Pasteurization, as a meaningful part of food processing, has received growing attention for regulating Pickering emulsion stability. In this research, the role of pasteurization and konjac glucomannan (KGM) in the modulation of Pickering emulsion properties was investigated. The results showed that the network structure formed by KGM inhibited the agglomeration of droplets due to pasteurization, which improved the heat stability of the Pickering emulsion. Increasing the concentration of KGM improved the densification of its network structure, as evidenced by the enhanced viscoelasticity of the emulsion after pasteurization. The retention rate of β-carotene encapsulated in the Pickering emulsion could reach 99% after pasteurization at 65 °C for 30 min. Moreover, pasteurization further enhanced the inhibitory effect of KGM on free fatty acid release and implemented a manageable release of β-carotene. This research offers theoretical guidance for the construction of highly stable Pickering emulsions for delivering temperature-sensitive hydrophobic ingredients.

LncRNA H19 has been reported to regulate apoptosis and neurological diseases. Hippocampal neuron apoptosis damages cognitive ability. Methionine restriction (MR) can improve cognitive impairment. However, the effect of MR on hippocampal neuronal apoptosis induced by a high-fat diet (HFD) in middle-aged mice remains unclear. For 25 weeks, middle-aged mice (C57BL/6J) were given a control diet (CON, 0.86% methionine + 4.2% fat), a high-fat diet (HFD, 0.86% methionine + 24% fat), or an HFD + MR diet (HFMR, 0.17% methionine + 24% fat). The HT22 cells were used to establish the early apoptosis model induced by high glucose (HG). In vitro, the results showed that MR significantly improved cell viability, suppressed the generation of ROS, and rescued HT22 cell apoptosis in a gradient-dependent manner. In Vivo, MR inhibited the damage and apoptosis of hippocampal neurons caused by a high-fat diet, reduced hippocampal oxidative stress, improved hippocampal glucose metabolism, relieved insulin resistance, and enhanced cognitive ability. Furthermore, MR could inhibit the overexpression of H19 and caspase-3 induced by HFD, HG, or H₂O₂ in vivo and in vitro, and promoted let-7a, b, e expression. These results indicate that MR can protect neurons from HFD-, HG-, or H₂O₂-induced injury and apoptosis by inhibiting H19.

Growing evidence links processed red meat consumption to increased diabetes risk, with oxidized proteins and/or amino acids proposed as potential mediators. We investigated whether dityrosine (Dityr), a key oxidation biomarker in high-oxidative pork (HOP) and structural analog of thyroid hormone T3, mediates HOP-induced glucose dysregulation via thyroid hormone (TH) signaling disruption. C57BL/6J mice were fed control, low-oxidative pork (LOP), HOP, LOP + Dityr, or Dityr diets for 12 weeks. HOP and Dityr impaired glucose tolerance and induced hyperglycemia and hypoinsulinemia. Both induced oxidative stress and inflammation that partly contributed to pancreatic β-cell dysfunction and reduction in insulin secretion. Crucially, they downregulated pancreatic thyroid hormone receptor β1 (TRβ1) and monocarboxylate transporter 8 (MCT-8), impairing TH signaling. This reduced TH transport in pancreatic tissue and triggered β-cell apoptosis by modulating TRβ1-mediated expression of TH-responsive genes and proteins involved in pancreatic function, ultimately leading to diminished insulin secretion and elevated blood glucose levels. Dityr alone recapitulated the metabolic and molecular disruptions of HOP. We conclude that Dityr drives HOP-induced glucose metabolism disorders primarily by disrupting TH signaling, along with promoting oxidative stress and inflammation that collectively impair β-cell function. Minimizing dietary Dityr exposure via modified cooking methods or antioxidant-rich diets may mitigate diabetes risk.