Characterization of effective antioxidant components of tropical fruit and vegetable species

Ph.DDOCTOR OF PHILOSOPH

Characterization of Substrate Preference for Slc1p and Cst26p in Saccharomyces cerevisiae Using Lipidomic Approaches and an LPAAT Activity Assay

10.1371/journal.pone.0011956PLoS ONE58

Ablation of Dihydroceramide Desaturase Confers Resistance to Etoposide-Induced Apoptosis In Vitro

10.1371/journal.pone.0044042PLoS ONE79

Fld1p, a functional homologue of human seipin, regulates the size of lipid droplets in yeast

Lipid droplets (LDs) are emerging cellular organelles that are of crucial importance in cell biology and human diseases. In this study, we present our screen of ∼4,700 Saccharomyces cerevisiae mutants for abnormalities in the number and morphology of LDs; we identify 17 fld (few LDs) and 116 mld (many LDs) mutants. One of the fld mutants (fld1) is caused by the deletion of YLR404W, a previously uncharacterized open reading frame. Cells lacking FLD1 contain strikingly enlarged (supersized) LDs, and LDs from fld1Δ cells demonstrate significantly enhanced fusion activities both in vivo and in vitro. Interestingly, the expression of human seipin, whose mutant forms are associated with Berardinelli-Seip congenital lipodystrophy and motoneuron disorders, rescues LD-associated defects in fld1Δ cells. Lipid profiling reveals alterations in acyl chain compositions of major phospholipids in fld1Δ cells. These results suggest that an evolutionally conserved function of seipin in phospholipid metabolism and LD formation may be functionally important in human adipogenesis

Constant Light Exposure Alters Gut Microbiota and Promotes the Progression of Steatohepatitis in High Fat Diet Rats

Background: Non-alcoholic fatty liver disease (NAFLD) poses a significant health concern worldwide. With the progression of urbanization, light pollution may be a previously unrecognized risk factor for NAFLD/NASH development. However, the role of light pollution on NAFLD is insufficiently understood, and the underlying mechanism remains unclear. Interestingly, recent studies indicate the gut microbiota affects NAFLD/NASH development. Therefore, the present study explored effects of constant light exposure on NAFLD and its related microbiotic mechanisms. Material and method: Twenty-eight SD male rats were divided into four groups (n=7 each): rats fed a normal chow diet, and exposed to standard light-dark cycle (ND-LD); rats fed a normal chow diet, and exposed to constant light (ND-LL); rats fed a high fat diet, and exposed to standard light-dark cycle (HFD-LD); and rats on a high fat diet, and exposed to constant light (HFD-LL). Body weight, hepatic pathophysiology, gut microbiota, and short/medium chain fatty acids in colon contents, serum lipopolysaccharide (LPS) and liver LPS-binding protein (LBP) mRNA expression were documented post intervention and compared among groups. Result: In normal chow fed groups, rats exposed to constant light displayed glucose abnormalities and dyslipidemia. In HFD-fed rats, constant light exposure exacerbated glucose abnormalities, insulin resistance, inflammation and liver steatohepatitis. Constant light exposure altered composition of gut microbiota in both normal chow and HFD fed rats. Compared with HFD-LD group, HFD-LL rats displayed less Butyricicoccus, Clostridium and Turicibacter, butyrate levels in colon contents, decreased colon expression of occludin-1 and zonula occluden‐1 (ZO-1) , and increased serum LPS and liver LBP mRNA expression. Conclusion: Constant light exposure impacts gut microbiota and its metabolic products, impairs gut barrier function and gut-liver axis, promotes NAFLD/NASH progression in HFD rats

The translocator maintenance protein Tam41 is required for mitochondrial cardiolipin biosynthesis

The mitochondrial inner membrane contains different translocator systems for the import of presequence-carrying proteins and carrier proteins. The translocator assembly and maintenance protein 41 (Tam41/mitochondrial matrix protein 37) was identified as a new member of the mitochondrial protein translocator systems by its role in maintaining the integrity and activity of the presequence translocase of the inner membrane (TIM23 complex). Here we demonstrate that the assembly of proteins imported by the carrier translocase, TIM22 complex, is even more strongly affected by the lack of Tam41. Moreover, respiratory chain supercomplexes and the inner membrane potential are impaired by lack of Tam41. The phenotype of Tam41-deficient mitochondria thus resembles that of mitochondria lacking cardiolipin. Indeed, we found that Tam41 is required for the biosynthesis of the dimeric phospholipid cardiolipin. The pleiotropic effects of the translocator maintenance protein on preprotein import and respiratory chain can be attributed to its role in biosynthesis of mitochondrial cardiolipin

Maternal High Fat Diet in Lactation Impacts Hypothalamic Neurogenesis and Neurotrophic Development, Leading to Later Life Susceptibility to Obesity in Male but Not Female Mice

Research Funding National Key Research and Development Program of China. Grant Number: 2018YFA0801000 National Natural Science Foundation of China. Grant Number: 92057206 A Wolfson merit professorship from UK Royal Society Postdoctoral Research Foundation of China. Grant Numbers: 2013M540157, 2014T70135 The KC Wong Education Foundation Grants from the "1000 talents" recruitment program A PIFI professional fellowship from CASPeer reviewedPublisher PD

Microbiota Depletion Impairs Thermogenesis of Brown Adipose Tissue and Browning of White Adipose Tissue

This work was supported by the Strategic Priority Research Program of the Chinese Academy of Sciences (XDB13030000) and Natural Science Foundation of China (NSFC; 91649108), the Chinese Academy of Sciences-Novo Nordisk Foundation, as well as grants from the Chinese Academy of Sciences “1000 Talents” recruitment program and a “Great-Wall Professorship” from the Chinese Academy of Sciences-Novo Nordisk Foundation. J.R.S. was also supported by a Wolfson merit professorship from The UK Royal Society. We are grateful to all of the members of the Molecular Energetics Group for their support and discussion of the results. We would like to thank Dr. Jia and Dr. Sun from the Core Facility for Protein Research from the Institute of Biophysics, Chinese Academy of Sciences for flow cytometry, and Peter Thomson and Marina Samatiou for technical assistance with the DLW measurements.Peer reviewedPublisher PD