Displaying publications 1 - 20 of 39 in total

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  1. Metabolomics - the complementary field in systems biology: a review on obesity and type 2 diabetes
    Abu Bakar MH, Sarmidi MR, Cheng KK, Ali Khan A, Suan CL, Zaman Huri H, et al.
    Mol Biosyst, 2015 Jul;11(7):1742-74.
    PMID: 25919044 DOI: 10.1039/c5mb00158g
    Metabolomic studies on obesity and type 2 diabetes mellitus have led to a number of mechanistic insights into biomarker discovery and comprehension of disease progression at metabolic levels. This article reviews a series of metabolomic studies carried out in previous and recent years on obesity and type 2 diabetes, which have shown potential metabolic biomarkers for further evaluation of the diseases. Literature including journals and books from Web of Science, Pubmed and related databases reporting on the metabolomics in these particular disorders are reviewed. We herein discuss the potential of reported metabolic biomarkers for a novel understanding of disease processes. These biomarkers include fatty acids, TCA cycle intermediates, carbohydrates, amino acids, choline and bile acids. The biological activities and aetiological pathways of metabolites of interest in driving these intricate processes are explained. The data from various publications supported metabolomics as an effective strategy in the identification of novel biomarkers for obesity and type 2 diabetes. Accelerating interest in the perspective of metabolomics to complement other fields in systems biology towards the in-depth understanding of the molecular mechanisms underlying the diseases is also well appreciated. In conclusion, metabolomics can be used as one of the alternative approaches in biomarker discovery and the novel understanding of pathophysiological mechanisms in obesity and type 2 diabetes. It can be foreseen that there will be an increasing research interest to combine metabolomics with other omics platforms towards the establishment of detailed mechanistic evidence associated with the disease processes.
  2. Celastrol attenuates mitochondrial dysfunction and inflammation in palmitate-mediated insulin resistance in C3A hepatocytes
    Abu Bakar MH, Sarmidi MR, Tan JS, Mohamad Rosdi MN
    Eur J Pharmacol, 2017 Mar 15;799:73-83.
    PMID: 28161417 DOI: 10.1016/j.ejphar.2017.01.043
    Accumulating evidence indicates that mitochondrial dysfunction-induced inflammation is among the convergence points for the greatest hallmarks of hepatic insulin resistance. Celastrol, an anti-inflammatory compound from the root of Tripterygium Wilfordii has been reported to mitigate insulin resistance and inflammation in animal disease models. Nevertheless, the specific mechanistic actions of celastrol in modulating such improvements at the cellular level remain obscure. The present study sought to explore the mechanistic roles of celastrol upon insulin resistance induced by palmitate in C3A human hepatocytes. The hepatocytes exposed to palmitate (0.75mM) for 48h exhibited reduced both basal and insulin-stimulated glucose uptake, mitochondrial dysfunction, leading to increased mitochondrial oxidative stress with diminished fatty acid oxidation. Elevated expressions of nuclear factor-kappa B p65 (NF-κB p65), c-Jun NH(2)-terminal kinase (JNK) signaling pathways and the amplified release of pro-inflammatory cytokines including IL-8, IL-6, TNF-α and CRP were observed following palmitate treatment. Consistently, palmitate reduced and augmented phosphorylated Tyrosine-612 and Serine-307 of insulin receptor substrate-1 (IRS-1) proteins, respectively in hepatocytes. However, celastrol at the optimum concentration of 30nM was able to reverse these deleterious occasions and protected the cells from mitochondrial dysfunction and insulin resistance. Importantly, we presented evidence for the first time that celastrol efficiently prevented palmitate-induced insulin resistance in hepatocytes at least, via improved mitochondrial functions and insulin signaling pathways. In summary, the present investigation underlines a conceivable mechanism to elucidate the cytoprotective potential of celastrol in attenuating mitochondrial dysfunction and inflammation against the development of hepatic insulin resistance.
  3. Fulltext Celastrol Protects against Antimycin A-Induced Insulin Resistance in Human Skeletal Muscle Cells
    Abu Bakar MH, Cheng KK, Sarmidi MR, Yaakob H, Huri HZ
    Molecules, 2015 May 07;20(5):8242-69.
    PMID: 25961164 DOI: 10.3390/molecules20058242
    Mitochondrial dysfunction and inflammation are widely accepted as key hallmarks of obesity-induced skeletal muscle insulin resistance. The aim of the present study was to evaluate the functional roles of an anti-inflammatory compound, celastrol, in mitochondrial dysfunction and insulin resistance induced by antimycin A (AMA) in human skeletal muscle cells. We found that celastrol treatment improved insulin-stimulated glucose uptake activity of AMA-treated cells, apparently via PI3K/Akt pathways, with significant enhancement of mitochondrial activities. Furthermore, celastrol prevented increased levels of cellular oxidative damage where the production of several pro-inflammatory cytokines in cultures cells was greatly reduced. Celastrol significantly increased protein phosphorylation of insulin signaling cascades with amplified expression of AMPK protein and attenuated NF-κB and PKC θ activation in human skeletal muscle treated with AMA. The improvement of insulin signaling pathways by celastrol was also accompanied by augmented GLUT4 protein expression. Taken together, these results suggest that celastrol may be advocated for use as a potential therapeutic molecule to protect against mitochondrial dysfunction-induced insulin resistance in human skeletal muscle cells.
  4. Improvement of mitochondrial function by celastrol in palmitate-treated C2C12 myotubes via activation of PI3K-Akt signaling pathway
    Abu Bakar MH, Tan JS
    Biomed Pharmacother, 2017 Sep;93:903-912.
    PMID: 28715871 DOI: 10.1016/j.biopha.2017.07.021
    Compelling evidences posited that high level of saturated fatty acid gives rise to mitochondrial dysfunction and inflammation in the development of insulin resistance in skeletal muscle. Celastrol is a pentacyclic triterpenoid derived from the root extracts of Tripterygium wilfordii that possesses potent anti-inflammatory properties in a number of animal models with metabolic diseases. However, the cellular mechanistic action of celastrol in alleviating obesity-induced insulin resistance in skeletal muscle remains largely unknown. Therefore, the present investigation evaluated the attributive properties of celastrol at different concentrations (10, 20, 30 and 40nM) on insulin resistance in C2C12 myotubes evoked by palmitate. We demonstrated that celastrol improved mitochondrial functions through significant enhancement of intracellular ATP content, mitochondrial membrane potential, citrate synthase activity and decrease of mitochondrial superoxide productions. Meanwhile, augmented mitochondrial DNA (mtDNA) content with suppressed DNA oxidative damage were observed following celastrol treatment. Celastrol significantly enhanced fatty acid oxidation rate and increased the level of tricarboxylic acid (TCA) cycle intermediates in palmitate-treated cells. Further analysis revealed that the improvement of glucose uptake activity in palmitate-loaded myotubes was partly mediated by celastrol via activation of PI3K-Akt insulin signaling pathway. Collectively, these findings provided evidence for the first time that the protection from palmitate-mediated insulin resistance in C2C12 myotubes by celastrol is likely associated with the improvement of mitochondrial functions-related metabolic activities.
  5. Celastrol attenuates inflammatory responses in adipose tissues and improves skeletal muscle mitochondrial functions in high fat diet-induced obese rats via upregulation of AMPK/SIRT1 signaling pathways
    Abu Bakar MH, Shariff KA, Tan JS, Lee LK
    Eur J Pharmacol, 2020 Sep 15;883:173371.
    PMID: 32712089 DOI: 10.1016/j.ejphar.2020.173371
    Accumulating evidence indicates that adipose tissue inflammation and mitochondrial dysfunction in skeletal muscle are inextricably linked to obesity and insulin resistance. Celastrol, a bioactive compound derived from the root of Tripterygium wilfordii exhibits a number of attributive properties to attenuate metabolic dysfunction in various cellular and animal disease models. However, the underlying therapeutic mechanisms of celastrol in the obesogenic environment in vivo remain elusive. Therefore, the current study investigated the metabolic effects of celastrol on insulin sensitivity, inflammatory response in adipose tissue and mitochondrial functions in skeletal muscle of the high fat diet (HFD)-induced obese rats. Our study revealed that celastrol supplementation at 3 mg/kg/day for 8 weeks significantly reduced the final body weight and enhanced insulin sensitivity of the HFD-fed rats. Celastrol noticeably improved insulin-stimulated glucose uptake activity and increased expression of plasma membrane GLUT4 protein in skeletal muscle. Moreover, celastrol-treated HFD-fed rats showed attenuated inflammatory responses via decreased NF-κB activity and diminished mRNA expression responsible for classically activated macrophage (M1) polarization in adipose tissues. Significant improvement of muscle mitochondrial functions and enhanced antioxidant defense machinery via restoration of mitochondrial complexes I + III linked activity were effectively exhibited by celastrol treatment. Mechanistically, celastrol stimulated mitochondrial biogenesis attributed by upregulation of the adenosine monophosphate-activated protein kinase (AMPK) and sirtuin 1 (SIRT1) signaling pathways. Together, these results further demonstrate heretofore the conceivable therapeutic mechanisms of celastrol in vivo against HFD-induced obesity mediated through attenuation of inflammatory response in adipose tissue and enhanced mitochondrial functions in skeletal muscle.
  6. Association of cultured myotubes and fasting plasma metabolite profiles with mitochondrial dysfunction in type 2 diabetes subjects
    Abu Bakar MH, Sarmidi MR
    Mol Biosyst, 2017 Aug 22;13(9):1838-1853.
    PMID: 28726959 DOI: 10.1039/c7mb00333a
    Accumulating evidence implicates mitochondrial dysfunction-induced insulin resistance in skeletal muscle as the root cause for the greatest hallmarks of type 2 diabetes (T2D). However, the identification of specific metabolite-based markers linked to mitochondrial dysfunction in T2D has not been adequately addressed. Therefore, we sought to identify the markers-based metabolomics for mitochondrial dysfunction associated with T2D. First, a cellular disease model was established using human myotubes treated with antimycin A, an oxidative phosphorylation inhibitor. Non-targeted metabolomic profiling of intracellular-defined metabolites on the cultured myotubes with mitochondrial dysfunction was then determined. Further, a targeted MS-based metabolic profiling of fasting blood plasma from normal (n = 32) and T2D (n = 37) subjects in a cross-sectional study was verified. Multinomial logical regression analyses for defining the top 5% of the metabolites within a 95% group were employed to determine the differentiating metabolites. The myotubes with mitochondrial dysfunction exhibited insulin resistance, oxidative stress and inflammation with impaired insulin signalling activities. Four metabolic pathways were found to be strongly associated with mitochondrial dysfunction in the cultured myotubes. Metabolites derived from these pathways were validated in an independent pilot investigation of the fasting blood plasma of healthy and diseased subjects. Targeted metabolic analysis of the fasting blood plasma with specific baseline adjustment revealed 245 significant features based on orthogonal partial least square discriminant analysis (PLS-DA) with a p-value < 0.05. Among these features, 20 significant metabolites comprised primarily of branched chain and aromatic amino acids, glutamine, aminobutyric acid, hydroxyisobutyric acid, pyroglutamic acid, acylcarnitine species (acetylcarnitine, propionylcarnitine, dodecenoylcarnitine, tetradecenoylcarnitine hexadecadienoylcarnitine and oleylcarnitine), free fatty acids (palmitate, arachidonate, stearate and linoleate) and sphingomyelin (d18:2/16:0) were identified as predictive markers for mitochondrial dysfunction in T2D subjects. The current study illustrates how cellular metabolites provide potential signatures associated with the biochemical changes in the dysregulated body metabolism of diseased subjects. Our finding yields additional insights into the identification of robust biomarkers for T2D associated with mitochondrial dysfunction in cultured myotubes.
  7. Withaferin A Protects Against High-Fat Diet-Induced Obesity Via Attenuation of Oxidative Stress, Inflammation, and Insulin Resistance
    Abu Bakar MH, Azmi MN, Shariff KA, Tan JS
    Appl Biochem Biotechnol, 2019 May;188(1):241-259.
    PMID: 30417321 DOI: 10.1007/s12010-018-2920-2
    Withaferin A (WA), a bioactive constituent derived from Withania somnifera plant, has been shown to exhibit many qualifying properties in attenuating several metabolic diseases. The current investigation sought to elucidate the protective mechanisms of WA (1.25 mg/kg/day) on pre-existing obese mice mediated by high-fat diet (HFD) for 12 weeks. Following dietary administration of WA, significant metabolic improvements in hepatic insulin sensitivity, adipocytokines with enhanced glucose tolerance were observed. The hepatic oxidative functions of obese mice treated with WA were improved via augmented antioxidant enzyme activities. The levels of serum pro-inflammatory cytokines and hepatic mRNA expressions of toll-like receptor (TLR4), nuclear factor κB (NF-κB), tumor necrosis factor-α (TNF-α), chemokine (C-C motif) ligand-receptor, and cyclooxygenase 2 (COX2) in HFD-induced obese mice were reduced. Mechanistically, WA increased hepatic mRNA expression of peroxisome proliferator-activated receptors (PPARs), cluster of differentiation 36 (CD36), fatty acid synthase (FAS), carnitine palmitoyltransferase 1 (CPT1), glucokinase (GCK), phosphofructokinase (PFK), and phosphoenolpyruvate carboxykinase (PCK1) that were associated with enhanced lipid and glucose metabolism. Taken together, these results indicate that WA exhibits protective effects against HFD-induced obesity through attenuation of hepatic inflammation, oxidative stress, and insulin resistance in mice.
  8. Celastrol attenuates high-fructose diet-induced inflammation and insulin resistance via inhibition of 11β-hydroxysteroid dehydrogenase type 1 activity in rat adipose tissues
    Abu Bakar MH, Mohamad Khalid MSF, Nor Shahril NS, Shariff KA, Karunakaran T
    Biofactors, 2022 Jan;48(1):111-134.
    PMID: 34676604 DOI: 10.1002/biof.1793
    High fructose consumption has been linked to low-grade inflammation and insulin resistance that results in increased intracellular 11ß-hydroxysteroid dehydrogenase type 1 (11β-HSD1) activity. Celastrol, a pentacyclic triterpene, has been demonstrated to exhibit multifaceted targets to attenuate various metabolic diseases associated with inflammation. However, the underlying mechanisms by which celastrol exerts its attributive properties on high fructose diet (HFrD)-induced metabolic syndrome remain elusive. Herein, the present study was aimed to elucidate the mechanistic targets of celastrol co-administrations upon HFrD in rats and evaluate its potential to modulate 11β-HSD1 activity. Celastrol remarkably improved glucose tolerance, lipid profiles, and insulin sensitivity along with suppression of hepatic glucose production. In rat adipose tissues, celastrol attenuated nuclear factor-kappa B (NF-κB)-driven inflammation, reduced c-Jun N-terminal kinases (JNK) phosphorylation, and mitigated oxidative stress via upregulated genes expression involved in mitochondrial biogenesis. Furthermore, insulin signaling pathways were significantly improved through the restoration of Akt phosphorylation levels at Ser473 and Thr308 residues. Celastrol exhibited a potent, selective and specific inhibitor of intracellular 11β-HSD1 towards oxidoreductase activity (IC50 value = 4.3 nM) in comparison to other HSD-related enzymes. Inhibition of 11β-HSD1 expression in rat adipose microsomes reduced the availability of its cofactor NADPH and substrate H6PDH in couple to upregulated mRNA and protein expressions of glucocorticoid receptor. In conclusion, our results underscore the most likely conceivable mechanisms exhibited by celastrol against HFrD-induced metabolic dysregulations mainly through attenuating inflammation and insulin resistance, at least via specific inhibitions on 11β-HSD1 activity in adipose tissues.
  9. Reduced mitochondrial DNA content in lymphocytes is associated with insulin resistance and inflammation in patients with impaired fasting glucose
    Abu Bakar MH, Hairunisa N, Zaman Huri H
    Clin Exp Med, 2018 Aug;18(3):373-382.
    PMID: 29550985 DOI: 10.1007/s10238-018-0495-4
    Altered mitochondrial DNA (mtDNA) is the most common denominator to numerous metabolic diseases. The present study sought to investigate the correlation between mtDNA content in lymphocytes and associated clinical risk factors for impaired fasting glucose (IFG). We included 23 healthy control and 42 IFG participants in this cross-sectional study. The measurements of mtDNA content in lymphocytes and pro-inflammatory markers derived from both normal and diseased individuals were quantified. Spearman partial correlation and multivariate statistical analyses were employed to evaluate the association between mtDNA content and other metabolic covariates in IFG. Reduced mtDNA content was observed in the IFG group with microvascular complications than those without complications. The IFG patients with lowest median of mtDNA content had considerably elevated hyperglycemia, insulin resistance and inflammation. The adjusted partial correlation analysis showed that mtDNA content was positively correlated with HDL-cholesterol and IL-10 (P 
  10. Fulltext Effect of Active Site Modification towards Performance Enhancement in Biopolymer κ-Carrageenan Derivatives
    Abu Bakar MH, Azeman NH, Mobarak NN, Mokhtar MHH, A Bakar AA
    Polymers (Basel), 2020 Sep 08;12(9).
    PMID: 32911662 DOI: 10.3390/polym12092040
    This research demonstrates a one-step modification process of biopolymer carrageenan active sites through functional group substitution in κ-carrageenan structures. The modification process improves the electronegative properties of κ-carrageenan derivatives, leading to enhancement of the material's performance. Synthesized succinyl κ-carrageenan with a high degree of substitution provides more active sites for interaction with analytes. The FTIR analysis of succinyl κ-carrageenan showed the presence of new peaks at 1068 cm-1, 1218 cm-1, and 1626 cm-1 that corresponded to the vibrations of C-O and C=O from the carbonyl group. A new peak at 2.86 ppm in 1H NMR represented the methyl proton neighboring with C=O. The appearance of new peaks at 177.05 and 177.15 ppm in 13C NMR proves the substitution of the succinyl group in the κ-carrageenan structure. The elemental analysis was carried out to calculate the degree of substitution with the highest value of 1.78 at 24 h of reaction. The XRD diffractogram of derivatives exhibited a higher degree of crystallinity compared to pristine κ-carrageenan at 23.8% and 9.2%, respectively. Modification of κ-carrageenan with a succinyl group improved its interaction with ions and the conductivity of the salt solution compared to its pristine form. This work has a high potential to be applied in various applications such as sensors, drug delivery, and polymer electrolytes.
  11. Fulltext Succinyl-κ-carrageenan Silver Nanotriangles Composite for Ammonium Localized Surface Plasmon Resonance Sensor
    Abu Bakar MH, Azeman NH, Mobarak NN, Ahmad Nazri NA, Tengku Abdul Aziz TH, Md Zain AR, et al.
    Polymers (Basel), 2022 Jan 14;14(2).
    PMID: 35054734 DOI: 10.3390/polym14020329
    This research investigates the physicochemical properties of biopolymer succinyl-κ-carrageenan as a potential sensing material for NH4+ Localized Surface Plasmon Resonance (LSPR) sensor. Succinyl-κ-carrageenan was synthesised by reacting κ-carrageenan with succinic anhydride. FESEM analysis shows succinyl-κ-carrageenan has an even and featureless topology compared to its pristine form. Succinyl-κ-carrageenan was composited with silver nanoparticles (AgNP) as LSPR sensing material. AFM analysis shows that AgNP-Succinyl-κ-carrageenan was rougher than AgNP-Succinyl-κ-carrageenan, indicating an increase in density of electronegative atom from oxygen compared to pristine κ-carrageenan. The sensitivity of AgNP-Succinyl-κ-carrageenan LSPR is higher than AgNP-κ-carrageenan LSPR. The reported LOD and LOQ of AgNP-Succinyl-κ-carrageenan LSPR are 0.5964 and 2.7192 ppm, respectively. Thus, AgNP-Succinyl-κ-carrageenan LSPR has a higher performance than AgNP-κ-carrageenan LSPR, broader detection range than the conventional method and high selectivity toward NH4+. Interaction mechanism studies show the adsorption of NH4+ on κ-carrageenan and succinyl-κ-carrageenan were through multilayer and chemisorption process that follows Freundlich and pseudo-second-order kinetic model.
  12. Uv-vis spectroscopy for simple chloride content analysis in edible oil using charged amino-functionalized carbon quantum dots fluorophore reagent
    Abu Bakar MH, Azeman NH, Mobarak NN, Nazri NAA, Daniyal WMEMM, Othman MQ, et al.
    Spectrochim Acta A Mol Biomol Spectrosc, 2024 May 07;317:124419.
    PMID: 38733916 DOI: 10.1016/j.saa.2024.124419
    The utilization of UV-Vis spectroscopy with amino-functionalized carbon quantum dots (NCQD) as a positive fluorophore reagent for chloride sensing in oil marks a notable advancement in analytical spectroscopy chemistry. This approach streamlines the detection process by eliminating the need for lengthy procedures and pretreatment steps typically associated with chloride detection in edible oil. By incorporating NCQD in chloride detection within the oil matrix, the wavelength analysis transitions from the UV to the visible region. This shift eliminates interference from oil matrix interactions, ensuring more accurate results. Molecular analysis of NCQD reveals significant shifts in its Fourier Transformation Infrared and photoluminescence spectroscopy peaks due to interaction with chloride in edible oil. It has two impressive sensitivity ranges spanning from 0.1-1.0 to 1.0-8.0 ppm, with a value of -0.4656 au. ppm-1 (R2 = 0.998) and -0.0361 au. ppm-1 (R2 = 0.931), respectively, the technique meets regulatory standards while achieving a low limit of detection (LOD) of 0.1 ppm. This places it on par with conventional methods and commercial sensors. The NCQD-UV-Vis spectroscopy method not only enhances the efficiency and accuracy of chloride detection but also holds promise for various industrial applications requiring simple and precise monitoring of chloride levels in oil samples.
  13. Fulltext Optical-based sensors for monitoring corrosion of reinforcement rebar via an etched cladding Bragg grating
    Abu Hassan MR, Abu Bakar MH, Dambul K, Adikan FR
    Sensors (Basel), 2012;12(11):15820-6.
    PMID: 23202233 DOI: 10.3390/s121115820
    In this paper, we present the development and testing of an optical-based sensor for monitoring the corrosion of reinforcement rebar. The testing was carried out using an 80% etched-cladding Fibre Bragg grating sensor to monitor the production of corrosion waste in a localized region of the rebar. Progression of corrosion can be sensed by observing the reflected wavelength shift of the FBG sensor. With the presence of corrosion, the etched-FBG reflected spectrum was shifted by 1.0 nm. In addition, with an increase in fringe pattern and continuously, step-like drop in power of the Bragg reflected spectrum was also displayed.
  14. Analytical analysis of second-order Stokes wave in Brillouin ring fiber laser
    Al-Asadi HA, Abu Bakar MH, Al-Mansoori MH, Adikan FR, Mahdi MA
    Opt Express, 2011 Dec 5;19(25):25741-8.
    PMID: 22273966 DOI: 10.1364/OE.19.025741
    This paper details a theoretical modeling of Brillouin ring fiber laser which incorporates the interaction between multiple Brillouin Stokes signals. The ring cavity was pumped at several Brillouin pump (BP) powers and the output was measured through an optical coupler with various coupling ratios. The first-order Brillouin Stokes signal was saturated with the presence of the second-order Stokes signal in the cavity as a result of energy transfer between them. The outcome of the study found that the optimum point for the first-order Stokes wave performance is at laser power reduction of 10%. Resultantly, at the optimum output coupling ratio of 90%, the BFL was able to produce 19.2 mW output power at BP power and Brillouin threshold power of 60 and 21.3 mW respectively. The findings also exhibited the feasibility of the theoretical models application to ring-type Brillouin fiber laser of various design parameters.
  15. Fulltext Amelioration of mitochondrial dysfunction-induced insulin resistance in differentiated 3T3-L1 adipocytes via inhibition of NF-κB pathways
    Bakar MH, Sarmidi MR, Kai CK, Huri HZ, Yaakob H
    Int J Mol Sci, 2014 Dec 02;15(12):22227-57.
    PMID: 25474091 DOI: 10.3390/ijms151222227
    A growing body of evidence suggests that activation of nuclear factor kappa B (NF-κB) signaling pathways is among the inflammatory mechanism involved in the development of insulin resistance and chronic low-grade inflammation in adipose tissues derived from obese animal and human subjects. Nevertheless, little is known about the roles of NF-κB pathways in regulating mitochondrial function of the adipose tissues. In the present study, we sought to investigate the direct effects of celastrol (potent NF-κB inhibitor) upon mitochondrial dysfunction-induced insulin resistance in 3T3-L1 adipocytes. Celastrol ameliorates mitochondrial dysfunction by altering mitochondrial fusion and fission in adipocytes. The levels of oxidative DNA damage, protein carbonylation and lipid peroxidation were down-regulated. Further, the morphology and quantification of intracellular lipid droplets revealed the decrease of intracellular lipid accumulation with reduced lipolysis. Moreover, massive production of the pro-inflammatory mediators tumor necrosis factor-α (TNF-α) and interleukin-1β (IL-1β) were markedly depleted. Insulin-stimulated glucose uptake activity was restored with the enhancement of insulin signaling pathways. This study signified that the treatments modulated towards knockdown of NF-κB transcription factor may counteract these metabolic insults exacerbated in our model of synergy between mitochondrial dysfunction and inflammation. These results demonstrate for the first time that NF-κB inhibition modulates mitochondrial dysfunction induced insulin resistance in 3T3-L1 adipocytes.
  16. Chemical constituents from the stem barks of Calophyllum recurvatum P.F. Stevens and Calophyllum andersonii P.F. Stevens, and their in-vitro hepatotoxic activity
    Firouz NS, Karunakaran T, Mokhtar N, Santhanam R, Jong VYM, Abu Bakar MH
    Nat Prod Res, 2024 Jan 22.
    PMID: 38247357 DOI: 10.1080/14786419.2024.2305222
    Bioactive phenolics can be found in abundance in Calophyllum species. Phytochemical studies are carried out on the stem bark of Calophyllum recurvatum and Calophyllum andersonii, which has led to the isolation and elucidation of phytochemicals, thwaitesixanthone (1), teysmanone A (2), soulattrolide (3), calanone (4), isocalanone (5) and friedelin (6), respectively. The cytotoxic activities of compounds (2), (3), (4) and (5) as well as plant extracts were tested against HeLa Chang liver, HepG2 and HL-7702 cell lines. Phenylpyranocoumarins, teysmanone A (2) and soulattrolide (3) portrayed appreciable cytotoxicity activities at 42.57 ± 1.20 and 34.53 ± 3.41 µg/mL, respectively against HepG2 cell line comparable to the positive control, curcumin. Meanwhile, n-hexane extract from C. recurvatum exhibited cytotoxicity with the IC50 value of 36.43 ± 0.64 and 26.25 ± 4.83 µg/mL against HeLa Chang liver and HepG2 cell lines. All the tested compounds and plant extracts displayed non-cytotoxic properties on HL-7702 cell line.
  17. Fulltext Accelerated Solvent Extractions (ASE) of Mitragyna speciosa Korth. (Kratom) Leaves: Evaluation of Its Cytotoxicity and Antinociceptive Activity
    Goh YS, Karunakaran T, Murugaiyah V, Santhanam R, Abu Bakar MH, Ramanathan S
    Molecules, 2021 Jun 17;26(12).
    PMID: 34204457 DOI: 10.3390/molecules26123704
    Mitragyna speciosa Korth (kratom) is known for its psychoactive and analgesic properties. Mitragynine is the primary constituent present in kratom leaves. This study highlights the utilisation of the green accelerated solvent extraction technique to produce a better, non-toxic and antinociceptive active botanical extract of kratom. ASE M. speciosa extract had a dry yield (0.53-2.91 g) and showed a constant mitragynine content (6.53-7.19%) when extracted with organic solvents of different polarities. It only requires a shorter extraction time (5 min) and a reduced amount of solvents (less than 100 mL). A substantial amount of total phenolic (407.83 ± 2.50 GAE mg/g and flavonoids (194.00 ± 5.00 QE mg/g) were found in ASE kratom ethanol extract. The MTT test indicated that the ASE kratom ethanolic leaf extract is non-cytotoxic towards HEK-293 and HeLa Chang liver cells. In mice, ASE kratom ethanolic extract (200 mg/kg) demonstrated a better antinociceptive effect compared to methanol and ethyl acetate leaf extracts. The presence of bioactive indole alkaloids and flavonols such as mitragynine, paynantheine, quercetin, and rutin in ASE kratom ethanolic leaf extract was detected using UHPLC-ESI-QTOF-MS/MS analysis supports its antinociceptive properties. ASE ethanolic leaf extract offers a better, safe, and cost-effective choice of test botanical extract for further preclinical studies.
  18. Fulltext Role of microbial electrosynthesis system in CO2 capture and conversion: a recent advancement toward cathode development
    Ibrahim I, Salehmin MNI, Balachandran K, Hil Me MF, Loh KS, Abu Bakar MH, et al.
    Front Microbiol, 2023;14:1192187.
    PMID: 37520357 DOI: 10.3389/fmicb.2023.1192187
    Microbial electrosynthesis (MES) is an emerging electrochemical technology currently being researched as a CO2 sequestration method to address climate change. MES can convert CO2 from pollution or waste materials into various carbon compounds with low energy requirements using electrogenic microbes as biocatalysts. However, the critical component in this technology, the cathode, still needs to perform more effectively than other conventional CO2 reduction methods because of poor selectivity, complex metabolism pathways of microbes, and high material cost. These characteristics lead to the weak interactions of microbes and cathode electrocatalytic activities. These approaches range from cathode modification using conventional engineering approaches to new fabrication methods. Aside from cathode development, the operating procedure also plays a critical function and strategy to optimize electrosynthesis production in reducing operating costs, such as hybridization and integration of MES. If this technology could be realized, it would offer a new way to utilize excess CO2 from industries and generate profitable commodities in the future to replace fossil fuel-derived products. In recent years, several potential approaches have been tested and studied to boost the capabilities of CO2-reducing bio-cathodes regarding surface morphology, current density, and biocompatibility, which would be further elaborated. This compilation aims to showcase that the achievements of MES have significantly improved and the future direction this is going with some recommendations. Highlights - MES approach in carbon sequestration using the biotic component.- The role of microbes as biocatalysts in MES and their metabolic pathways are discussed.- Methods and materials used to modify biocathode for enhancing CO2 reduction are presented.
  19. Factors associated with anxiety among elderly hypertensive in primary care setting
    Ismail Z, Mohamad M, Isa MR, Fadzil MA, Yassin SM, Ma KT, et al.
    J Ment Health, 2015 Feb;24(1):29-32.
    PMID: 25358109 DOI: 10.3109/09638237.2014.971148
    BACKGROUND: There is increasing evidence showing that anxiety is associated with morbidity in the older age group. Factors contributing to anxiety may vary among different diseases and settings.
    AIMS: The aim of this study was to determine the factors associated with anxiety symptoms among elderly hypertensive at the primary care level.
    METHODS: A cross-sectional study and face-to-face interviews using Hospital Anxiety and Depression Scale (HADS) were conducted among elderly hypertensive.
    RESULTS: The mean (SD) age of subjects was 68.8 (6.76) years and comprised of 49.5% and 50.5% of males and females, respectively. The majority of respondents were Malays (76.1%), followed by Chinese (14.3%), and Indians (9.5%). The mean (SD) duration of hypertension was 8.44 (7.29) years and the prevalence of anxiety symptoms was 13.3% (95% CI: 9.9, 16.7). Multiple logistic regression analysis showed that elderly hypertensive with a past history of stroke (adjusted OR: 4.472; 95% CI: 1.754, 11.405; p = 0.002) and depression (adjusted OR: 3.715; 95% CI: 2.009, 6.872; p 
  20. Fulltext The role of lycopene for the amelioration of glycaemic status and peripheral antioxidant capacity among the Type II diabetes mellitus patients: a case-control study
    Leh HE, Mohd Sopian M, Abu Bakar MH, Lee LK
    Ann Med, 2021 12;53(1):1059-1065.
    PMID: 34180336 DOI: 10.1080/07853890.2021.1943515
    BACKGROUND: The use of lycopene as a complementary medicine for Type II diabetes mellitus (T2DM) is limited and controversial. This study evaluated the effect of lycopene intake on the changes of glycaemic status and antioxidant capacity among the T2DM patients.

    PATIENTS AND METHODS: This case-control study involved the participation of 87 patients and 122 healthy individuals. Lycopene intake was assessed by using a food frequency questionnaire. The peripheral antioxidant capacity among the T2DM patients was evaluated. Glycated haemoglobin (HbA1c) and fasting plasma glucose (FPG) were measured as indications of glycaemic status.

    RESULTS: Peripheral antioxidant capacity was significantly lower in the T2DM group. Direct positive correlations were found between the lycopene intake and peripheral antioxidant level among the T2DM patients. Contrarily, HbA1c and FPG levels decreased significantly with the higher lycopene intake.

    CONCLUSIONS: T2DM patients with a higher lycopene intake showed a greater peripheral antioxidant capacity and better glycaemic control. Lycopene may act to ameliorate oxidative stress and improve the pathophysiology of T2DM.

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