composed of PW from two oilfields in the Central Valley of California that differed drastically in the concentration of inorganic and organic constituents. Specifically, we measured the carrying capacity of these media, the maximum growth rates of P. tricornutum, its cellular lipid accumulation capacity, and its capacity to remediate the most polluted PW source. Our study shows that P. tricornutum can successfully adjust to the tested cultivation media through processes of short-term acclimation and long-term adaptation. Furthermore, the cultivation of P. tricornutum in the most heavily polluted PW source led to significant increases in cell yield and improved photosynthetic capacity during the stationary phase, which could be attributed chiefly to the higher levels of nitrate present in this PW source. Chemical water analyses also demonstrated the capability of P. tricornutum to remediate major nutrient content and potentially harmful elements like fluorine and copper. Because P. tricornutum is amenable to advanced genetic engineering, which could be taken advantage of to improve its cultivation resilience and productivity in an economic setting, we propose this study as a step towards essential follow-up studies that will identify the genetic regulation behind its growth in oilfield PW media and its remediation of the PW constituents.

Fatty acids suppress the steroidogenesis of the MA-10 mouse Leydig cell line by downregulating CYP11A1 and inhibiting late-stage autophagy

Obese men have lower circulating testosterone than men with an optimal body mass index. Elevated fatty acids (FAs) caused by obesity have been reported to suppress the steroidogenesis of Leydig cells. Recent studies have demonstrated that autophagy regulates steroidogenesis in endocrine cells; however, few studies have investigated the molecular mechanisms of FA-impaired steroidogenesis. To study FA regulation in the steroidogenesis of Leydig cells, MA-10 cells were treated with an FA mixture and co-treated with 8-Br-cAMP to stimulate the steroidogenesis capacity. We showed that FAs led to cellular lipid accumulation and decreased steroidogenesis of MA-10 cells, and FA-suppressed steroidogenesis was largely recovered by P5 treatment but not by 22R-OHC treatment, suggesting the primary defect was the deficiency of CYP11A1. To examine the involvement of autophagy in the steroidogenesis of Leydig cells, we treated MA-10 cells with autophagy regulators, including rapamycin, bafilomycin, and chloroquine. Inhibition of late-stage autophagy including FA-upregulated Rubicon suppressed the steroidogenesis of MA-10 cells. More interestingly, Rubicon played a novel regulatory role in the steroidogenesis of MA-10 cells, independent of inhibitors of late-stage autophagy. Collectively, this study provides novel targets to investigate the interaction between FAs and steroidogenesis in steroidogenic cells.

Antioxidant Effect of Wheat Germ Extracts and Their Antilipidemic Effect in Palmitic Acid-Induced Steatosis in HepG2 and 3T3-L1 Cells

Wheat germ (WG) is a by-product of wheat milling and comprises many bioactive compounds. This study aimed to compare the antioxidant and antilipidemic effects of different WG extracts (WGEs) by analyzing candidate bioactive compounds such as carotenoids, tocopherols, γ-oryzanol, and biogenic amines by reversed-phase high-performance liquid chromatography. Antioxidant activity was determined using the ABTS, DPPH, and FRAP assays. The antilipidemic effect was evaluated in palmitic acid-induced steatosis in HepG2 hepatocytes and 3T3-L1 adipocytes. Cellular lipid accumulation was assessed by Oil Red O staining and a cellular triglyceride content assay. All analyzed WGEs showed significant antioxidant potential, although some bioactive compounds, such as carotenoids, tocopherols, and γ-oryzanol, were the highest in the ethanol extract. Correlation analysis revealed the antioxidant potential of all identified biogenic amines except for spermidine. Ethanol and n-hexane extracts significantly inhibited cellular lipid accumulation in cell models. These results suggest that WGEs exhibit promising antioxidant potential, with a variety of bioactive compounds. Collectively, the findings of this study suggest that bioactive compounds in WGEs attenuate plasma lipid and oxidation levels. In conclusion, WG can be used as a natural antioxidant and nutraceutical using appropriate solvents and extraction methods.

Jaceosidin Inhibits Adipogenesis in 3T3-L1 Adipocytes through the PPARγ Pathway

Jaceosidin, a natural flavone, has been reported to have anti-tumorigenic, anti-oxidant, and anti-inflammatory activities. However, the anti-adipogenic effects of jaceosidin have not been investigated. In this study, we demonstrate that jaceosidin suppresses adipocyte differentiation and cellular lipid accumulation without cytotoxicity. Jaceosidin also suppresses the mRNA and protein expression of adipogenesis-related genes. To our knowledge, these results are the first evidence of the anti-adipogenic effects of jaceosidin in 3T3-L1 adipocytes and suggest the use of jaceosidin as a treatment for obesity.

2-Bromo-4′-methoxychalcone and 2-Iodo-4′-methoxychalcone Prevent Progression of Hyperglycemia and Obesity via 5′-Adenosine-Monophosphate-Activated Protein Kinase in Diet-Induced Obese Mice

Obesity and diabetes are global health-threatening issues. Interestingly, the mechanism of these pathologies is quite different among individuals. The discovery and development of new categories of medicines from diverse sources are urgently needed for preventing and treating diabetes and other metabolic disorders. Previously, we reported that chalcones are important for preventing biological disorders, such as diabetes. In this study, we demonstrate that the synthetic halogen-containing chalcone derivatives 2-bromo-4′-methoxychalcone (compound 5) and 2-iodo-4′-methoxychalcone (compound 6) can promote glucose consumption and inhibit cellular lipid accumulation via 5′-adenosine-monophosphate-activated protein kinase (AMPK) activation and acetyl-CoA carboxylase 1 (ACC) phosphorylation in 3T3-L1 adipocytes and C2C12 skeletal myotubes. In addition, the two compounds significantly prevented body weight gain and impaired glucose tolerance, hyperinsulinemia, and insulin resistance, which collectively help to delay the progression of hyperglycemia in high-fat-diet-induced obese C57BL/6 mice. These findings indicate that 2-bromo-4′-methoxychalcone and 2-iodo-4′-methoxychalcone could act as AMPK activators, and may serve as lead compounds for a new class of medicines that target obesity and diabetes.

Role of miR-383 and miR-146b in different propensities to obesity in male mice

The study was designed to investigate the possible mechanisms of hepatic microRNAs (miRs) in regulating local thyroid hormone (TH) action and ultimately different propensities to high-fat diet (HFD)-induced obesity. When obesity-prone (OP) and obesity-resistant (OR) mice were fed HFD for 7 weeks, OP mice showed apparent hepatic steatosis, with significantly higher body weight and lower hepatic TH receptor b (TRb) expression and type 1 deiodinase (DIO1) activity than OR mice. Next-generation sequencing technology revealed that 13 miRs in liver were dysregulated between the two phenotypes, of which 8 miRs were predicted to target on Dio1 or TRb. When mice were fed for 17 weeks, OR mice had mild hepatic steatosis and increased Dio1 and TRb expression than OP mice, with downregulation of T3 target genes (including Srebp1c, Acc1, Scd1 and Fasn) and upregulation of Cpt1α, Atp5c1, Cox7c and Cyp7a1. A stem-loop qRT-PCR analysis confirmed that the levels of miR-383, miR-34a and miR-146b were inversely correlated with those of DIO1 or TRb. Down-regulated expression of miR-383 or miR-146b by miR-383 inhibitor (anti-miR-383) or miR-146b inhibitor (anti-miR-146b) in free fatty acid-treated primary mouse hepatocytes led to increased DIO1 and TRb expressions, respectively, and subsequently decreased cellular lipid accumulation, while miR-34a inhibitor (anti-miR-34a) transfection had on effects on TRb expression. Luciferase reporter assay illustrated that miR-146b could directly target TRb 3′untranslated region (3′UTR). These findings suggested that miR-383 and miR-146b might play critical roles in different propensities to diet-induced obesity via targeting on Dio1 and TRb, respectively.