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The arrestin domain-containing 3 protein regulates body mass and energy expenditure.

https://arctichealth.org/en/permalink/ahliterature130643
Source
Cell Metab. 2011 Nov 2;14(5):671-83
Publication Type
Article
Date
Nov-2-2011
Author
Parth Patwari
Valur Emilsson
Eric E Schadt
William A Chutkow
Samuel Lee
Alessandro Marsili
Yongzhao Zhang
Radu Dobrin
David E Cohen
P Reed Larsen
Ann Marie Zavacki
Loren G Fong
Stephen G Young
Richard T Lee
Author Affiliation
Cardiovascular Division, Department of Medicine, Brigham and Women's Hospital and Harvard Medical School, Boston, MA 02115, USA. parth@alum.mit.edu
Source
Cell Metab. 2011 Nov 2;14(5):671-83
Date
Nov-2-2011
Language
English
Publication Type
Article
Keywords
Adipose Tissue, Brown - metabolism
Adipose Tissue, White - metabolism
Adrenergic beta-Agonists - pharmacology
Animals
Arrestins - genetics - metabolism
Body mass index
Chromosomes, Human, Pair 5
Cohort Studies
Energy Metabolism - genetics
Female
Genetic Loci
Humans
Iceland - epidemiology
Linkage Disequilibrium
Male
Mice
Mice, Knockout
Obesity - epidemiology - genetics - metabolism
Receptors, Adrenergic, beta - metabolism
Sequence Homology, Amino Acid
Sex Factors
Signal Transduction
Thermogenesis - genetics
Abstract
A human genome-wide linkage scan for obesity identified a linkage peak on chromosome 5q13-15. Positional cloning revealed an association of a rare haplotype to high body-mass index (BMI) in males but not females. The risk locus contains a single gene, "arrestin domain-containing 3" (ARRDC3), an uncharacterized a-arrestin. Inactivating Arrdc3 in mice led to a striking resistance to obesity, with greater impact on male mice. Mice with decreased ARRDC3 levels were protected from obesity due to increased energy expenditure through increased activity levels and increased thermogenesis of both brown and white adipose tissues. ARRDC3 interacted directly with ß-adrenergic receptors, and loss of ARRDC3 increased the response to ß-adrenergic stimulation in isolated adipose tissue. These results demonstrate that ARRDC3 is a gender-sensitive regulator of obesity and energy expenditure and reveal a surprising diversity for arrestin family protein functions.
Notes
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PubMed ID
21982743 View in PubMed
Less detail

Associations between physical activity and fat mass in adolescents: the Stockholm Weight Development Study.

https://arctichealth.org/en/permalink/ahliterature49632
Source
Am J Clin Nutr. 2005 Feb;81(2):355-60
Publication Type
Article
Date
Feb-2005
Author
Ulf Ekelund
Martin Neovius
Yvonné Linné
Søren Brage
Nicholas J Wareham
Stephan Rössner
Author Affiliation
Medical Research Council Epidemiology Unit, Cambridge, United Kingdom. ue202@medschl.cam.ac.uk
Source
Am J Clin Nutr. 2005 Feb;81(2):355-60
Date
Feb-2005
Language
English
Publication Type
Article
Keywords
Adipose Tissue - metabolism
Adolescent
Anthropometry
Body Composition - physiology
Cohort Studies
Cross-Sectional Studies
Energy Metabolism - genetics - physiology
Exercise - physiology
Female
Humans
Longitudinal Studies
Male
Middle Aged
Mothers
Obesity - epidemiology - etiology - metabolism
Plethysmography, Whole Body - methods
Questionnaires
Research Support, Non-U.S. Gov't
Self Disclosure
Sex Factors
Socioeconomic Factors
Sweden - epidemiology
Abstract
BACKGROUND: Obesity is multifactorial. However, the accumulation of fat mass (FM) is proposed to be due to a positive energy balance, which may be caused by reduced physical activity (PA). OBJECTIVE: The objectives of the study were to describe the independent associations between PA and FM in adolescents and to describe the intergenerational association of FM between mothers and their offspring. DESIGN: We conducted a cross-sectional study in 445 (190 M, 255 F) 17-y-old adolescents and their mothers. PA was assessed with a self-reported questionnaire and validated by comparison with accelerometric data in a subsample of the cohort. Body composition was measured by using air-displacement plethysmography. RESULTS: Males were significantly more active than were females (P
Notes
Comment In: Am J Clin Nutr. 2005 Feb;81(2):337-815699218
PubMed ID
15699221 View in PubMed
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Coffee Consumption and Whole-Blood Gene Expression in the Norwegian Women and Cancer Post-Genome Cohort.

https://arctichealth.org/en/permalink/ahliterature296172
Source
Nutrients. 2018 Aug 09; 10(8):
Publication Type
Comparative Study
Journal Article
Date
Aug-09-2018
Author
Runa B Barnung
Therese H Nøst
Stine M Ulven
Guri Skeie
Karina S Olsen
Author Affiliation
Department of Community Medicine, Faculty of Health Sciences, University of Tromsø-The Arctic University of Norway, 9037 Tromsø, Norway. runa.b.barnung@uit.no.
Source
Nutrients. 2018 Aug 09; 10(8):
Date
Aug-09-2018
Language
English
Publication Type
Comparative Study
Journal Article
Keywords
Adult
Aged
Coffee
Cross-Sectional Studies
Energy Metabolism - genetics
Female
Gene Expression Profiling - methods
Gene Expression Regulation
Humans
Inflammation - epidemiology - genetics
Life Style
Middle Aged
Norway - epidemiology
Oligonucleotide Array Sequence Analysis
RNA, Messenger - blood - genetics
Risk factors
Surveys and Questionnaires
Transcriptome
Abstract
Norwegians are the second highest consumers of coffee in the world. Lately, several studies have suggested that beneficial health effects are associated with coffee consumption. By analyzing whole-blood derived, microarray based mRNA gene expression data from 958 cancer-free women from the Norwegian Women and Cancer Post-Genome Cohort, we assessed the potential associations between coffee consumption and gene expression profiles and elucidated functional interpretation. Of the 958 women included, 132 were considered low coffee consumers (3 cups of coffee/day). At a false discovery rate
Notes
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PubMed ID
30096876 View in PubMed
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Common variants near MC4R in relation to body fat, body fat distribution, metabolic traits and energy expenditure.

https://arctichealth.org/en/permalink/ahliterature147829
Source
Int J Obes (Lond). 2010 Jan;34(1):182-9
Publication Type
Article
Date
Jan-2010
Author
S I I Kring
C. Holst
S. Toubro
A. Astrup
T. Hansen
O. Pedersen
T I A Sørensen
Author Affiliation
Institute of Preventive Medicine, Copenhagen University Hospital, Centre for Health and Society, Copenhagen, Denmark.
Source
Int J Obes (Lond). 2010 Jan;34(1):182-9
Date
Jan-2010
Language
English
Publication Type
Article
Keywords
Adolescent
Adult
Alleles
Body Fat Distribution
Body mass index
Cholesterol, HDL - blood - genetics
Denmark - epidemiology
Energy Metabolism - genetics
Genetic Variation - genetics
Genotype
Humans
Male
Middle Aged
Obesity - blood - epidemiology - genetics - physiopathology
Phenotype
Receptor, Melanocortin, Type 4 - genetics
Young Adult
Abstract
Common variants near melanocortin receptor 4 (MC4R) have been related to fatness and type 2 diabetes. We examined the associations of rs17782313 and rs17700633 in relation to body fat, body fat distribution, metabolic traits, weight development and energy expenditure.
Obese young men (n = 753, BMI > or = 31.0 kg m(-2)) and a randomly selected group (n = 874) identified from a population of 174 800 men were re-examined in three surveys at mean ages 35, 46 and 49 years (S-35, S-46 and S-49). Measurements were available at upto eight times from birth to adulthood. Logistic regression analysis was used to assess odds ratio (OR) for the presence of the carrier allele for a given difference in phenotypic values.
Rs17782313 minor C-allele was associated with overall, abdominal and peripheral fatness (range of OR = 1.06-1.14 per z-score units) at all three surveys, although only consistently significant at S-35 and S-46. Rs17700633 minor A-allele was also associated with the fatness measures, but significantly so only at S-49 for overall and abdominal fatness (range of OR = 1.03-1.15 per z-score units), and peripheral fatness (OR = 1.15-1.20 per z-score units). There were only few significant associations with metabolic traits. The rs17782313 C-allele and the rs17700633 A-allele were both associated with lower high-density lipoprotein cholesterol (range of OR = 0.64-0.84 per mol l(-1)), significantly at S-46. The rs17700633 A-allele was significantly associated with insulin (OR = 1.25 per 50 pmol l(-1)), leptin (OR = 1.42 per 10 ng microl(-1)) and insulin sensitivity (OR = 0.81 per model unit). The rs17782313 C-allele and the rs17700633 A-allele were both associated with BMI in childhood and adolescence (range of OR = 1.04-1.17 per z-score units), significant for the rs17782313 C-allele at the age of 13-19 years and for rs17700633 A-allele at age 7, 10, 13 and 19 years. No significant associations were found for energy expenditure.
Near MC4R variants appear to contribute to body fat, body fat distribution, some metabolic traits, weight development during childhood, but not to energy expenditure.
PubMed ID
19844209 View in PubMed
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Diurnal profiles of hypothalamic energy balance gene expression with photoperiod manipulation in the Siberian hamster, Phodopus sungorus.

https://arctichealth.org/en/permalink/ahliterature86674
Source
Am J Physiol Regul Integr Comp Physiol. 2008 Apr;294(4):R1148-53
Publication Type
Article
Date
Apr-2008
Author
Ellis Claire
Moar Kim M
Logie Tracy J
Ross Alexander W
Morgan Peter J
Mercer Julian G
Author Affiliation
Division of Obesity and Metabolic Health, Rowett Research Institute, Aberdeen Centre for Energy Regulation and Obesity, Aberdeen AB21 9SB, UK.
Source
Am J Physiol Regul Integr Comp Physiol. 2008 Apr;294(4):R1148-53
Date
Apr-2008
Language
English
Publication Type
Article
Keywords
Animals
Body Weight - genetics
Circadian Rhythm
Cricetinae
Eating - genetics
Energy Metabolism - genetics
Gene Expression Regulation
Hypothalamus - metabolism
Leptin - blood
Male
Nerve Tissue Proteins - genetics - metabolism
Neuropeptides - genetics - metabolism
Nuclear Proteins - genetics - metabolism
Phodopus
Photoperiod
RNA, Messenger - metabolism
Receptors, Cell Surface - genetics - metabolism
Seasons
Suppressor of Cytokine Signaling Proteins - genetics - metabolism
Suprachiasmatic Nucleus - metabolism
Abstract
Hypothalamic energy balance genes have been examined in the context of seasonal body weight regulation in the Siberian hamster. Most of these long photoperiod (LD)/short photoperiod (SD) comparisons have been of tissues collected at a single point in the light-dark cycle. We examined the diurnal expression profile of hypothalamic genes in hamsters killed at 3-h intervals throughout the light-dark cycle after housing in LD or SD for 12 wk. Gene expression of neuropeptide Y, agouti-related peptide, proopiomelanocortin, cocaine- and amphetamine-regulated transcript, long-form leptin receptor, suppressor of cytokine signaling-3, melanocortin-3 receptor, melanocortin-4 receptor, and the clock gene Per1 as control were measured by in situ hybridization in hypothalamic nuclei. Effects of photoperiod on gene expression and leptin levels were generally consistent with previous reports. A clear diurnal variation was observed for Per1 in the suprachiasmatic nucleus in both photoperiods. Temporal effects on expression of energy balance genes were restricted to long-form leptin receptor in the arcuate nucleus and ventromedial nucleus, where similar diurnal expression profiles were observed, and melanocortin-4 receptor in the paraventricular nucleus; these effects were only observed in LD hamsters. There was no variation in serum leptin concentration. The 24-h profiles of hypothalamic energy balance gene expression broadly confirm photoperiodic differences that were observed previously, based on single time point comparisons, support the growing consensus that these genes have a limited role in seasonal body weight regulation, and further suggest limited involvement in daily rhythms of food intake.
PubMed ID
18234745 View in PubMed
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Does the ability to metabolically downregulate alter the hypoxia tolerance of fishes? A comparative study using cunner (T. adspersus) and Greenland cod (G. ogac).

https://arctichealth.org/en/permalink/ahliterature89919
Source
J Exp Zool Part A Ecol Genet Physiol. 2009 Apr 1;311(4):231-9
Publication Type
Article
Date
Apr-1-2009
Author
Corkum Chris P
Gamperl A Kurt
Author Affiliation
Ocean Sciences Centre, Memorial University of Newfoundland, St. John's, Nfld., Canada.
Source
J Exp Zool Part A Ecol Genet Physiol. 2009 Apr 1;311(4):231-9
Date
Apr-1-2009
Language
English
Publication Type
Article
Keywords
Adaptation, Biological - physiology
Analysis of Variance
Animals
Anoxia - metabolism
Energy Metabolism - genetics
Gadiformes - physiology
Newfoundland and Labrador
Oxygen Consumption - physiology
Perciformes - physiology
Abstract
In this study, the metabolic response and tolerance of cunner (a temperate wrasse species capable of metabolic depression) to graded hypoxia (water O(2) saturation 100-10%) was measured at two temperatures ( approximately 1 and 8 degrees C), and compared with that of the Greenland cod (Gadus ogac). Cunner had significantly lower oxygen consumption (MO(2)) values at both 1 (21.2+/-2.4 mg O(2) kg(-0.83) hr(-1)) and 8 degrees C (31.6+/-1.5 mg O(2) kg(-0.83) hr(-1)) as compared with the Greenland cod (64.0+/-4.3 and 92.5+/-6.3 mg O(2) kg(-0.83) hr(-1), respectively) when measured under normoxia. In addition, this species was considerably more hypoxia tolerant than Greenland cod, as evidenced by an ability to tolerate lower water O(2) saturations and their significantly lower critical oxygen saturation (S(crit)) values (16.9 and 21.4% vs. 40.4 and 54.8% water O(2) saturation at 1 and 8 degrees C, respectively). Surprisingly, the normoxic Q(10) value for cunner MO(2) (1.77) was not indicative of a hypometabolic state at 1 degrees C (based on previous experiments on this species). However, 1 degrees C cunner immediately decreased their MO(2) to a new steady state (44% below normoxic levels) when water O(2) saturation was lowered, and this resulted in a Q(10) of approximately 4.5 at oxygen levels between 80 and 20% saturation. This study provides the first data to suggest that fish capable of metabolic depression have an enhanced hypoxia tolerance, and that the cunner's hypometabolic state at cold temperatures is plastic and dependent on other environmental parameters.
PubMed ID
19235899 View in PubMed
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The effects of a HTR2B stop codon and testosterone on energy metabolism and beta cell function among antisocial Finnish males.

https://arctichealth.org/en/permalink/ahliterature285571
Source
J Psychiatr Res. 2016 Oct;81:79-86
Publication Type
Article
Date
Oct-2016
Author
Roope Tikkanen
Tero Saukkonen
Malin Fex
Hedvig Bennet
Marja-Riitta Rautiainen
Tiina Paunio
Mika Koskinen
Rony Panarsky
Laura Bevilacqua
Rickard L Sjöberg
Jari Tiihonen
Matti Virkkunen
Source
J Psychiatr Res. 2016 Oct;81:79-86
Date
Oct-2016
Language
English
Publication Type
Article
Keywords
Adult
Antisocial Personality Disorder - genetics - metabolism - pathology
Area Under Curve
Blood glucose - genetics
Body mass index
Codon, Terminator - genetics
Cohort Studies
Energy Metabolism - genetics
Finland
Glucose Tolerance Test
Humans
Indoles - cerebrospinal fluid
Insulin - blood
Insulin-Secreting Cells - physiology
Male
Psychiatric Status Rating Scales
Receptor, Serotonin, 5-HT2B - genetics
Testosterone - blood
Young Adult
Abstract
Herein, we examined insulin resistance (IR), insulin sensitivity (IS), beta cell activity, and glucose metabolism in subjects with antisocial personality disorder (ASPD), and whether the serotonin 2B (5-HT2B) receptor and testosterone have a role in energy metabolism. A cohort of subjects belonging to a founder population that included 98 ASPD males, aged 25-30, was divided into groups based on the presence of a heterozygous 5-HT2B receptor loss-of-function gene mutation (HTR2B Q20*; n = 9) or not (n = 89). Serum glucose and insulin levels were measured in a 5 h oral glucose tolerance test (75 g) and indices describing IR, IS, and beta cell activity were calculated. Body mass index (BMI) was also determined. Concentrations of the serotonin metabolite 5-hydroxyindoleacetic acid were measured in cerebrospinal fluid, and testosterone levels from serum. An IR-like state comprising high IR, low IS, and high beta cell activity indices was observed among ASPD subjects without the HTR2B Q20* allele. By contrast, being an ASPD HTR2B Q20* carrier appeared to be preventive of these pathophysiologies. The HTR2B Q20* allele and testosterone predicted lower BMI independently, but an interaction between HTR2B Q20* and testosterone lead to increased insulin sensitivity among HTR2B Q20* carriers with low testosterone levels. The HTR2B Q20* allele also predicted reduced beta cell activity and enhanced glucose metabolism. Reduced 5-HT2B receptor function at low or normal testosterone levels may be protective of obesity. Results were observed among Finnish males having an antisocial personality disorder, which limits the generality.
PubMed ID
27420381 View in PubMed
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Expression of beta-amyloid induced age-dependent presynaptic and axonal changes in Drosophila.

https://arctichealth.org/en/permalink/ahliterature98234
Source
J Neurosci. 2010 Jan 27;30(4):1512-22
Publication Type
Article
Date
Jan-27-2010
Author
Xiao-Liang Zhao
Wen-An Wang
Jiang-Xiu Tan
Jian-Kang Huang
Xiao Zhang
Bao-Zhu Zhang
Yu-Hang Wang
Han-Yu YangCheng
Hong-Lian Zhu
Xiao-Jiang Sun
Fu-De Huang
Author Affiliation
Institute of Neuroscience and State Key Laboratory of Neuroscience, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences, Shanghai 200031, China.
Source
J Neurosci. 2010 Jan 27;30(4):1512-22
Date
Jan-27-2010
Language
English
Publication Type
Article
Keywords
Aging - metabolism
Amyloid beta-Protein - genetics - metabolism
Animals
Axonal Transport - genetics
Central Nervous System - metabolism - pathology - ultrastructure
Disease Models, Animal
Down-Regulation - genetics
Drosophila - metabolism - ultrastructure
Energy Metabolism - genetics
Mitochondria - metabolism - pathology - ultrastructure
Nerve Degeneration - genetics - metabolism - pathology
Presynaptic Terminals - metabolism - pathology - ultrastructure
Synaptic Transmission - physiology
Synaptic Vesicles - metabolism - pathology - ultrastructure
Vacuoles - metabolism - pathology - ultrastructure
Wallerian Degeneration - genetics - metabolism - pathology
Abstract
Alzheimer's disease (AD) is attributable to synapse dysfunction and loss, but the nature and progression of the presynaptic structural and functional changes in AD are essentially unknown. We expressed wild-type or arctic form of beta amyloid(1-42) (Abeta) in a small group of neurons in the adult fly and performed extensive time course analysis of the function and structure of both axon and presynaptic terminals at the identified single-neuron level. Abeta accumulated intracellularly and induced a range of age-dependent changes, including depletion of presynaptic mitochondria, slowdown of bi-directional transports of axonal mitochondria, decreased synaptic vesicles, increased large vacuoles, and elevated synaptic fatigue. These structural and functional synaptic changes correlated with age-dependent deficit in motor behavior. All these alterations were accelerated in flies expressing the arctic form of Abeta. The depletion of presynaptic mitochondria was the earliest detected phenotype and was not caused by the change in axonal transport of mitochondria. Moreover, axonal mitochondria exhibited a dramatic reduction in number but a significant increase in size in aged Abeta-expressing flies, indicating a global depletion of mitochondria in the neuron and an impairment of mitochondria fission. These results suggest that Abeta accumulation depletes presynaptic and axonal mitochondria, leading to other presynaptic deficits.
PubMed ID
20107079 View in PubMed
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Fasting plasma total ghrelin concentrations in monozygotic twins discordant for obesity.

https://arctichealth.org/en/permalink/ahliterature90361
Source
Metabolism. 2009 Feb;58(2):174-9
Publication Type
Article
Date
Feb-2009
Author
Leskelä Piia
Ukkola Olavi
Vartiainen Johanna
Rönnemaa Tapani
Kaprio Jaakko
Bouchard Claude
Kesäniemi Y Antero
Author Affiliation
Department of Internal Medicine and Biocenter Oulu, Clinical Research Center Oulu, University of Oulu, Oulu University Hospital, P.O. Box 5000, FIN-90014, Finland.
Source
Metabolism. 2009 Feb;58(2):174-9
Date
Feb-2009
Language
English
Publication Type
Article
Keywords
Adult
Body Weight - genetics
Energy Metabolism - genetics
Fasting
Female
Gene Frequency
Genetic Variation
Genotype
Ghrelin - blood
Humans
Male
Middle Aged
Obesity - genetics - metabolism
Polymorphism, Genetic
Twins, Monozygotic - blood - genetics
Abstract
Ghrelin is a hormone that is involved in the regulation of food intake. Neuronal, endocrine, and genetic factors have been shown to regulate plasma ghrelin levels; but the determinants of fasting ghrelin concentrations are not yet fully understood. The main aim was to explore the roles of adiposity and genetic differences in determining fasting plasma total ghrelin levels. We measured total ghrelin levels in a population of 23 monozygotic twin pairs discordant for obesity. In addition, 2 variants of ghrelin gene, namely, Arg51Gln and Leu72Met, were genotyped in 3 populations of monozygotic twin pairs: 23 obesity-discordant, 43 lean-concordant, and 46 obesity-concordant twin pairs. In discordant twins, lean co-twins had higher fasting plasma total ghrelin levels (950 pg/mL, SD = 328 pg/mL) than obese twins (720 pg/mL, SD = 143 pg/mL; P = .003). Arg51Gln-polymorphism of the ghrelin gene was equally distributed between the twin groups. However, there were significant differences in genotype frequencies at the Leu72Met polymorphism between the discordant and obese-concordant groups (P = .003) and between the discordant and lean-concordant groups (P = .011), but not between the 2 concordant groups. In the discordant group, there were fewer Met carriers (4%) than among the obese (17%) or the lean-concordant groups (15%). Plasma total ghrelin levels are affected by acquired obesity independent of genetic background. The Leu72 allele is particularly common among monozygotic twins discordant for obesity, suggesting that this ghrelin allele is more permissive in the regulation of energy balance. The ghrelin gene may thus play a role in the regulation of variability of body weight, such that Leu72 allele carriers are more prone to weight variability in response to environmental factors.
PubMed ID
19154949 View in PubMed
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Flight-induced changes in gene expression in the Glanville fritillary butterfly.

https://arctichealth.org/en/permalink/ahliterature269219
Source
Mol Ecol. 2015 Oct;24(19):4886-900
Publication Type
Article
Date
Oct-2015
Author
Jouni Kvist
Anniina L K Mattila
Panu Somervuo
Virpi Ahola
Patrik Koskinen
Lars Paulin
Leena Salmela
Toby Fountain
Pasi Rastas
Annukka Ruokolainen
Minna Taipale
Liisa Holm
Petri Auvinen
Rainer Lehtonen
Mikko J Frilander
Ilkka Hanski
Source
Mol Ecol. 2015 Oct;24(19):4886-900
Date
Oct-2015
Language
English
Publication Type
Article
Keywords
Animals
Butterflies - genetics - physiology
Energy Metabolism - genetics
Female
Finland
Flight, Animal
Gene Expression
Male
Molecular Sequence Data
Polymorphism, Single Nucleotide
Sequence Analysis, RNA
Sex Characteristics
Transcriptome
Abstract
Insect flight is one of the most energetically demanding activities in the animal kingdom, yet for many insects flight is necessary for reproduction and foraging. Moreover, dispersal by flight is essential for the viability of species living in fragmented landscapes. Here, working on the Glanville fritillary butterfly (Melitaea cinxia), we use transcriptome sequencing to investigate gene expression changes caused by 15 min of flight in two contrasting populations and the two sexes. Male butterflies and individuals from a large metapopulation had significantly higher peak flight metabolic rate (FMR) than female butterflies and those from a small inbred population. In the pooled data, FMR was significantly positively correlated with genome-wide heterozygosity, a surrogate of individual inbreeding. The flight experiment changed the expression level of 1513 genes, including genes related to major energy metabolism pathways, ribosome biogenesis and RNA processing, and stress and immune responses. Males and butterflies from the population with high FMR had higher basal expression of genes related to energy metabolism, whereas females and butterflies from the small population with low FMR had higher expression of genes related to ribosome/RNA processing and immune response. Following the flight treatment, genes related to energy metabolism were generally down-regulated, while genes related to ribosome/RNA processing and immune response were up-regulated. These results suggest that common molecular mechanisms respond to flight and can influence differences in flight metabolic capacity between populations and sexes.
PubMed ID
26331775 View in PubMed
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