Background & Aims
Obesity promotes the development of nonalcoholic fatty liver diseases (NAFLDs), yet not all obese patients develop NAFLD. The underlying causes for this discrepancy remain elusive. LPGAT1 is an acyltransferase that catalyzes the remodeling of phosphatidylglycerol (PG), a mitochondrial phospholipid implicated in various metabolic diseases. Here, we investigated the role of LPGAT1 in regulating the onset of diet-induced obesity and its related hepatosteatosis because polymorphisms of the
LPGAT1
gene promoter were strongly associated with susceptibility to obesity in Pima Indians.
Methods
Mice with whole-body knockout of LPGAT1 were generated to investigate the role of PG remodeling in NAFLD.
Results
LPGAT1 deficiency protected mice from diet-induced obesity, but led to hepatopathy, insulin resistance, and NAFLD as a consequence of oxidative stress, mitochondrial DNA depletion, and mitochondrial dysfunction.
Conclusions
This study identified an unexpected role of PG remodeling in obesity, linking mitochondrial dysfunction to NAFLD.
Cancer stem cells (CSCs) have been demonstrated in a variety of tumors and are thought to act as a clonogenic core for the genesis of new tumor growth. This small subpopulation of cancer cells has been proposed to help drive tumorigenesis, metastasis, recurrence and conventional therapy resistance. CSCs show self-renewal and flexible clonogenic properties and help define specific tumor microenvironments (TME). The interaction between CSCs and TME is thought to function as a dynamic support system that fosters the generation and maintenance of CSCs. Investigation of the interaction between CSCs and the TME is shedding light on the biologic mechanisms underlying the process of tumor malignancy, metastasis, and therapy resistance. We summarize recent advances in CSC biology and their environment, and discuss the challenges and future strategies for targeting this biology as a new therapeutic approach.
The sintering of supported metal nanoparticles is a major route to the deactivation of industrial heterogeneous catalysts, which largely increase the cost and decrease the productivity. Here, we discover that supported palladium/gold/platinum nanoparticles distributed at the interface of oxide supports and nitrogen-doped carbon shells would undergo an unexpected nitrogen-doped carbon atomization process against the sintering at high temperatures, during which the nanoparticles can be transformed into more active atomic species. The in situ transmission electron microscopy images reveal the abundant nitrogen defects in carbon shells provide atomic diffusion sites for the mobile atomistic palladium species detached from the palladium nanoparticles. More important, the catalytic activity of sintered and deactivated palladium catalyst can be recovered by this unique N-doped carbon atomization process. Our findings open up a window to preparation of sintering-resistant single atoms catalysts and regeneration of deactivated industrial catalysts.
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