Paraoxonase responses to exercise and niacin therapy in men with metabolic syndrome

Our purpose was to characterize changes in paraoxonase 1 (PON1) activity and concentration after single aerobic exercise sessions conducted before and after 6 weeks of niacin therapy in men with metabolic syndrome (MetS). Twelve men with MetS expended 500 kcal by walking at 65% of VO2max before and after a 6-week regimen of niacin. Niacin doses were titrated by 500 mg/week from 500 to 1500 mg/day and maintained at 1500 mg/day for the last 4 weeks. Fasting blood samples were collected before and 24 hours after each exercise session and analyzed for PON1 activity, PON1 concentration, myeloperoxidase (MPO), apolipoprotein A1, oxidized low-density lipoprotein (oLDL), lipoprotein particle sizes and concentrations. PON1 activity, PON1 concentration, MPO, and oLDL were unaltered following the independent effects of exercise and niacin (P > 0.05 for all). High-density lipoprotein particle size decreased by 3% (P = 0.040) and concentrations of small very low-density lipoprotein increased (P = 0.016) following exercise. PON1 activity increased 6.1% (P = 0.037) and PON1 concentrations increased 11.3% (P = 0.015) with the combination of exercise and niacin. Exercise and niacin works synergistically to increase PON1 activity and concentration with little or no changes in lipoproteins or markers of lipid oxidation.UCR::Vicerrectoría de Investigación::Unidades de Investigación::Ciencias Sociales::Centro de Investigación en Ciencias del Movimiento Humano (CIMOHU)UCR::Vicerrectoría de Docencia::Ciencias Sociales::Facultad de Educación::Escuela de Educación Físic

Life on Arginine for Mycoplasma hominis: Clues from Its Minimal Genome and Comparison with Other Human Urogenital Mycoplasmas

Mycoplasma hominis is an opportunistic human mycoplasma. Two other pathogenic human species, M. genitalium and Ureaplasma parvum, reside within the same natural niche as M. hominis: the urogenital tract. These three species have overlapping, but distinct, pathogenic roles. They have minimal genomes and, thus, reduced metabolic capabilities characterized by distinct energy-generating pathways. Analysis of the M. hominis PG21 genome sequence revealed that it is the second smallest genome among self-replicating free living organisms (665,445 bp, 537 coding sequences (CDSs)). Five clusters of genes were predicted to have undergone horizontal gene transfer (HGT) between M. hominis and the phylogenetically distant U. parvum species. We reconstructed M. hominis metabolic pathways from the predicted genes, with particular emphasis on energy-generating pathways. The Embden–Meyerhoff–Parnas pathway was incomplete, with a single enzyme absent. We identified the three proteins constituting the arginine dihydrolase pathway. This pathway was found essential to promote growth in vivo. The predicted presence of dimethylarginine dimethylaminohydrolase suggested that arginine catabolism is more complex than initially described. This enzyme may have been acquired by HGT from non-mollicute bacteria. Comparison of the three minimal mollicute genomes showed that 247 CDSs were common to all three genomes, whereas 220 CDSs were specific to M. hominis, 172 CDSs were specific to M. genitalium, and 280 CDSs were specific to U. parvum. Within these species-specific genes, two major sets of genes could be identified: one including genes involved in various energy-generating pathways, depending on the energy source used (glucose, urea, or arginine) and another involved in cytadherence and virulence. Therefore, a minimal mycoplasma cell, not including cytadherence and virulence-related genes, could be envisaged containing a core genome (247 genes), plus a set of genes required for providing energy. For M. hominis, this set would include 247+9 genes, resulting in a theoretical minimal genome of 256 genes

Sterility and Gene Expression in Hybrid Males of Xenopus laevis and X. muelleri

BACKGROUND: Reproductive isolation is a defining characteristic of populations that represent unique biological species, yet we know very little about the gene expression basis for reproductive isolation. The advent of powerful molecular biology tools provides the ability to identify genes involved in reproductive isolation and focuses attention on the molecular mechanisms that separate biological species. Herein we quantify the sterility pattern of hybrid males in African Clawed Frogs (Xenopus) and apply microarray analysis of the expression pattern found in testes to identify genes that are misexpressed in hybrid males relative to their two parental species (Xenopus laevis and X. muelleri). METHODOLOGY/PRINCIPAL FINDINGS: Phenotypic characteristics of spermatogenesis in sterile male hybrids (X. laevis x X. muelleri) were examined using a novel sperm assay that allowed quantification of live, dead, and undifferentiated sperm cells, the number of motile vs. immotile sperm, and sperm morphology. Hybrids exhibited a dramatically lower abundance of mature sperm relative to the parental species. Hybrid spermatozoa were larger in size and accompanied by numerous undifferentiated sperm cells. Microarray analysis of gene expression in testes was combined with a correction for sequence divergence derived from genomic hybridizations to identify candidate genes involved in the sterility phenotype. Analysis of the transcriptome revealed a striking asymmetric pattern of misexpression. There were only about 140 genes misexpressed in hybrids compared to X. laevis but nearly 4,000 genes misexpressed in hybrids compared to X. muelleri. CONCLUSIONS/SIGNIFICANCE: Our results provide an important correlation between phenotypic characteristics of sperm and gene expression in sterile hybrid males. The broad pattern of gene misexpression suggests intriguing mechanisms creating the dominance pattern of the X. laevis genome in hybrids. These findings significantly contribute to growing evidence for allelic dominance in hybrids and have implications for the mechanism of species differentiation at the transcriptome level

MITOCHONDRIAL TRANSCRIPTION AND TRANSLATION INITIATION FACTOR PROTEIN EXPRESSION ENHANCEMENT THROUGH HIGH-VOLUME RESISTANCE TRAINING

David E. Lee1, James D. Fluckey2, Mats I. Nilsson2, Lemuel A.Brown1, Kevin L. Shimkus2, Tyrone A. Washington1, Stephen F.Crouse, FACSM3, and Nicholas P.Greene123 1Human Performance Laboratory, Department of Health, Human Performance and Recreation, University of Arkansas, Fayetteville, AR, 2Muscle Biology Laboratory, Department of Health & Kinesiology, Texas A&M University, College Station, TX, 3Applied Exercise Science Laboratory, Department of Health & Kinesiology, Texas A&M University, College Station, TX Exercise is known to stimulate muscle protein synthesis through transcription and translation of nuclear DNA leading to muscular hypertrophy and mitochondrial biogenesis. To our knowledge, the effect of exercise on mitochondrial translation has yet to be tested even though proteins coded by the mitochondria are paramount to metabolic health. PURPOSE: This investigation aims to determine if transcription factor A of the mitochondria (TFAM) and mitochondrial translation initiation factor 2 (mtIF2) protein expression is enhanced following high-volume resistance training and see if any difference exists in obesity compared to lean controls. METHODS: Zucker Rats (N=30, 16 lean, 14 obese) engaged in either a resistance training protocol or remained sedentary. The exercised rats (n = 8 lean and 8 obese) undertook a resistance exercise protocol involving a hind limb ‘squat-like’ exercise while the remainder (n=8 lean and 6 obese) were sedentary. Sixteen hours following the final bout of resistance exercise, the animals were euthanized and mixed fiber gastrocnemius muscles were removed and immediately frozen in liquid nitrogen. Samples were later analyzed for TFAM and mtIF2 protein expression via Western blot analysis. Data were analyzed using a 2x2 ANOVA (exercise vs. sedentary X lean vs. obese); α was set at p≤0.05. RESULTS: TFAM protein content increased by 54.62%(p0.05). No significant difference in TFAM and mtIF2 was observed between lean and obese responses to exercise. CONCLUSION: Resistance exercise increased the expression of mitochondrial transcription factors and appears to increase expression of mitochondrial translation factors in lean and obese animals indicating enhanced capacity for transcription and translation of mitochondrially encoded genes with high volume exercise training. These data suggest that resistance training could lead to increased metabolic proteins derived from the mitochondrial DNA in mammals. Enhanced mitochondrial protein synthesis would likely lead to increased oxidative phosphorylation enzymes such as those used in the electron transport system indicating a possible pathway for resistance training improvements on whole organism metabolic health. This investigation was funded by the Sydney & J.L. Huffines Institue for Sports Medicine & Human Performance at Texas A&M University