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1.
Anim Reprod Sci ; 125(1-4): 180-8, 2011 May.
Article in English | MEDLINE | ID: mdl-21511415

ABSTRACT

Selenium (Se) is an essential component of at least 25 selenoproteins involved in a multitude of physiological functions, including reproduction. However, relatively little is known about the mechanisms by which Se exerts its physiological effects in reproductive tissue. The objective of this study was to compare the effect of long-term inorganic Se (sodium selenite, SS) and organic yeast-derived Se (Sel-Plex(®), SP) supplementations on tissue Se content and gene expression patterns in the oviduct of broiler-breeder hens. Hens were randomly assigned at 6 weeks of age to one of the three treatments: basal semi-purified diet (control), basal diet+0.3 ppm Se as SP or basal diet+0.3 ppm Se as SS. At 49 weeks, oviduct tissue from hens randomly selected from each treatment (n=7) was analyzed for Se content and gene expression profiles using the Affymetrix Chicken genome array. Gene expression data were evaluated using GeneSpring GX 10.0 (Silicon Genetics, Redwood, CA) and Ingenuity Pathways Analysis software (Ingenuity Systems, Redwood City, CA). Oviduct Se concentration was greater with Se supplementation compared with the control (P≤0.05) but did not differ between SS- and SP-supplemented groups. Gene expression analysis revealed that the quantity of gene transcripts associated with energy production and protein translation were greater in the oviduct with SP but not SS supplementation. Targets up-regulated by SP, but not SS, included genes encoding several subunits of the mitochondrial respiratory complexes, ubiquinone production and ribosomal subunits. SS hens showed a decrease in transcripts of genes involved in respiratory complexes, ATP synthesis and protein translation and metabolism in oviduct relative to control hens. In this study, although tissue Se concentrations did not differ between hens fed SS- and SP-supplemented diets, expression patterns of genes involved in energy production and protein synthesis pathways differed between treatments. These variations may partially explain the differences in reproductive performance reported in hens fed different forms of Se.


Subject(s)
Chickens/genetics , Gene Expression Regulation/drug effects , Oviducts/drug effects , Selenium/administration & dosage , Animals , Chickens/metabolism , Computational Biology , Dietary Supplements , Female , Gene Expression Profiling/methods , Gene Expression Profiling/veterinary , Oligonucleotide Array Sequence Analysis/veterinary , Oviducts/metabolism , Oviducts/physiology , RNA, Messenger/biosynthesis , RNA, Messenger/genetics , Random Allocation , Reverse Transcriptase Polymerase Chain Reaction/veterinary
2.
Exp Gerontol ; 43(9): 859-66, 2008 Sep.
Article in English | MEDLINE | ID: mdl-18657603

ABSTRACT

An active area of aging research is focused on identifying compounds having the ability to mimic the effects of caloric restriction (CR). From 2 to 5 months of age, we fed male B6C3F(1) mice either a 40% CR diet, a control diet supplemented with a commercially available nutraceutical mixture (NCM) containing resveratrol, quercetin and inositol hexaphosphate, or a diet supplemented with an equivalent dose of chemical-grade resveratrol (RES; 1.25 mg resveratrol kg(-1) day(-1)) from 2 to 5 months of age. Cardiac gene expression profiles were generated for the three groups of treated mice and compared to age-matched control (CO) mice. All three treatments were associated with changes in several cytoskeletal maintenance pathways, suggesting that RES and NCM are able to mimic short-term CR. CR uniquely affected several immune function pathways while RES uniquely affected multiple stress response pathways. Pathway analysis revealed that NCM (but not CR or RES) regulated multiple metabolic pathways that were also changed by long-term CR, including glucose and lipid metabolism, oxidative phosphorylation and chromatin assembly. Examination of key genes and pathways affected by NCM suggests that Foxo1 is a critical upstream mediator of its actions.


Subject(s)
Caloric Restriction , Dietary Supplements , Gene Expression Regulation/drug effects , Myocardium/metabolism , Stilbenes/pharmacology , Aging/drug effects , Aging/genetics , Aging/metabolism , Animals , Blood Glucose/analysis , Body Weight , Drug Evaluation, Preclinical/methods , Gene Expression Profiling/methods , Insulin/blood , Male , Mice , Mice, Inbred Strains , Oligonucleotide Array Sequence Analysis/methods , Resveratrol , Reverse Transcriptase Polymerase Chain Reaction/methods , Signal Transduction/drug effects
3.
Int J Obes (Lond) ; 30(11): 1585-94, 2006 Nov.
Article in English | MEDLINE | ID: mdl-16801930

ABSTRACT

OBJECTIVE: To investigate plausible contributors to the obesity epidemic beyond the two most commonly suggested factors, reduced physical activity and food marketing practices. DESIGN: A narrative review of data and published materials that provide evidence of the role of additional putative factors in contributing to the increasing prevalence of obesity. DATA: Information was drawn from ecological and epidemiological studies of humans, animal studies and studies addressing physiological mechanisms, when available. RESULTS: For at least 10 putative additional explanations for the increased prevalence of obesity over the recent decades, we found supportive (although not conclusive) evidence that in many cases is as compelling as the evidence for more commonly discussed putative explanations. CONCLUSION: Undue attention has been devoted to reduced physical activity and food marketing practices as postulated causes for increases in the prevalence of obesity, leading to neglect of other plausible mechanisms and well-intentioned, but potentially ill-founded proposals for reducing obesity rates.


Subject(s)
Disease Outbreaks , Obesity/etiology , Age Factors , Body Mass Index , Drug-Related Side Effects and Adverse Reactions , Endocrine System/drug effects , Epigenesis, Genetic/physiology , Female , Humans , Maternal Age , Obesity/epidemiology , Obesity/ethnology , Prevalence , Selection, Genetic , Sleep/physiology , Smoking/epidemiology , Temperature
4.
Am J Physiol Endocrinol Metab ; 279(2): E433-46, 2000 Aug.
Article in English | MEDLINE | ID: mdl-10913045

ABSTRACT

Linking tissue uncoupling protein (UCP) homolog abundance with functional metabolic outcomes and with expression of putative genetic regulators promises to better clarify UCP homolog physiological function. A murine endotoxemia model characterized by marked alterations in thermoregulation was employed to examine the association between heat production, UCP homolog expression, and mitochondrial proton leak ("uncoupling"). After intraperitoneal lipopolysaccharide (LPS, approximately 6 mg/kg) injection, colonic temperature (T(c)) in adult female C57BL6/J mice dropped to a nadir of approximately 30 degrees C by 8 h, preceded by a four- to fivefold drop in liver UCP2 and UCP5/brain mitochondrial carrier protein 1 mRNA levels, with no change in their hindlimb skeletal muscle (SKM) expression. SKM UCP3 mRNA rose fivefold during development of hypothermia and was correlated with an LPS-induced increase in plasma free fatty acid concentration. UCP2 and UCP5 transcripts recovered about three- to sixfold in both tissues starting at 6-8 h, preceding a recovery of T(c) between 16 and 24 h. SKM UCP3 followed an opposite pattern. Such results are not consistent with an important influence of UCP3 in driving heat production but do not preclude a role for UCP2 or UCP5 in this process. The transcription coactivator PGC-1 displayed a transient LPS-evoked rise (threefold) or drop (two- to fivefold) in SKM and liver expression, respectively. No differences between control and LPS-treated mouse liver or SKM in vitro mitochondrial proton leak were evident at time points corresponding to large differences in UCP homolog expression.


Subject(s)
Carrier Proteins/metabolism , Endotoxemia/metabolism , Membrane Transport Proteins , Mitochondrial Proteins , Nerve Tissue Proteins/metabolism , Proteins/metabolism , RNA, Messenger/metabolism , Animals , Body Temperature , Body Temperature Regulation/drug effects , Carrier Proteins/genetics , Disease Models, Animal , Endotoxemia/chemically induced , Fatty Acids, Nonesterified/blood , Female , Ion Channels , Lipopolysaccharides/pharmacology , Liver/cytology , Liver/metabolism , Membrane Potentials/drug effects , Mice , Mice, Inbred C57BL , Mitochondria, Liver/drug effects , Mitochondria, Liver/metabolism , Mitochondria, Muscle/drug effects , Mitochondria, Muscle/metabolism , Mitochondrial Swelling , Mitochondrial Uncoupling Proteins , Muscle, Skeletal/metabolism , Nerve Tissue Proteins/genetics , Oxygen Consumption/drug effects , Proteins/genetics , Protons , Transcription Factors/metabolism , Transcription, Genetic , Uncoupling Protein 2 , Uncoupling Protein 3
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