Cancer cachexia is a multifactorial syndrome characterized by progressive muscle and fat loss, driven by systemic inflammation and metabolic dysfunction. The role of adipose tissue in modulating muscle wasting through endocrine signaling remains underexplored. This study investigates the therapeutic potential of a high-fat diet (HFD) in mitigating muscle atrophy in cancer cachexia through adiponectin signaling. Lewis lung carcinoma (LLC) cells (1.5 × 10⁶ cells per mouse) were subcutaneously implanted in C57BL/6J mice to induce cachexia. Mice were randomized to receive either a standard diet (CD) or an HFD (65% energy from fat) for 21 days post-tumor implantation. Serum and tissue samples were analyzed for inflammatory markers, muscle mass, adiponectin expression, and muscle function using enzyme-linked immunosorbent assay (ELISA), quantitative real-time PCR (qRT-PCR), hematoxylin-eosin (H&E) staining, and functional assays. The HFD did not affect tumor size or energy intake but reduced hepatosplenomegaly (liver: P = 0.0282, spleen: P < 0.0001) and circulating inflammatory factor levels (tumor necrosis factor alpha (TNFα): 22.9%, interleukin 6 (IL6): 30.4%, interleukin 1 beta (IL1β): 33.6%, compared to LLC+CD) in cachectic mice. The HFD attenuated the loss of muscle mass (P = 0.0115), functional decline, reduction in myofiber cross-sectional area, and the expression of atrophy-related genes. It also mitigated weight loss (inguinal white adipose tissue (iWAT) mass loss: 54% in CD vs. 12% in HFD; epididymal white adipose tissue (eWAT) mass loss: 49% in CD vs. 19% in HFD) and adipocyte atrophy in both iWAT and eWAT, concurrently reducing adipose browning and inflammatory factor expression. Mechanistically, transcriptome analysis of muscle and iWAT implicated adiponectin-related pathways. The HFD enhanced adiponectin expression in iWAT, partially restored circulating adiponectin levels (9.6%, P = 0.0220, compared to LLC+CD), and upregulated AdipoR1 expression in muscle. This increased adiponectin expression in adipose tissue appeared to be mediated by peroxisome proliferator-activated receptor gamma (PPARγ) and CCAAT/enhancer-binding protein alpha (C/EBPα). Consequently, gene expression associated with mitochondrial biogenesis, muscle cell regeneration, and fatty acid utilization was activated in muscle tissue. An HFD mitigates fat loss and muscle atrophy in cancer cachexia. It restores adiponectin secretion in adipose tissue and attenuates systemic inflammation. These findings underscore the therapeutic potential of dietary modulation in cachexia and highlight the fat-to-muscle axis as a promising target for future interventions.

Maillard reaction (MR) is a non-enzymatic browning reaction commonly seen in food processing, which occurs between reducing sugars and compounds with amino groups. Despite certain advantages based on Maillard reaction products (MRPs) found in some food for health and storage application have appeared, however, the MR occurring in human physiological environment can produce advanced glycation end products (AGEs) by non-enzymatic modif ication of macromolecules such as proteins, lipids and nucleic acid, which could change the structure and functional activity of the molecules themselves. In this review, we take AGEs as our main object, on the one hand, discuss physiologic aging, that is, age-dependent covalent cross-linking and modif ication of proteins such as collagen that occur in eyes and skin containing connective tissue. On the other hand, pathological aging associated with autoimmune and inflammatory diseases, neurodegenerative diseases, diabetes and diabetic nephropathy, cardiovascular diseases and bone degenerative diseases have been mainly proposed. Based on the series of adverse effects of accelerated aging and disease pathologies caused by MRPs, the possible harm caused by some MR can be slowed down or inhibited by artif icial drug intervention,dietary pattern and lifestyle control. It also stimulates people’s curiosity to continue to explore the potential link between the MR and human aging and health, which should be paid more attention to for the development of life sciences.

Despite cisplatin has been widely used in the treatment of various cancers, the noteworthy nephrotoxicity greatly constrained its clinical value. For this reason, finding novel targeted therapies to attenuate the nephrotoxicity of cisplatin should be pretty significant. Our previous study found that histone deacetylase sirtuin 6 (SIRT6) could be an ideal target for the treatment of cisplatin-induced acute kidney injury. In this study, we explored the protective effects of ellagic acid, a natural polyphenol compound that activates SIRT6, on cisplatin-induced nephrotoxicity. Pre-treatment of ellagic acid attenuated cytotoxicity of cisplatin in primary renal cells and TCMK-1 cells. Moreover, ellagic acid ameliorated renal dysfunction, apoptosis and fibrosis induced by cisplatin in mice. Furthermore, ellagic acid reduced nephrotoxicity-associated inflammatory factor interleukin (IL)-1β and IL-6 expression both in vitro and in vivo. Mechanistically, ellagic acid reversed cisplatin-reduced SIRT6 expression and diminished cisplatin-induced tumor necrosis factor (TNF)-α expression. And SIRT6 knockdown abrogated the protective effects of ellagic acid on cisplatin-induced cell apoptosis, indicating the renal-protective effects of ellagic acid are mainly dependent on ellagic acid-mediated SIRT6 activation. Our results provide preclinical rationale for using ellagic acid as a feasible and promising agent to ameliorate cisplatin-induced acute kidney injury, and support ellagic acid as a potential adjunctive therapy for future cancer treatment.

Previous study have demonstrated that a compound composed of water-soluable Ganoderma lucidum polysaccharides (GLP) and Polyporus umbellatus polysaccharides (PUP) in a ratio of 3:1 named GPP enhances innate immune function in mice through enhancing the function of macrophage cells and activity of natural killer (NK) cells. Here in our research, we further investigated the effect of GPP on the diversity and composition of intestinal flora, and explored its effect on colitis model mice. The immunoregulatory verification experiments of GPP were conducted in both normal and DSS-induced mice model. Our research showed that GPP increased the diversity of intestinal microorganisms in mice with the extension of administration time. Daily GPP intake attenuated DSS-induced colon injury, protected the splenic lymphocyte proliferation ability, enhanced the serum hemolysin synthesis, and increased peripheral phagocytes and NK cell activity in model mice. Comparisons of the predominant gene pathways of the bacterial microbiota showed that DNA repair and recombination, base mismatch repair pathways was stronger in GPP-treatment group than in control group, indicating the possible molecular mechanisms of immune function regulation. Our study showed that GPP regulated immune function in both health and colitis model, and had a positive effect on maintaining intestinal flora homeostasis.

Oral microbiota is an important part of the human microbiota. Oral microbes can be colonized into the intestine in various ways. Oral microbiota is associated with a variety of oral diseases. Recently, increasing evidence has shown that the oral microbiota is closely related to the physical state of humans, such as diabetes, obesity, and cancer. In the future, oral microbiota will become a new target for improving the physical state of humans.