Publications by authors named "T Pilot"
Macrophages are innate immune cells present in all tissues, in which they participate in immune responses and maintenance of tissue homeostasis. They develop either from embryonic precursors or from circulating monocytes, and their functions are in part dictated by their origin. We previously observed robust monocyte recruitment and contribution to the macrophage pool in brown adipose tissue.
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- - The study investigates the role of the enzyme ELOVL5 in the biosynthesis of Polyunsaturated Fatty Acids (PUFAs) and its implications for liver conditions, specifically MASH (metabolic-associated steatotic liver disease), revealing how enzyme disruption affects liver metabolism.
- - Research showed that ELOVL5 levels increase during MASH progression and that its absence in mice leads to significant liver issues after a high-fat, high-sucrose diet, including fat accumulation, inflammation, and fibrosis.
- - The findings suggest that the loss of ELOVL5 disrupts mitochondrial function, contributes to liver damage from dietary factors, and alters fatty acid metabolism, indicating a critical link between enzyme activity and liver health.
Article Synopsis
- Monocytes play a crucial role in atherosclerosis by turning into macrophages when they migrate to plaques, and this study explores how their glucose metabolism influences their behavior and contribution to the disease.
- Researchers found that higher serum glucose levels are linked to increased monocyte numbers, while restricted diets hinder monocytes from switching energy sources, which reduces their presence in the blood.
- The study highlights that glucose metabolism is vital for maintaining specific monocyte characteristics and functions, but inhibiting glucose uptake alone doesn't prevent atherosclerosis, likely because the remaining monocytes become more migratory.
Background: Type 2 diabetes mellitus (T2DM) is a major global health issue and a significant risk factor for atherosclerosis. Atherosclerosis in T2DM patients has been associated with inflammation, insulin resistance, hyperglycemia, dyslipidemia, and oxidative stress. Identifying molecular features of atherosclerotic plaques in T2DM patients could provide valuable insights into the pathogenesis of the disease.
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- * Mice lacking PLTP (KO) on a high-fat diet experienced more weight gain, insulin resistance, and increased inflammation compared to normal mice (WT), indicating PLTP's protective role against endotoxemia.
- * When given LPS, PLTP-deficient mice showed higher LPS absorption from the gut and disrupted metabolism of triglyceride-rich lipoproteins, suggesting PLTP is crucial for managing LPS effects and preventing diet-induced metabolic issues.