Chemerin as an Inducer of ß Cell Proliferation Mediates Mitochondrial Homeostasis and Promotes ß Cell Mass Expansion.

Loss of the ß cell population is a crucial feature of type 2 diabetes. Restoring the ß cell mass by stimulating ß cell proliferation and preventing its apoptosis was proposed as a therapeutic approach to treating diabetes. Therefore, researchers have been increasingly interested in identifying exogenous factors that can stimulate ß cell proliferation in situ and in vitro. Adipokine chemerin, which is secreted from adipose tissue and the liver, has been identified as a chemokine that plays a critical role in the regulation of metabolism. In this study, we demonstrate that chemerin as a circulating adipokine promotes ß cell proliferation in vivo and in vitro. Chemerin serum levels and the expression of the main receptors within islets are highly regulated under a variety of challenging conditions, including obesity and type 2 diabetes. As compared to their littermates, mice overexpressing chemerin had a larger islet area and increased ß cell mass with both a normal and high-fat diet. Moreover, in chemerin-overexpressed mice, we observed improved mitochondrial homeostasis and increased insulin synthesis. In summary, our findings confirm the potential role of chemerin as an inducer of ß cell proliferation, and they provide novel insights into the helpful strategy to expand ß cell population.

Study on the adsorption of polystyrene microplastics by three-dimensional reduced graphene oxide.

In this paper, a study on the removal of imitated polystyrene (PS) microplastics in water was carried out based on the adsorption capacity of three-dimensional reduced graphene oxide (3D RGO). Scanning electron microscopy and X-ray diffractometry characterization showed that the freeze-dried 3D RGO formed a distinct porous spatial structure. Different experimental parameters, such as pH, ion concentration (C0), contact time (t), and temperature (T), were studied to investigate the PS microplastic adsorption performance of 3D RGO. The adsorption mechanism was mainly attributed to the strong π-π interaction between the carbon ring of 3D RGO and the benzene ring of PS microplastics. Sorption kinetic and isothermal data were obtained by the well-fitted Langmuir adsorption isotherm model and pseudo-second-order kinetic model. Furthermore, the result of thermodynamic analysis showed that the adsorption of PS microplastics was a spontaneous endothermic process. Under the optimal conditions of pH = 6, C0 = 600 mg/L, t = 120 min, and T = 26 °C, the maximum adsorption capacity of the prepared 3D RGO on PS microplastics was 617.28 mg/g. Furthermore, this method exhibited good feasibility in tap water and lake water.

m6A Reader HNRNPC Facilitates Adipogenesis by Regulating Cytoskeletal Remodeling through Enhanced Lcp1 mRNA Stability.

Reduced adipogenesis is a prominent characteristic of aging adipose tissue and is closely tied to the development of metabolic disorders associated with aging. Epigenetic modification plays a crucial role in the aging process, yet the role of N6-methyladenosine (m6A), the most prevalent RNA modification, in regulating adipose tissue aging remains uncertain. Our study found that levels of m6A and its recognition protein, heterogeneous nuclear ribonucleoprotein C (HNRNPC), decrease in adipose tissue as individuals age. Lower levels of HNRNPC were also linked to reduced adipogenesis during aging. Through loss and gain of function experiments with HNRNPC, we established a positive correlation between HNRNPC and adipogenesis in vitro. Hnrnpc-APKO mice displayed decreased adipogenesis, increased insulin resistance, elevated expression of aging-related and inflammation-related genes, decreased lipogenesis-related genes, and other metabolic disorders compared to their littermates. Additionally, we discovered that HNRNPC facilitated the stability of lymphocyte cytosolic protein 1 (Lcp1) mRNA by binding to the m6A motif of LCP1. Overexpression of LCP1 mitigated the inhibition of adipogenesis caused by decreased HNRNPC through modulation of cytoskeletal remodeling. Finally, our findings demonstrate that anti-aging treatments could enhance HNRNPC levels. In conclusion, HNRNPC is positively associated with reduced adipogenesis during aging, and increacing HNRNPC levels through anti-aging treatments highlights its potential as a therapeutic target for addressing metabolic imbalances in adipose tissue related to aging.

Supported-catalyst CuO/AC with reduced cost and enhanced activity for the degradation of heavy oil refinery wastewater by catalytic ozonation process.

In this work, activated carbon-supported copper(II) oxide (CuO/AC) was prepared and used to degrade heavy oil refinery wastewater (HORW) by catalytic ozonation with the aim to develop low-cost and high-efficient supported-catalysts for degrading real recalcitrant industrial wastewater. Supported-catalyst CuO/AC was characterized by X-ray diffraction (XRD), N2-physisorption, scanning electronic microscope (SEM), transmission electron microscope (TEM), and X-ray fluorescence (XRF). The degradation was mainly evaluated by chemical oxygen demand (COD), total organic carbon (TOC), 5-day biochemical oxygen demand (BOD5), biodegradability and toxicity. Compared with unsupported-catalyst CuO or the mixed system of activated-AC and unsupported-catalyst CuO, supported-catalyst CuO/AC with reduced cost exhibited significantly enhanced activity for degrading HORW (5.0 g CuO-5%/AC, 90 mg/L O3, and 7.3 pH). TEM analysis showed that the high activity of supported-catalyst CuO-5%/AC might be ascribed to the fact that CuO particles were small and highly dispersed on AC. Mass spectrum spectrometry (MS) analysis revealed that the organic components in HORW were first degraded to small molecule oxidation products, which were then oxidized or mineralized further. The influence of CuO loading, CuO/AC dose, ozone dose and initial pH on the degradation efficiency was also investigated. The results of the present work showed that CuO/AC could be a promising supported-catalyst for catalyzing ozonation degradation of HORW.