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Author

Catherine Hambly

Other affiliations: Rowett Research Institute
Bio: Catherine Hambly is an academic researcher from University of Aberdeen. The author has contributed to research in topics: Medicine & Basal metabolic rate. The author has an hindex of 24, co-authored 92 publications receiving 2564 citations. Previous affiliations of Catherine Hambly include Rowett Research Institute.


Papers
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Journal ArticleDOI
TL;DR: A consolidated view of the complexity and challenges of designing studies for measurement of energy metabolism in mouse models is presented, including a practical guide to the assessment of energy expenditure, energy intake and body composition and statistical analysis thereof.
Abstract: We present a consolidated view of the complexity and challenges of designing studies for measurement of energy metabolism in mouse models, including a practical guide to the assessment of energy expenditure, energy intake and body composition and statistical analysis thereof. We hope this guide will facilitate comparisons across studies and minimize spurious interpretations of data. We recommend that division of energy expenditure data by either body weight or lean body weight and that presentation of group effects as histograms should be replaced by plotting individual data and analyzing both group and body-composition effects using analysis of covariance (ANCOVA).

644 citations

Journal ArticleDOI
TL;DR: This review provides some examples of the animal work that has been performed, and focuses on the variation in approaches that have been taken and their potential, rather than aiming to be a comprehensive summary.
Abstract: Background Obesity stems from a prolonged imbalance between the levels of energy intake and expenditure, with the resultant surplus being stored as body lipids. Our understanding of the regulation of food intake and the physiological basis of differences in energy expenditure is owed, in large part, to studies made on animals. Moreover, animal models have been a cornerstone of studies of environmental effects, such as epigenetics, responses to high-fat and low-calorie diets and the identification and development of pharmaceuticals for obesity treatment. This review provides some examples of the animal work that has been performed, and focuses on the variation in approaches that have been taken and their potential, rather than aiming to be a comprehensive summary.

157 citations

Journal ArticleDOI
TL;DR: Gavage of the bacterial metabolite butyrate increased the thermogenic capacity of ABX-treated mice, reversing the deficit and indicating that gut microbiota contributes to upregulated thermogenesis in the cold environment and that this may be partially mediated viabutyrate.

150 citations

Journal ArticleDOI
Herman Pontzer1, Yosuke Yamada2, Hiroyuki Sagayama3, Philip N. Ainslie4, Lene Frost Andersen5, Liam Anderson4, Lenore Arab6, Issaad Baddou7, Kweku Bedu-Addo8, Ellen E. Blaak9, Stéphane Blanc10, Stéphane Blanc11, Alberto G. Bonomi12, Carlijn V. C. Bouten9, Pascal Bovet13, Maciej S. Buchowski14, Nancy F. Butte15, Stefan G J A Camps9, Graeme L. Close4, Jamie A. Cooper11, Richard Cooper16, Sai Krupa Das17, Lara R. Dugas16, Ulf Ekelund18, Sonja Entringer19, Sonja Entringer20, Terrence Forrester21, Barry W. Fudge22, Annelies H. C. Goris9, Michael Gurven23, Catherine Hambly24, Asmaa El Hamdouchi7, Marjije B. Hoos9, Sumei Hu25, Noorjehan Joonas, Annemiek M. C. P. Joosen9, Peter T. Katzmarzyk26, Kitty P. Kempen9, Misaka Kimura2, William E. Kraus1, Robert F. Kushner27, Estelle V. Lambert28, William R. Leonard27, Nader Lessan29, Corby K. Martin26, Anine Christine Medin5, Anine Christine Medin30, Erwin P. Meijer9, James C Morehen31, James C Morehen4, James P. Morton4, Marian L. Neuhouser32, Teresa A. Nicklas15, Robert Ojiambo33, Kirsi H. Pietiläinen34, Yannis P. Pitsiladis35, Jacob Plange-Rhule8, Guy Plasqui9, Ross L. Prentice32, Roberto A Rabinovich36, Susan B. Racette37, David A. Raichlen38, Eric Ravussin26, Rebecca M. Reynolds36, Susan B. Roberts17, Albertine J. Schuit39, Anders Sjödin40, Eric Stice41, Samuel S. Urlacher42, Giulio Valenti12, Giulio Valenti9, Ludo M. Van Etten9, Edgar A. Van Mil9, Jonathan C. K. Wells43, George S. Wilson4, Brian M. Wood6, Brian M. Wood44, Jack A. Yanovski, Tsukasa Yoshida, Xueying Zhang24, Xueying Zhang25, Alexia J. Murphy-Alford45, Cornelia U Loechl45, Amy Luke46, Jennifer Rood26, Dale A. Schoeller11, Klaas R. Westerterp47, William W. Wong15, John R. Speakman 
13 Aug 2021-Science
TL;DR: In this article, the authors analyzed a large, diverse database of total expenditure measured by the doubly labeled water method for males and females aged 8 days to 95 years and found that fat-free mass-adjusted expenditure accelerates rapidly in neonates to ~50% above adult values at ~1 year; declines slowly to adult levels by ~20 years; remains stable in adulthood (20 to 60 years), even during pregnancy; then declines in older adults.
Abstract: Total daily energy expenditure ("total expenditure") reflects daily energy needs and is a critical variable in human health and physiology, but its trajectory over the life course is poorly studied. We analyzed a large, diverse database of total expenditure measured by the doubly labeled water method for males and females aged 8 days to 95 years. Total expenditure increased with fat-free mass in a power-law manner, with four distinct life stages. Fat-free mass-adjusted expenditure accelerates rapidly in neonates to ~50% above adult values at ~1 year; declines slowly to adult levels by ~20 years; remains stable in adulthood (20 to 60 years), even during pregnancy; then declines in older adults. These changes shed light on human development and aging and should help shape nutrition and health strategies across the life span.

146 citations

Journal ArticleDOI
10 Jul 2015-Science
TL;DR: Morphological, behavioral, physiological, and genetic adaptations allow pandas to survive on their low-energy bamboo diet, and a unique mutation in the DUOX2 gene might explain these low thyroid hormone levels.
Abstract: The carnivoran giant panda has a specialized bamboo diet, to which its alimentary tract is poorly adapted. Measurements of daily energy expenditure across five captive and three wild pandas averaged 5.2 megajoules (MJ)/day, only 37.7% of the predicted value (13.8 MJ/day). For the wild pandas, the mean was 6.2 MJ/day, or 45% of the mammalian expectation. Pandas achieve this exceptionally low expenditure in part by reduced sizes of several vital organs and low physical activity. In addition, circulating levels of thyroid hormones thyroxine (T4) and triiodothyronine (T3) averaged 46.9 and 64%, respectively, of the levels expected for a eutherian mammal of comparable size. A giant panda–unique mutation in the DUOX2 gene, critical for thyroid hormone synthesis, might explain these low thyroid hormone levels. A combination of morphological, behavioral, physiological, and genetic adaptations, leading to low energy expenditure, likely enables giant pandas to survive on a bamboo diet.

141 citations


Cited by
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Journal ArticleDOI
TL;DR: The elevated plus maze is a widely used behavioral assay for rodents and it has been validated to assess the anti-anxiety effects of pharmacological agents and steroid hormones, and to define brain regions and mechanisms underlying anxiety-related behavior.
Abstract: The elevated plus maze is a widely used behavioral assay for rodents and it has been validated to assess the anti-anxiety effects of pharmacological agents and steroid hormones, and to define brain regions and mechanisms underlying anxiety-related behavior. Briefly, rats or mice are placed at the junction of the four arms of the maze, facing an open arm, and entries/duration in each arm are recorded by a video-tracking system and observer simultaneously for 5 min. Other ethological parameters (i.e., rears, head dips and stretched-attend postures) can also be observed. An increase in open arm activity (duration and/or entries) reflects anti-anxiety behavior. In our laboratory, rats or mice are exposed to the plus maze on one occasion; thus, results can be obtained in 5 min per rodent.

2,221 citations

Journal ArticleDOI
Tamar Frankel1
TL;DR: The Essay concludes that practitioners theorize, and theorists practice, use these intellectual tools differently because the goals and orientations of theorists and practitioners, and the constraints under which they act, differ.
Abstract: Much has been written about theory and practice in the law, and the tension between practitioners and theorists. Judges do not cite theoretical articles often; they rarely "apply" theories to particular cases. These arguments are not revisited. Instead the Essay explores the working and interaction of theory and practice, practitioners and theorists. The Essay starts with a story about solving a legal issue using our intellectual tools - theory, practice, and their progenies: experience and "gut." Next the Essay elaborates on the nature of theory, practice, experience and "gut." The third part of the Essay discusses theories that are helpful to practitioners and those that are less helpful. The Essay concludes that practitioners theorize, and theorists practice. They use these intellectual tools differently because the goals and orientations of theorists and practitioners, and the constraints under which they act, differ. Theory, practice, experience and "gut" help us think, remember, decide and create. They complement each other like the two sides of the same coin: distinct but inseparable.

2,077 citations

Journal ArticleDOI
TL;DR: How the gut microbiota and derived microbial compounds may contribute to human metabolic health and to the pathogenesis of common metabolic diseases are discussed, and examples of microbiota-targeted interventions aiming to optimize metabolic health are highlighted.
Abstract: Observational findings achieved during the past two decades suggest that the intestinal microbiota may contribute to the metabolic health of the human host and, when aberrant, to the pathogenesis of various common metabolic disorders including obesity, type 2 diabetes, non-alcoholic liver disease, cardio-metabolic diseases and malnutrition. However, to gain a mechanistic understanding of how the gut microbiota affects host metabolism, research is moving from descriptive microbiota census analyses to cause-and-effect studies. Joint analyses of high-throughput human multi-omics data, including metagenomics and metabolomics data, together with measures of host physiology and mechanistic experiments in humans, animals and cells hold potential as initial steps in the identification of potential molecular mechanisms behind reported associations. In this Review, we discuss the current knowledge on how gut microbiota and derived microbial compounds may link to metabolism of the healthy host or to the pathogenesis of common metabolic diseases. We highlight examples of microbiota-targeted interventions aiming to optimize metabolic health, and we provide perspectives for future basic and translational investigations within the nascent and promising research field. In this Review, Fan and Pedersen discuss how the gut microbiota and derived microbial compounds may contribute to human metabolic health and to the pathogenesis of common metabolic diseases, and highlight examples of microbiota-targeted interventions aiming to optimize metabolic health.

1,445 citations

Journal ArticleDOI
01 Apr 2006-Obesity
TL;DR: The 12th update of the human obesity gene map is presented, which incorporates published results up to the end of October 2005, and shows putative loci on all chromosomes except Y.
Abstract: This paper presents the 12th update of the human obesity gene map, which incorporates published results up to the end of October 2005. Evidence from single-gene mutation obesity cases, Mendelian disorders exhibiting obesity as a clinical feature, transgenic and knockout murine models relevant to obesity, quantitative trait loci (QTL) from animal cross-breeding experiments, association studies with candidate genes, and linkages from genome scans is reviewed. As of October 2005, 176 human obesity cases due to single-gene mutations in 11 different genes have been reported, 50 loci related to Mendelian syndromes relevant to human obesity have been mapped to a genomic region, and causal genes or strong candidates have been identified for most of these syndromes. There are 244 genes that, when mutated or expressed as transgenes in the mouse, result in phenotypes that affect body weight and adiposity. The number of QTLs reported from animal models currently reaches 408. The number of human obesity QTLs derived from genome scans continues to grow, and we now have 253 QTLs for obesity-related phenotypes from 61 genome-wide scans. A total of 52 genomic regions harbor QTLs supported by two or more studies. The number of studies reporting associations between DNA sequence variation in specific genes and obesity phenotypes has also increased considerably, with 426 findings of positive associations with 127 candidate genes. A promising observation is that 22 genes are each supported by at least five positive studies. The obesity gene map shows putative loci on all chromosomes except Y. The electronic version of the map with links to useful publications and relevant sites can be found at http://obesitygene.pbrc.edu.

1,205 citations

Journal ArticleDOI
13 Sep 2012-Nature
TL;DR: A separation between health effects, morbidity and mortality, and similar to what has been shown in rodents, study design, husbandry and diet composition may strongly affect the life-prolonging effect of CR in a long-lived nonhuman primate is suggested.
Abstract: Calorie restriction (CR), a reduction of 10–40% in intake of a nutritious diet, is often reported as the most robust non-genetic mechanism to extend lifespan and healthspan. CR is frequently used as a tool to understand mechanisms behind ageing and age-associated diseases. In addition to and independently of increasing lifespan, CR has been reported to delay or prevent the occurrence of many chronic diseases in a variety of animals. Beneficial effects of CR on outcomes such as immune function, motor coordination and resistance to sarcopenia in rhesus monkeys have recently been reported. We report here that a CR regimen implemented in young and older age rhesus monkeys at the National Institute on Aging (NIA) has not improved survival outcomes. Our findings contrast with an ongoing study at the Wisconsin National Primate Research Center (WNPRC), which reported improved survival associated with 30% CR initiated in adult rhesus monkeys (7–14 years) and a preliminary report with a small number of CR monkeys. Over the years, both NIA and WNPRC have extensively documented beneficial health effects of CR in these two apparently parallel studies. The implications of the WNPRC findings were important as they extended CR findings beyond the laboratory rodent and to a long-lived primate. Our study suggests a separation between health effects, morbidity and mortality, and similar to what has been shown in rodents, study design, husbandry and diet composition may strongly affect the life-prolonging effect of CR in a long-lived nonhuman primate.

979 citations