Effects of postponing nitrogen topdressing on starch structural properties of superior and inferior grains in hybrid indica rice cultivars with different taste values.

Introduction: Nitrogen (N) fertilizer management, especially postponing N topdressing can affect rice eating quality by regulating starch quality of superior and inferior grains, but the details are unclear. This study aimed to evaluate the effects of N topdressing on starch structure and properties of superior and inferior grains in hybrid indica rice with different tastes and to clarify the relationship between starch structure, properties, and taste quality. Methods: Two hybrid indica rice varieties, namely the low-taste Fyou 498 and high-taste Shuangyou 573, were used as experimental materials. Based on 150 kg·N hm-2, three N fertilizer treatments were established: zero N (N0), local farmer practice (basal fertilizer: tillering fertilizer: panicle fertilizer=7:3:0) (N1), postponing N topdressing (basal fertilizer: tillering fertilizer: panicle fertilizer=3:1:6) (N2). Results: The starch granules of superior grains were more complete, and the decrease in small granules content and the stability of starch crystals were a certain extent less than those of inferior grains. Compared with N1, under N2, low-taste and high-taste varieties large starch granules content were significantly reduced by 6.89%, 0.74% in superior grains and 4.26%, 2.71% in inferior grains, the (B2 + B3) chains was significantly reduced by 1.61%, 0.98% in superior grains, and 1.18%, 0.97% in inferior grains, both reduced the relative crystallinity and 1045/1022 cm-1, thereby decreasing the stability of the starch crystalline region and the orderliness of starch granules. N2 treatment reduced the ΔHgel of two varieties. These changes ultimately contributed to the enhancement of the taste values in superior and inferior grains in both varieties, especially the inferior grains. Correlation analysis showed that the average starch volume diameter (D[4,3]) and relative crystallinity were significantly positively correlated with the taste value of superior and inferior sgrains, suggesting their potential use as an evaluation index for the simultaneous enhancement of the taste value of rice with superior and inferior grains. Discussion: Based on 150 kg·N hm-2, postponing N topdressing (basal fertilizer: tillering fertilizer: panicle fertilizer=3:1:6) promotes the enhancement of the overall taste value and provides theoretical information for the production of rice with high quality.

ZIP Genes Are Involved in the Retransfer of Zinc Ions during the Senescence of Zinc-Deficient Rice Leaves.

Rice lacks sufficient amounts of zinc despite its vitality for human health. Leaf senescence enables redistribution of nutrients to other organs, yet Zn retransfer during deficiency is often overlooked. In this hydroponic experiment, we studied the effect of Zn deficiency on rice seedlings, focusing on the fourth leaf under control and deficient conditions. Growth phenotype analysis showed that the growth of rice nodal roots was inhibited in Zn deficiency, and the fourth leaf exhibited accelerated senescence and increased Zn ion transfer. Analyzing differentially expressed genes showed that Zn deficiency regulates more ZIP family genes involved in Zn ion retransfer. OsZIP3 upregulation under Zn-deficient conditions may not be induced by Zn deficiency, whereas OsZIP4 is only induced during Zn deficiency. Gene ontology enrichment analysis showed that Zn-deficient leaves mobilized more biological pathways (BPs) during aging, and the enrichment function differed from that of normal aging leaves. The most apparent "zinc ion transport" BP was stronger than that of normal senescence, possibly due to Zn-deficient leaves mobilizing large amounts of BP related to lipid metabolism during senescence. These results provide a basis for further functional analyses of genes and the study of trace element transfer during rice leaf senescence.

The Nuclear Orphan Receptor Nur77 Alleviates Palmitate-induced Fat Accumulation by Down-regulating G0S2 in HepG2 Cells.

Excessive triglyceride accumulation in hepatocytes is the hallmark of obesity-associated nonalcoholic fatty liver disease (NAFLD). Elevated levels of the saturated free fatty acid palmitate in obesity are a major contributor to excessive hepatic lipid accumulation. The nuclear orphan receptor Nur77 is a transcriptional regulator and a lipotoxicity sensor. Using human HepG2 hepatoma cells, this study aimed to investigate the functional role of Nur77 in palmitate-induced hepatic steatosis. The results revealed that palmitate significantly induced lipid accumulation and suppressed lipolysis in hepatocytes. In addition, palmitate significantly suppressed Nur77 expression and stimulated the expression of peroxisome proliferator-activated receptor γ (PPARγ) and its target genes. Nur77 overexpression significantly reduced palmitate-induced expression of PPARγ and its target genes. Moreover, Nur77 overexpression attenuated lipid accumulation and augmented lipolysis in palmitate-treated hepatocytes. Importantly, G0S2 knockdown significantly attenuated lipid accumulation and augmented lipolysis in palmitate-treated hepatocytes, whereas G0S2 knockdown had no effect on the palmitate-induced expression of Nur77, PPARγ, or PPARγ target genes. In summary, palmitate suppresses Nur77 expression in HepG2 cells, and Nur77 overexpression alleviates palmitate-induced hepatic fat accumulation by down-regulating G0S2. These results display a novel molecular mechanism linking Nur77-regulated G0S2 expression to palmitate-induced hepatic steatosis.

Palmitate induces fat accumulation by activating C/EBPß-mediated G0S2 expression in HepG2 cells.

AIM: To determine the role of G0/G1 switch gene 2 (G0S2) and its transcriptional regulation in palmitate-induced hepatic lipid accumulation. METHODS: HepG2 cells were treated with palmitate, or palmitate in combination with CCAAT/enhancer binding protein (C/EBP)ß siRNA or G0S2 siRNA. The mRNA expression of C/EBPß, peroxisome proliferator-activated receptor (PPAR)γ and PPARγ target genes (G0S2, GPR81, GPR109A and Adipoq) was examined by qPCR. The protein expression of C/EBPß, PPARγ, and G0S2 was determined by Western blotting. Lipid accumulation was detected with Oil Red O staining and quantified by absorbance value of the extracted Oil Red O dye. Lipolysis was evaluated by measuring the amount of glycerol released into the medium. RESULTS: Palmitate caused a dose-dependent increase in lipid accumulation and a dose-dependent decrease in lipolysis in HepG2 cells. In addition, palmitate increased the mRNA expression of C/EBPß, PPARγ, and PPARγ target genes (G0S2, GPR81, GPR109A, and Adipoq) and the protein expression of C/EBPß, PPARγ, and G0S2 in a dose-dependent manner. Knockdown of C/EBPß decreased palmitate-induced PPARγ and its target genes (G0S2, GPR81, GPR109A, and Adipoq) mRNA expression and palmitate-induced PPARγ and G0S2 protein expression in HepG2 cells. Knockdown of C/EBPß also attenuated lipid accumulation and augmented lipolysis in palmitate-treated HepG2 cells. G0S2 knockdown attenuated lipid accumulation and augmented lipolysis, while G0S2 knockdown had no effects on the mRNA expression of C/EBPß, PPARγ, and PPARγ target genes (GPR81, GPR109A and Adipoq) in palmitate-treated HepG2 cells. CONCLUSION: Palmitate can induce lipid accumulation in HepG2 cells by activating C/EBPß-mediated G0S2 expression.

Protective effects of intestinal trefoil factor (ITF) on gastric mucosal epithelium through activation of extracellular signal-regulated kinase 1/2 (ERK1/2).

The rapid repair of gastric mucosa is critical upon exposure to injurious agents. Intestinal trefoil factor (ITF) is a member of the trefoil factor family domain peptides, which play an important role in the cytoprotection of gastric epithelium. However, the underlying molecular mechanisms that are responsible for ITF-induced gastric epithelial repair remain unclear. In the present study, we demonstrate that ITF enhances the proliferation and migration of GES-1 gastric endothelial cells in a dose- and time-dependent manner through the activation of extracellular signal-regulated kinase 1/2 (ERK1/2). Furthermore, the ITF-mediated protection of GES-1 cells from a NS398 (nonsteroidal anti-inflammatory drug) was dependent on the ERK1/2 signaling pathway. Taken together, the results provide a mechanistic explanation for ITF-mediated protection of gastric epithelial mucosa cells, suggesting that activation of the ERK1/2 signaling pathway may provide a new therapeutic strategy for repairing gastric injury.