Jingya Guo

Background: Skin photoaging is primarily caused by prolonged ultraviolet (UV) exposure, which manifests as dryness and wrinkle formation. Recent studies highlight that beneficial microorganisms have garnered considerable attention for their emerging role in modulating host health, especially in skin photoaging. Methods: To investigate the role of two strains, Bifidobacterium animalis subsp. lactis BL-G101 (BL-G101) and Lactobacillus acidophilus LA-G80 (LA-G80), in UVB-induced photoaging, we conducted experiments on human Hs68 dermal fibroblasts. Using untargeted metabolomics, we explored the potential mechanisms underlying BL-G101 treatment in Hs68 cells by profiling differential metabolites in the intracellular and extracellular metabolomes. Results: Our results demonstrated that BL-G101 significantly inhibited UVB-induced reduction in collagen and hyaluronic acid (HA), whereas LA-G80 showed no notable effects. BL-G101 treatment also protects against UVB-induced oxidative stress, which was evidenced by significantly decreased MDA levels and enhanced SOD activity. Moreover, BL-G101 suppressed UVB-induced inflammation by significantly decreasing IL-1β and TNF-α levels. SA-β-gal staining revealed a reduction in senescent fibroblasts following BL-G101 treatment. Untargeted metabolomics suggested that the anti-photoaging effects of BL-G101 may involve the modulation of metabolic pathways of biosynthesis of cofactors, glycine, serine and threonine metabolism, and arginine biosynthesis. Conclusions: These preclinical findings demonstrate that BL-G101 reduces dermal photoaging, supporting its potential as a functional food ingredient against skin aging.

Odorant receptors (ORs) have long been thought to serve as chemosensors located on the cilia of olfactory sensory neurons (OSNs) in the olfactory epithelium, where they recognize odorant molecules and comprise the largest family of seven transmembrane-domain G protein-coupled receptors (GPCRs). Over the last three decades, accumulating evidence has suggested that ORs are distributed in a variety of peripheral tissues beyond their supposed typical tissue expression in the olfactory epithelium. These ectopic ORs play a role in regulating various cellular, physiological, and pathophysiological phenomena in the body, such as regulation of hypertension, hepatic glucose production, cancer development, and chronic skin disease. Adipose tissue, the key organ in regulating obesity and energy metabolism, has been reported to take advantage of ectopic OR-mediated signaling. In this review, we summarize and provide an in-depth analysis of the current research on the key biological functions of adipose tissue ORs in response to food-derived odorants, as well as the molecular mechanisms underlying their activity.

Previous studies have reported the therapeutic effects of oleuropein (OP) consumption on the early stage of diabetic nephropathy and diabetic cardiomyopathy. However, the efficacy of OP on the long-course of these diabetes complications has not been investigated. Therefore, in this study, to investigate the relieving effects of OP intake on these diseases, and to explore the underlying mechanisms, db/db mice (17-week-old) were orally administrated with OP (200 mg/kg bodyweight) for 15 weeks. We found that OP reduced expansion of the glomerular mesangial matrix, renal inflammation, renal fibrosis, and renal apoptosis. Meanwhile, OP treatment exerted cardiac anti-fibrotic, anti-inflammatory, and anti-apoptosis effects. Notably, transcriptomic and bioinformatic analyses indicated 290 and 267 differentially expressed genes in the kidney and heart replying to OP treatment, respectively. For long-course diabetic nephropathy, OP supplementation significantly upregulated the cyclic guanosine monophosphate-dependent protein kinase (cGMP–PKG) signaling pathway. For long-course diabetic cardiomyopathy, p53 and cellular senescence signaling pathways were significantly downregulated in response to OP supplementation. Furthermore, OP treatment could significantly upregulate the transcriptional expression of the ATPase Na⁺/K⁺ transporting subunit alpha 3, which was enriched in the cGMP–PKG signaling pathway. In contrast, OP treatment could significantly downregulate the transcriptional expressions of cyclin-dependent kinase 1, G two S phase expressed protein 1, and cyclin B2, which were enriched in p53 and cellular senescence signal pathways; these genes were confirmed by qPCR validation. Overall, our findings demonstrate that OP ameliorated long-course diabetic nephropathy and cardiomyopathy in db/db mice and highlight the potential benefits of OP as a functional dietary supplement in diabetes complications treatment.

Cedryl acetate (CA), also called acetyl cedrene, is approved by the FDA as a flavoring or adjuvant to be added to foods. In this study, we aimed to investigate the preventive benefits of CA on obesity and obesity-related metabolic syndrome caused by a high-fat diet (HFD). Three groups of C57BL/6J mice (ten-week-old) were fed Chow, an HFD, or an HFD with CA supplementation (100 mg/kg) for 19 weeks. We observed that CA supplementation significantly reduced weight gain induced by an HFD, decreased the weight of the visceral fat pads, and prevented adipocyte hypertrophy in mice. Moreover, mice in the CA group showed significant improvements in hepatic lipid accumulation, glucose intolerance, insulin resistance, and gluconeogenesis compared with the mice in the HFD group. Since 16S rRNA analysis revealed that the gut microbiota in the CA and HFD groups were of similar compositions at the phylum and family levels, CA may have limited effects on gut microbiota in HFD-fed mice. The beneficial effects on the metabolic parameters of CA were reflected by CA’s regulation of metabolism-related gene expression in the liver (including Pepck, G6Pase, and Fbp1) and the epididymal white adipose tissues (including PPARγ, C/EBPα, FABP4, FAS, Cytc, PGC-1α, PRDM16, Cidea, and COX4) of the mice. In summary, a potent preventive effect of CA on HFD-induced obesity and related metabolic syndrome was highlighted by our results, and CA could be a promising dietary component for obesity intervention.

Genetic modification (GM) offers an alternative strategy to conventional animal breeding. The present study was carried out to investigate the potential health effects of the consumption of growth hormone-transgenic triploid carp (GH-ttc) through a 90-day subchronic rodent feeding study. Wistar rats (n = 10/sex/group) were given formulated diets containing GH-ttc or non-GM carp at an incorporated rate of 2.5%, 5%, or 10% (w/w) for 90 days. An additional control group of rats (n = 10/sex/group) was fed a basic rodent diet. During the 90-day study, clinical observation, ophthalmic examination, body weight, and food intake were evaluated. At the end of the study, rats were killed, and the hematology, serum chemistry, urine test, necropsy, and histopathology were assessed. Compared with the non-GM carp and the basic control groups, no biologically significant differences were observed on clinical signs of toxicity, body weights, food intake, hematology, serum chemistry, urinalysis, organ weight, and histopathology on selected organs for the GH-ttc group. The results of this 90-day subchronic feeding study indicated that, at the dose level used in this study, consumption of GH-ttc showed no subchronic toxicity to Wistar rats.