Author information: Solocinski K1,2, Holzworth M1, Wen X1, Cheng KY1, Lynch IJ1,3, Cain BD2, Wingo CS1,3, Gumz ML4,5,6.
1Department of Medicine, University of Florida.
2Department of Biochemistry and Molecular Biology, University of Florida.
3North Florida/South Georgia Veterans Health System, Gainesville, FL.
4Department of Medicine, University of Florida. Michelle.Gumz@medicine.ufl.edu.
5Department of Biochemistry and Molecular Biology, University of Florida. Michelle.Gumz@medicine.ufl.edu.
6North Florida/South Georgia Veterans Health System, Gainesville, FL. Michelle.Gumz@medicine.ufl.edu.
Journal: Acta Physiologica
Date of e-pub: September 2016
Abstract: Increasing evidence demonstrates that circadian clock proteins are important regulators of physiological functions including blood pressure. An established risk factor for developing cardiovascular disease is the absence of a blood pressure dip during the inactive period. The goal of the present study was to determine the effects of a high salt diet plus mineralocorticoid on PER1-mediated blood pressure regulation in a salt-resistant, normotensive mouse model, C57BL/6J.
Blood pressure was measured using radiotelemetry. After control diet, wild type and Per1 knockout mice were given a high salt diet (4% NaCl) and the long-acting mineralocorticoid deoxycorticosterone pivalate. Blood pressure and activity rhythms were analyzed to evaluate changes over time.
Bloodpressure in wild type mice was not affected by a high salt diet plus mineralocorticoid. In contrast, Per1 knockout mice exhibited significantly increased mean arterial pressure in response to a high salt diet plus mineralocorticoid. The inactive/active phase ratio of mean arterial pressure in wild type mice was unchanged by high salt plus mineralocorticoid treatment. Importantly, this treatment caused Per1 knockout mice to lose the expected decrease or “dip” in blood pressure during the inactive compared to the active phase.
Loss of PER1 increased sensitivity to the high salt plus mineralocorticoid treatment. Italso resulted in a non-dipper phenotype in this model of salt-sensitive hypertension and provides a unique model of non-dipping. Together these data support an important role for the circadian clock protein PER1 in the modulation of blood pressure in a high salt/mineralocorticoid model of hypertension.
Improvements in Metabolic Health with Consumption of Ellagic Acid and Subsequent Conversion into Urolithins: Evidence and Mechanisms.
Author information: Kang I1, Buckner T1, Shay NF2, Gu L3, Chung S4.
1Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE;
2Department of Food Science and Technology, Oregon State University, Corvallis, OR; and.
3Food Science and Human Nutrition Department, University of Florida, Gainesville, FL.
4Department of Nutrition and Health Sciences, University of Nebraska-Lincoln, Lincoln, NE; firstname.lastname@example.org.
Journal: Advances in Nutrition
Date of e-pub: September 2016
Abstract: Ellagic acid (EA) is a naturally occurring polyphenol found in some fruits and nuts, including berries, pomegranates, grapes, and walnuts. EA has been investigated extensively because of its antiproliferative action in some cancers, along with its anti-inflammatory effects. A growing body of evidence suggests that the intake of EA is effective in attenuating obesity and ameliorating obesity-mediated metabolic complications, such as insulin resistance, type 2 diabetes, nonalcoholic fatty liver disease, and atherosclerosis. In this review, we summarize how intake of EA regulates lipid metabolism in vitro and in vivo, and delineate the potential mechanisms of action of EA on obesity-mediated metabolic complications. We also discuss EA as an epigenetic effector, as well as a modulator of the gut microbiome, suggesting that EA may exert a broader spectrum of health benefits than has been demonstrated to date. Therefore, this review aims to suggest the potential metabolic benefits of consumption of EA-containing fruits and nuts against obesity-associated health conditions.
Maintenance of host DNA integrity in field-preserved mosquito (Diptera: Culicidae) blood meals for identification by DNA barcoding.
Author information: Reeves LE1, Holderman CJ2, Gillett-Kaufman JL3, Kawahara AY4, Kaufman PE3.
1Entomology and Nematology Department, University of Florida, PO Box 110620, 1881 Natural Area Drive, Gainesville, FL, 32611, USA. email@example.com.
2Biosecurity Research Institute, Kansas State University, 1041 Pat Roberts Hall, Manhattan, KS, 66506, USA.
3Entomology and Nematology Department, University of Florida, PO Box 110620, 1881 Natural Area Drive, Gainesville, FL, 32611, USA.
4McGuire Center for Lepidoptera and Biodiversity, Florida Museum of Natural History, University of Florida, 3215 Hull Road, Gainesville, FL, 32611, USA.
Journal: Parasite Vectors
Date of e-pub: September 2016
Abstract: Determination of the interactions between hematophagous arthropods and their hosts is a necessary component to understanding the transmission dynamics of arthropod-vectored pathogens. Current molecular methods to identify hosts of blood-fed arthropods require the preservation of host DNA to serve as an amplification template. During transportation to the laboratory and storage prior to molecular analysis, genetic samples need to be protected from nucleases, and the degradation effects of hydrolysis, oxidation and radiation. Preservation of host DNA contained in field-collected blood-fed specimens has an additional caveat: suspension of the degradative effects of arthropod digestion on host DNA. Unless effective preservation methods are implemented promptly after blood-fed specimens are collected, host DNA will continue to degrade. Preservation methods vary in their efficacy, and need to be selected based on the logistical constraints of the research program.
We compared four preservation methods (cold storage at -20 °C, desiccation, ethanol storage of intact mosquito specimens and crushed specimens on filter paper) for field storage of host DNA from blood-fed mosquitoes across a range of storage and post-feeding time periods. The efficacy of these techniques in maintaining host DNA integrity was evaluated using a polymerase chain reaction (PCR) to detect the presence of a sufficient concentration of intact host DNA templates for blood meal analysis. We applied a logistic regression model to assess the effects of preservation method, storage time and post-feeding time on the binomial response variable, amplification success.
Preservation method, storage time and post-feeding time all significantly impacted PCR amplification success. Filter papers and, to a lesser extent, 95 % ethanol, were the most effective methods for the maintenance of host DNA templates. Amplification success of host DNA preserved in cold storage at -20 °C and desiccation was poor.
Our data suggest that, of the methods tested, host DNA template integrity was most stable when blood meals were preserved using filter papers. Filter paper preservation is effective over short- and long-term storage, while ethanol preservation is only suitable for short-term storage. Cold storage at -20 °C, and desiccation of blood meal specimens, even for short time periods, should be avoided.
Cold adaptation increases rates of nutrient flow and metabolic plasticity during cold exposure in Drosophila melanogaster.
Author information: Williams CM1, McCue MD2, Sunny NE3, Szejner-Sigal A4, Morgan TJ5, Allison DB6, Hahn DA7.
1Department of Entomology and Nematology, University of Florida, Gainesville, FL 32611, USA Department of Integrative Biology, University of California, Berkeley, CA 94720, USA firstname.lastname@example.org.
2Department of Biological Sciences, St Mary’s University, San Antonio, TX 78228, USA.
3Department of Medicine, University of Florida, Gainesville, FL 32601, USA.
4Department of Entomology and Nematology, University of Florida, Gainesville, FL 32611, USA Department of Integrative Biology, University of California, Berkeley, CA 94720, USA.
5Division of Biology, Kansas State University, Manhattan, KS 66506, USA.
6Section on Statistical Genetics, Department of Biostatistics, University of Alabama at Birmingham, Birmingham, AL 35294, USA.
7Department of Entomology and Nematology, University of Florida, Gainesville, FL 32611, USA Genetics Institute, University of Florida, Gainesville, FL 32610, USA.
Journal: Proceedings: Biological Sciences
Date of e-pub: September 2016
Abstract: Metabolic flexibility is an important component of adaptation to stressful environments, including thermal stress and latitudinal adaptation. A long history of population genetic studies suggest that selection on core metabolic enzymes may shape life histories by altering metabolic flux. However, the direct relationship between selection on thermal stress hardiness and metabolic flux has not previously been tested. We investigated flexibility of nutrient catabolism during cold stress in Drosophila melanogaster artificially selected for fast or slow recovery from chill coma (i.e. cold-hardy or -susceptible), specifically testing the hypothesis that stress adaptation increases metabolic turnover. Using (13)C-labelled glucose, we first showed that cold-hardy flies more rapidly incorporate ingested carbon into amino acids and newly synthesized glucose, permitting rapid synthesis of proline, a compound shown elsewhere to improve survival of cold stress. Second, using glucose and leucine tracers we showed that cold-hardy flies had higher oxidation rates than cold-susceptible flies before cold exposure, similar oxidation rates during cold exposure, and returned to higher oxidation rates during recovery. Additionally, cold-hardy flies transferred compounds among body pools more rapidly during cold exposure and recovery. Increased metabolic turnover may allow cold-adapted flies to better prepare for, resist and repair/tolerate cold damage. This work illustrates for the first time differences in nutrient fluxes associated with cold adaptation, suggesting that metabolic costs associated with cold hardiness could invoke resource-based trade-offs that shape life histories.
Aging amplifies multiple phenotypic defects in mice with zinc transporter Zip14 (Slc39a14) deletion.
Author information: Aydemir TB1, Troche C1, Kim J1, Kim MH1, Teran OY1, Leeuwenburgh C2, Cousins RJ3.
1Food Science and Human Nutrition Department, Center for Nutritional Sciences, College of Agriculture and Life Sciences, University of Florida,Gainesville, FL, United States.
2Department of Aging and Geriatric Research, College of Medicine, University of Florida, Gainesville, FL, United States; Institute on Aging, College of Medicine, University of Florida, Gainesville, FL, United States.
3Food Science and Human Nutrition Department, Center for Nutritional Sciences, College of Agriculture and Life Sciences, University of Florida,Gainesville, FL, United States. Electronic address: email@example.com.
Journal: Proceedings: Experimental Gerontology
Date of e-pub: September 2016
Abstract: Inflammation and zinc dyshomeostasis are two common hallmarks of aging. A major zinc transporter ZIP14 (slc39a14) is upregulated by proinflammatory stimuli, e.g. interleukin-6. We have evaluated the influence of age on the Zip14 KO phenotype using wild-type (WT) and Zip14 knockout (KO) mice. Aging produced a major increase in serum IL-6 concentrations that was dramatically augmented in the Zip14 KO mice. In keeping with enhanced serum IL-6 concentrations, aging produced tissue-specific increases in zinc concentration of skeletal muscle and white adipose tissue. Metabolic endotoxemia produced by Zip14 ablation is maintained in aged KO mice. Muscle non-heme iron (NHI) was increased in aged WT mice but not in aged Zip14 KO mice demonstrating NHI uptake by muscle is ZIP14-dependent and increases with age. NF-κB and STAT3 activation was greater in aged mice, but was tissue specific and inversely related to tissue zinc. Micro-CT analysis revealed that Zip14 KO mice had markedly reduced trabecular bone that was greatly amplified with aging. These results demonstrate that the inflammation-responsive zinc transporter ZIP14 has phenotypic effects that are amplified with aging.
NOTE: These abstracts were retrieved from the U.S. National Library of Medicine website managed in collaboration with the U.S. National Library of Medicine