Semaglutide improves liver health in mice with MASH through intrahepatic sinusoidal endothelial GLP-1 receptors, independent of weight loss, with a substantial effect on fibrosis and immune remodeling.
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Cell Press · Cell & Molecular Biology · ISSN 1550-4131, 1932-7420
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Semaglutide improves liver health in mice with MASH through intrahepatic sinusoidal endothelial GLP-1 receptors, independent of weight loss, with a substantial effect on fibrosis and immune remodeling.
Malignant cells depend on NAD metabolism, especially via NAMPT, to support proliferation, stress tolerance, and immune evasion, revealing a potential therapeutic vulnerability.
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Malignant cells depend on NAD metabolism, especially via NAMPT, to support proliferation, stress tolerance, and immune evasion, revealing a potential therapeutic vulnerability.
Elevated NAD+ in adipose tissue triggers Serpina3n release, which protects muscle mass across aging, disuse, and cancer cachexia models.
Histone H3K9 lactylation in colonic macrophages persists after colitis resolution and promotes susceptibility to metabolic liver disease under high-fat diet in mice.
UBT251 achieved up to a 19.7% reduction in body weight in adults with overweight or obesity over 24 weeks, significantly exceeding placebo with all p < 0.001.
Aging reduces hepatic β-hydroxybutyrate synthesis, inducing CD8(+) T cell exhaustion and impairing antiviral and antitumor immunity in mice.
Hepatic glutamine depletion is linked with increased CD4+ T cell inflammation and worsened liver damage in MASLD patients and mouse models.
Loss of host MTDH in hepatocytes and CD8+ T cells enhances antitumor immunity and suppresses tumor growth and metastasis in mouse models.
Extracellular arginine directly remodels the tRNA-codon axis, regulating MHC class I translation independently of amino acid stress signaling.
Immunometabolism is now a central feature of immune responses, influencing most aspects of immune research and evolving rapidly as a key scientific focus.
Lactate promotes necroptosis through RIPK3 K63 lactylation, with PCAF-mediated modification enhancing kinase activity and membrane disruption in mice and humans.
Hepatic dysfunction disrupts selenium delivery to cartilage, promoting osteoarthritis in mice and humans, with a 20% higher OA prevalence among individuals with liver disease.
GDF15 activates the GFRAL-HPA axis to suppress liver inflammation independently of weight loss in mouse models of MASH.
Glutamine metabolism through glutaminolysis restrains inflammatory cytokine production by hepatic CD4(+) T cells during MASLD.
A very-low-carbohydrate diet yields 2-3 times greater improvements in hepatic insulin sensitivity than Mediterranean or very-low-fat diets during 10% weight loss in metabolically unhealthy obesity.
The gut microbiota is a central mediator between environmental neurotoxicants and neurological health, influencing exposure outcomes through microbial and host interactions.
Renaming polyendocrine metabolic ovarian syndrome emphasizes its core metabolic dysfunction, highlighting its link to increased cardiovascular and metabolic disease risk.
Microbiome-derived metabolites modulate immune cells through molecular pathways, influencing metabolic health or chronic inflammation linked to cardiometabolic diseases.
GLP-1 receptor agonists may improve reproductive and metabolic disturbances in women with polyendocrine metabolic ovarian syndrome.
A high-protein, low-carbohydrate diet improves hepatic glucose and lipid metabolism in patients with prediabetes and steatosis, even with equal weight loss of 10%.
Diet-dependent remodeling of the gut microbiome enhances anti-tumor immunity and may explain improved immune checkpoint blockade efficacy in obesity.
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