• Journal of Nutrition and Health
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• v.57 no.4
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• pp.376-388
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• 2024

Purpose: Adipocyte dysfunction has been reported in diabetes, and stimulating thermogenesis and suppressing senescence in adipocytes potentially alleviates metabolic dysregulation. This study aimed to investigate thermogenesis and cellular senescence in diabetic adipocytes under basal conditions and in response to stimuli. Methods: White and brown primary adipocytes derived from control (CON) and db/db (DB) mice were treated with β-agonists, such as norepinephrine (NE) and CL316,243, and 18-carbon fatty acids, including stearic acid, oleic acid (OLA), linoleic acid (LNA), and α-linolenic acid, and the expression of the genes related to thermogenesis and cellular senescence was measured. Results: Although no difference in the thermogenic and cellular senescence gene expression in white adipose tissue (WAT) was noted between the CON and DB mice, brown adipose tissue (BAT) from the DB mice exhibited lower uncoupling protein 1 (Ucp1) expression and higher cyclin-dependent kinase inhibitor (Cdkn)1a and Cdkn2a expression levels compared to that from the CON mice. Stromal vascular cells isolated from the BAT of the DB mice displayed higher peroxisome proliferator-activated receptor gamma (Pparg), CCAAT/enhancer-binding protein alpha (Cebpa), Cdkn1a, and Cdkn2a expression levels. White adipocytes from the DB mice exhibited lower Ucp1, peroxisome proliferator-activated receptor-gamma coactivator 1 alpha (Pgc1a), and PR domain containing 16 (Prdm16) expression levels regardless of β-agonist treatment. NE upregulated Pgc1a in both white and brown adipocytes from the CON mice, but not in those from the DB mice. Although none of the fatty acids were observed to downregulate the cellular senescence genes in fully differentiated adipocytes, the OLA-treated brown adipocytes derived from DB mice exhibited lower Cdkn1a and Cdkn2b expression levels than the LNA-treated cells. Conclusion: These results indicate that the lower thermogenic capacity of diabetic adipocytes may be related to their cellular senescence, and different fatty acids potentially exert divergent effects on the expression of cellular senescence genes.

• Journal of Microbiology and Biotechnology
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• v.10 no.2
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• pp.143-146
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• 2000

This study was conducted to compare the cellular fatty acid composition and genotypic analysis of Bifidobacterium longum MK-G7 originated from Koreans with other commercial type strains of bifidobacteria. The cellular fatty acid of Bif. longum MK-G7 was shown to be composed of $C_{160FAME},C_{181\;c18DMA},C_{18.1\;CIS9\; FAME},C_{14.0FAME},C_{19\;0cye9,10 DMA},Feature7(C_{17.2 FAME), and Feature 10(C_{181\; Cll/t9/t6 FAME}$. Bif. longum MK-G7 showed 99.9% homology and the highest relatedness with Bif. longum ATCC 15707 type strain. Both Bif. longum MK-G7 and Bif. longum ATCC 15707 showed 153 bp products on RAPD (randomly amplified polymorphic DNA) analysis, however, they showed quite different band patterns on PFGE (pulsed-field gel electrophoresis) analysis. Consequently, our present study showed that Bif. longum MK-G7 was different from any commercial type strains of Bif. longum tested.

• BMB Reports
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• v.56 no.12
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• pp.651-656
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• 2023

Senescence, a cellular process through which damaged or dysfunctional cells suppress the cell cycle, contributes to aging or age-related functional decline. Cell metabolism has been closely correlated with aging processes, and it has been widely recognized that metabolic changes underlie the cellular alterations that occur with aging. Here, we report that fatty acid oxidation (FAO) serves as a critical regulator of cellular senescence and uncover the underlying mechanism by which FAO inhibition induces senescence. Pharmacological or genetic ablation of FAO results in a p53-dependent induction of cellular senescence in human fibroblasts, whereas enhancing FAO suppresses replicative senescence. We found that FAO inhibition promotes cellular senescence through acetyl-CoA, independent of energy depletion. Mechanistically, increased formation of autophagosomes following FAO inhibition leads to a reduction in SIRT1 protein levels, thereby contributing to senescence induction. Finally, we found that inhibition of autophagy or enforced expression of SIRT1 can rescue the induction of senescence as a result of FAO inhibition. Collectively, our study reveals a distinctive role for the FAO-autophagy-SIRT1 axis in the regulation of cellular senescence.

• Journal of Microbiology and Biotechnology
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• v.33 no.12
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• pp.1563-1575
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• 2023

Acyl-coenzyme A (CoA):diacylglycerol acyltransferase 2 (DGAT2) catalyzes the last stage of triacylglycerol (TAG) synthesis, a process that forms ester bonds with diacylglycerols (DAG) and fatty acyl-CoA substrates. The enzymatic role of Dgat2 has been studied in various biological species. Still, the full description of how Dgat2 channels fatty acids in skeletal myocytes and the consequence thereof in glucose uptake have yet to be well established. Therefore, this study explored the mediating role of Dgat2 in glucose uptake and fatty acid partitioning under short interfering ribonucleic acid (siRNA)-mediated Dgat2 knockdown conditions. Cells transfected with Dgat2 siRNA downregulated glucose transporter type 4 (Glut4) messenger RNA (mRNA) expression and decreased the cellular uptake of [1-¹⁴C]-labeled 2-deoxyglucose up to 24.3% (p < 0.05). Suppression of Dgat2 deteriorated insulin-induced Akt phosphorylation. Dgat2 siRNA reduced [1-¹⁴C]-labeled oleic acid incorporation into TAG, but increased the level of [1-¹⁴C]-labeled free fatty acids at 3 h after initial fatty acid loading. In an experiment of chasing radioisotope-labeled fatty acids, Dgat2 suppression augmented the level of cellular free fatty acids. It decreased the level of re-esterification of free fatty acids to TAG by 67.6% during the chase period, and the remaining pulses of phospholipids and cholesteryl esters were decreased by 34.5% and 61%, respectively. Incorporating labeled fatty acids into beta-oxidation products increased in Dgat2 siRNA transfected cells without gene expression involving fatty acid oxidation. These results indicate that Dgat2 has regulatory function in glucose uptake, possibly through the reaction of TAG with endogenously released or recycled fatty acids.

• Biomedical Science Letters
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• v.10 no.3
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• pp.293-298
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• 2004

This study was performed to compare the growth rates, cellular fatty acid compositions and morphology by using electron microscope of Escherichia coli (E. coli) grown in various conditions including different concentrations of phenol, CdCl₂ and HgCl₂. Ninety eight E. coli strains were isolated from Naktong river and human feces. The content of unsaturated fatty acids, especially 16:1ω7c and 18:1ωc increased as the concentration of phenol and CdCl₂ increased. The content of unsaturated fatty acid increased up to 50 ppb of HgCl₂, but decreased at 75 ppb of HgCl₂. There were more unsaturated fatty acids than saturated fatty acid in the presence of toxic substances. However, the ration was reversed when the affected E. coli was transferred to toxic substance free fresh trypticase soy broth medium. Also, by using transmission electron microscope these cells were observed to various morphological deformation by heavy metals and their deposition on the surface. From these results, we suggested that the changes of major fatty acids composition and morphology of E. coli may be considered to indicate contaminated levels of heavy metals or organic solvents. The information presented here may be useful in predicting effects of heavy-metal and organic solvent contamination in streams and provides a basis for further studies of metal or organic solvent effects on microbial communities.

• The Korean Journal of Food And Nutrition
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• v.24 no.4
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• pp.501-508
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• 2011

Previous studies suggest that polyunsaturated fatty acids with long carbon chains such as eicosapentaenoic acid(EPA) and docosahexaenoic acid(DHA) have several health benefits. However metabolic consequences of these fatty acids themselves and their regulation of transcriptional activity involving glucose utilization are not well established. Thus, the purpose of this study was to investigate how EPA influx affects cellular lipid accumulation and gene expressions involving $de$ $novo$ lipogenesis in hepatocyte cultures. Compared to oleic acid treatment, EPA treatment showed remarkably decreased cellular TG conversion and accumulation, along with phospholipids at a lower extent. As expected, EPA increased mRNA expression involving fatty acid influx and lipid droplet formation, but did not affect mRNA expression involving glucose utilization. EPA increased transcriptional activity of PPAR-${\alpha}$ and glucose responsive transcription factor when transcription factor binding protein was activated. Taken together, these data suggest that EPA decreases lipid accumulation through increases of the ${\beta}$-oxidation pathway without interruption of glucose utilization.

• Asian-Australasian Journal of Animal Sciences
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• v.22 no.12
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• pp.1686-1692
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• 2009

Garlic oil (GAR, Allium sativum L.) has been studied as a feed additive to improve animal production performance and decrease methane emission in ruminants. The present study was designed to determine the possible effect of GAR on fatty acid composition and accumulation in animal fat tissue using a cell model. 3T3-L1 preadipocytes at $2{\times}10^{4}\;mL^{-1}$ were seeded to 24-well plates and allowed to proliferate to reach confluence. The cells were then treated with media containing 0, 2.5, 5, 10, 20 and 40 $\mu{g}$ $mL^{-1}$ of GAR during the differentiation period for 8 days. Media containing dexamethasone, methyl-isobutylxanthine and insulin was applied during the first 2 days of the early differentiation period. On day 8 sub-sets of the wells were stained with oil red-O and the remaining cells were harvested for determination of glycerol-3-phosphate dehydrogenase [EC 1.1.1.8] (GPDH) activity (n = 6) and cellular fatty acid concentration (n = 6). It was found that supplementation of GAR increased (p<0.05) the ratio of monounsaturated fatty acids/saturated fatty acids in the adipocytes and showed inhibitory effect (p<0.05) on the post-confluent proliferation. With relative low dosage, GAR (5-20 $\mu{g}$ $mL^{-1}$) increased (p<0.05) the GPDH activity without affecting the cellular fatty acid concentration, while a high dosage (40 $\mu{g}$ $mL^{-1}$) inhibited (p<0.05) fatty acid accumulation and decreased GPDH activity. Supplementation of GAR had an effect on cell post-confluent proliferation, differentiation and fatty acid accumulation. However, the effect may be diverse and depends on the dose applied.

• Journal of Microbiology and Biotechnology
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• v.25 no.2
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• pp.162-173
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• 2015

The cellular fatty acid composition is important for metabolic plasticity in Rhodobacter sphaeroides. We explored the effects of changing the cellular ratio of unsaturated fatty acids (UFAs) to saturated fatty acids (SFAs) in R. sphaeroides by overexpressing several key fatty acid biosynthetic enzymes through the use of expression plasmid pRK415. Bacteria containing the plasmid pRKfabI₁ with the fabI₁ gene that encodes enoyl-acyl carrier protein (ACP) reductase showed a reduction in the cellular UFA to SFA ratio from 4 (80% UFA) to 2 (65% UFA) and had decreased membrane fluidity and reduced cell growth. Additionally, the ratio of UFA to SFA of the chromatophore vesicles from pRKfabI₁-containing cells was similarly lowered, and the cell had decreased levels of light-harvesting complexes, but no change in intracytoplasmic membrane (ICM) content or photosynthetic (PS) gene expression. Both inhibition of enoyl-ACP reductase with diazaborine and addition of exogenous UFA restored membrane fluidity, cell growth, and the UFA to SFA ratio to wild-type levels in this strain. R. sphaeroides containing the pRKfabB plasmid with the fabB gene that encodes the enzyme β-ketoacyl-ACP synthase I exhibited an increased UFA to SFA ratio from 4 (80% UFA) to 9 (90% UFA), but showed no change in membrane fluidity or growth rate relative to control cells. Thus, membrane fluidity in R. sphaeroides remains fairly unchanged when membrane UFA levels are between 80% and 90%, whereas membrane fluidity, cell growth, and cellular composition are affected when UFA levels are below 80%.

• Journal of the Korean Society of Food Science and Nutrition
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• v.24 no.2
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• pp.280-285
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• 1995

To develop natural food preservatives, antimicrobial effect of the ethanol extract of leaf mustard against E. coli and S. aureus were examined in terms of compositions and leakage of cellular materials in the microorganisms treated with the extract. No effect of the concentration of ethanol extract on the fatty acid composition of E. coli and S. aureus at logarithmic phase was showen, but the content of palmitic and palmitoleic acid of E. coli slightly increased and decreased, respectively, and the content of palmitic and margaric acid of S. aureus slightly increased, when compared to each control. Ethanol extract did not affect most of the amino acids E. coli and S. aureus at logarithmic phase ; however, some of them(proline, glycine, valine and histidine of E. coli and proline, methionine and histidine of s. aureus) were elevated and some other amino acid(aspartic acid, glutamic acid, tyrosine and arginine of E. coli and aspartic acid, glutamic acid, glycine, alanine and lysine of Staph. aureus) found to be decreased. The amount of cell body protein leaked from E. coli and S. aureus increased to 1.02 and 0.22mg/g cell weight, respectively, as compared to controls. Similarly, the substances with absorbance at 260 nm from E. coli and s. aureus increased to 0.12 and 0.06mg/g cell weight, respectively.

• Journal of Medicine and Life Science
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• v.15 no.2
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• pp.37-41
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• 2018

Mitochondrial injury in renal tubule has been recognized as a major contributor in acute kidney injury (AKI) pathogenesis. Ischemic insult, nephrotoxin, endotoxin and contrast medium destroy mitochondrial structure and function as well as their biogenesis and dynamics, especially in renal proximal tubule, to elicit ATP depletion. Mitochondrial fatty acid ${\beta}$-oxidation (FAO) is the preferred source of ATP in the kidney, and its impairment is a critical factor in AKI pathogenesis. This review explores current knowledge of mitochondrial dysfunction and energy depletion in AKI and prospective views on developing therapeutic strategies targeting mitochondrial dysfunction in AKI.