Lean, but Not Healthy: the 'Metabolically Obese, Normal-Weight'

Total Page:16

File Type:pdf, Size:1020Kb

Lean, but Not Healthy: the 'Metabolically Obese, Normal-Weight' REVIEW CURRENT OPINION Lean, but not healthy: the ‘metabolically obese, normal-weight’ phenotype Cherlyn Dinga, Zhiling Chana, and Faidon Magkosa,b Purpose of review Obesity is commonly associated with metabolic dysfunction but there are obese persons who are 05/27/2020 on BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3XI41p+sDLxbvlJvgPKJYKCChu4AQ7aSiyxN6Txunm8aAM3UyKGgK1Q== by https://journals.lww.com/co-clinicalnutrition from Downloaded Downloaded metabolically healthy. On the opposite side of the coin, there are lean persons who carry multiple cardiometabolic risk factors, typically referred to as metabolically obese, normal-weight (MONW). This from has called into question our understanding of obesity and metabolic dysfunction, as an appearance of https://journals.lww.com/co-clinicalnutrition normal weight may mask significant comorbidities and delay health interventions. Recent findings High heterogeneity in MONW prevalence rates has been observed, with estimates ranging from as low as 5% to as high as 45%. Reasons for this include sample size effects, differences in MONW definition, social and demographic factors, as well as assumptions made in establishing normal weight. MONW study participants are often characterized by excess visceral adipose tissue and ectopic fat deposition, by adipose tissue inflammation, altered inflammatory and adipokine profiles, reduced skeletal muscle mass BhDMf5ePHKav1zEoum1tQfN4a+kJLhEZgbsIHo4XMi0hCywCX1AWnYQp/IlQrHD3XI41p+sDLxbvlJvgPKJYKCChu4AQ7aSiyxN6Txunm8aAM3UyKGgK1Q== and low cardiorespiratory fitness. However, more often than not, groups of MONW study participants have been somewhat ‘fatter’ than the control groups of metabolically healthy lean study participants, which in itself could be responsible for some of the observed differences. Very limited data are available regarding interventions to improve metabolic function in MONW study participants. Summary There is a need for more research to better understand the characteristics of the MONW phenotype, the cause of metabolic dysfunction in the absence of obesity, and evaluate potential therapies so as to facilitate the establishment of clinical guidelines. Keywords body fat, calorie restriction, exercise, normal weight, obesity INTRODUCTION led to sensible deductions that excess adipose tissue According to the definition provided by the WHO, is pathological, and provides a convenient etiological obesity and overweight are collectively defined as basis for common contemporary medical disorders. abnormal or excessive fat accumulation that may Indeed, several mechanistic studies have been central undermine health [1]. The WHO definition uses in the support of this dogma. the BMI as an indicator of body fat, and generally In the recent decades, however, the exponential considers a person with a BMI at least 25 kg/m2 to be increase in overweight and obesity [8] has revealed overweight, and a person with a BMI at least 30 kg/m2 interesting trends, which would otherwise be to be obese [1]. Obesity has become increasingly detrimental to society and quality of life. It burdens a on national healthcare systems, strains economic Clinical Nutrition Research Centre, Singapore Institute for Clinical 05/27/2020 Sciences, Agency for Science, Technology and Research (AÃSTAR) resources and has far reaching social consequences b [2–5]. With regards to its effects on health, strong and Department of Physiology, Yong Loo Lin School of Medicine, National University of Singapore, Singapore epidemiological evidence suggests that obesity is an Correspondence to Faidon Magkos, PhD, Clinical Nutrition Research independent risk factor for a myriad of diseases, Centre, Singapore Institute for Clinical Sciences, Agency for Science, including cardiovascular disease, type 2 diabetes mel- Technology and Research (AÃSTAR), Brenner Centre for Molecular litus (T2DM), nonalcoholic fatty liver disease, and Medicine, 30 Medical Drive, Singapore 117609. Tel: +65 6407 0323; has been linked to the development of several debil- e-mail: [email protected] itating health conditions, such as sleep apnea, Curr Opin Clin Nutr Metab Care 2016, 19:408–417 hypertension, stroke, and cancer [5–7]. This has DOI:10.1097/MCO.0000000000000317 www.co-clinicalnutrition.com Volume 19 Number 6 November 2016 Copyright © 2016 Wolters Kluwer Health, Inc. All rights reserved. Metabolically obese, normal-weight phenotype Ding et al. approximately 40% of individuals from a society KEY POINTS involved in the practice of self-imposed caloric Normal body weight is not a marker of metabolic restriction exhibited impaired glucose tolerance, health; approximately 5–45% of lean individuals have despite having low BMI values and total body fat metabolic abnormalities, which are typically associated [21]. There are good explanations to consider this an with obesity. exception rather than the norm, and most normal- weight individuals with significant obesity-related Metabolic dysfunction in lean people has been linked comorbidity consistently exhibit patterns of excess to increased intra-abdominal (visceral) adipose tissue, & increased liver and muscle fat content, increased fat body fat [22 ,23]. cell size, adipose tissue inflammation, altered From a clinical perspective, normal body weight inflammatory and adipokine profiles, reduced skeletal puts metabolically unhealthy individuals at height- muscle mass, lack of physical activity, and low ened risk of associated comorbidities by masking the cardiorespiratory fitness. need for screening and thus delaying diagnosis [23]. MONW study participants are typically somewhat The likely result is that individuals may seek medical fatter than comparison groups (even though within the attention only at more advanced stages of cardio- lean range), so it is not clear which of these metabolic disease, making treatment options more abnormalities are inherent to the phenotype and which complicated and harder to implement. It may also are the result of increased total body fat. lower drug efficacy and patient compliance rates, as There is very little information regarding therapeutic well as increase the exposure of affected individuals approaches (e.g., diet and exercise) to improve to unfavorable risk–benefit ratios for medication, metabolic abnormalities in lean people with surgery, or physical therapy. These possibilities may metabolic dysfunction. explain the stronger associations found between diabetes risk (and development) and common risk factors in normal-weight individuals compared with overweight or obese individuals [22&]. There is, obscured by low numbers in a situation of lower therefore, good reason to better understand the obesity rates. The existence of metabolically healthy metabolically obese, normal-weight (MONW) phe- obese (MHO) persons [9,10&&,11] and documented notype, and evaluate interventions for its reversal. associations of excess body fat with favorable health outcomes [12–14] have left the wider medical community baffled, and brought into question THE METABOLICALLY OBESE, NORMAL- our current understanding of how obesity-related WEIGHT PHENOTYPE comorbidities develop. There are perplexing indica- tions that overfeeding and mild weight gain do not Definition necessarily cause metabolic dysfunction in MHO Ruderman et al. [24] first described the MONW study participants [15&&]. Similarly, diet or exer- phenotype as individuals in the healthy range of cise-induced weight loss interventions may not standard body weight tables who have metabolic necessarily decrease cardiometabolic risk in MHO abnormalities commonly associated with adult- individuals [16], and may even lead to a paradoxical onset obesity. Much like patients with the classical response (e.g., a decrease in insulin sensitivity presentations of adult-onset obesity, Ruderman et al. instead of the expected increase) [17]. Studies also [24] explained that MONW individuals could seem to suggest that increased adipose tissue mass present with hyperinsulinemia, increased adipocyte may offer protection against the detrimental effects size, and hypertriglyceridemia, which could be cor- of metabolic syndrome, and has been associated rected with caloric restriction. Many years later, with improved survival rates of patients receiving De Lorenzo et al. [25] introduced the concept of inpatient care [12–14]. normal-weight obesity (NWO), defined as persons Conversely, several normal-weight individuals with normal BMI but increased body fat and reduced by virtue of BMI have been shown to exhibit the lean mass. Although both NWO and MONW phe- clustering of metabolic disorders normally associ- notypes are associated with increased cardiometa- ated with the obese, metabolically unhealthy phe- bolic risk, current NWO criteria may be far more notype [9,18&]. In studies examining cardiovascular inclusive – by definition they could comprise meta- events, cardiac and all-cause mortality in metabol- bolically healthy, normal-weight persons who meet ically unhealthy people, normal-weight individuals the criteria for excess body fat [25–27]. To facilitate were just as or more likely as overweight and obese scientific discussion, it would seem appropriate at persons to yield to cardiovascular and fatal events this juncture to conceptually discern the MONW [18&,19,20]. At the extreme end of this paradigm, from NWO for purposes of clarity. In assessing the 1363-1950 Copyright ß 2016 Wolters Kluwer Health, Inc. All rights reserved. www.co-clinicalnutrition.com 409 Copyright
Recommended publications
  • Abdominal Obesity and Cardiovascular Disease
    Advances in Obesity Weight Management & Control Mini Review Open Access Abdominal obesity and cardiovascular disease Abstract Volume 3 Issue 2 - 2015 There is no doubt that obesity has become a major disease in modern times and it Rayan Saleh is definitely associated with cancer, neurodegeneration and heart disease. Scientific Department of Food and Nutritional Sciences, University of studies have resulted in a growing consensus on the way abdominal obesity is Reading, UK associated with inflammation and cardiometabolic risk. Although the gender is a substantial factor of having abdominal fat, there are other protective factors including Correspondence: Rayan Saleh, Registered Dietitian, healthy eating and physical activity. Several techniques are used to assess obesity Department of Food and Nutritional sciences, University of and their utilization depends on their feasibility and economic cost. This research is Reading, White knights, Reading, RG6 6AH, Berkshire, UK, designed to address the important relationship between abdominal obesity and the risk Email [email protected] of developing cardiovascular disease. Received: August 19, 2015 | Published: September 15, 2015 Keywords: abdominal obesity, metabolic syndrome, cardiovascular disease, body shape, inflammation, insulin resistance Abbreviations: WHO, world health organization; T2D, type to hip ratio WHR), bioelectrical impedance analysis (BIA), Dual 2 diabetes; BMI, body mass index; WC, waist circumference; WHR, energy X-ray absorptiometry (DXA), Computed tomography (CT) waist
    [Show full text]
  • The Obesity Paradox: a Statistical Outcome Or a Real Effect of Clinical Relevance?
    Review J Hypertens Res (2019) 5(4):162–166 The obesity paradox: a statistical outcome or a real effect of clinical relevance? Ivona Mitu1, Cristina Daniela Dimitriu2, O. Mitu3*, Manuela Ciocoiu4 1“Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania, 2Department of Morpho-Functional Sciences (II), “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania 3Department of Medical Specialties (I), “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania 4Department of Morpho-Functional Sciences (II), “Grigore T. Popa” University of Medicine and Pharmacy, Iasi, Romania Received: October 10, 2019, Accepted: November 21, 2019 Abstract Obesity is one of the most important risk factors for morbidity and mortality, especially when referring to car- diovascular diseases. Different obesity phenotypes are presented in the medical literature, each one describing a different cardiovascular risk profile. The most important phenotype that is directly linked to the obesity paradox (OP) is the metabolically healthy obese phenotype, characterizing individuals with a BMI ≥ 30 kg/m2 and no metabolic abnormalities. This phenotype strengthens the true existence of the OP. In the same time we need to consider all the possible influencers when concluding if the OP is real and worth taking into consideration by clinicians. Analyzing studies that mention the OP, we observed several limitations either of the study itself or of the BMI used to classify obese patients. These limitations are described in the present review and they are of great importance in understanding how the OP is defined and how it should be interpreted. Keywords: obesity paradox, cardiovascular, BMI, obesity phenotypes. Introduction that the obesity prevalence has doubled since 1980, reaching 5% in children and 12% in adults [1].
    [Show full text]
  • Obesity, Diabetes and Longevity in the Gulf: Is There a Gulf Metabolic Syndrome?
    Obesity, diabetes and longevity in the Gulf: is there a Gulf Metabolic Syndrome? Article Published Version Open Access Guy, G. W., Nunn, A. V.W., Thomas, L. E. and Bell, J. D. (2009) Obesity, diabetes and longevity in the Gulf: is there a Gulf Metabolic Syndrome? International Journal of Diabetes Mellitus, 1 (1). pp. 43-54. ISSN 1877-5934 doi: https://doi.org/10.1016/j.ijdm.2009.05.001 Available at http://centaur.reading.ac.uk/35380/ It is advisable to refer to the publisher’s version if you intend to cite from the work. See Guidance on citing . To link to this article DOI: http://dx.doi.org/10.1016/j.ijdm.2009.05.001 Publisher: Elsevier All outputs in CentAUR are protected by Intellectual Property Rights law, including copyright law. Copyright and IPR is retained by the creators or other copyright holders. Terms and conditions for use of this material are defined in the End User Agreement . www.reading.ac.uk/centaur CentAUR Central Archive at the University of Reading Reading’s research outputs online This article appeared in a journal published by Elsevier. The attached copy is furnished to the author for internal non-commercial research and education use, including for instruction at the authors institution and sharing with colleagues. Other uses, including reproduction and distribution, or selling or licensing copies, or posting to personal, institutional or third party websites are prohibited. In most cases authors are permitted to post their version of the article (e.g. in Word or Tex form) to their personal website or institutional repository.
    [Show full text]
  • Understanding and Diagnosing Hyperinsulinaemia Catherine Crofts
    Understanding and Diagnosing Hyperinsulinaemia Catherine Crofts A thesis submitted to AUT University in fulfilment of the requirements for the degree of Doctor of Philosophy 2015 Human Potential Centre Primary Supervisor: Grant Schofield Secondary Supervisor: Caryn Zinn Tertiary Supervisor: Mark Wheldon Abstract Traditionally, insulin resistance is thought to be the precursor to many metabolic diseases. It is now believed that compensatory hyperinsulinaemia, previously thought to be a symptom of insulin resistance, may independently associated with metabolic disease and have its own pathological implications. Further understanding of compensatory hyperinsulinaemia may offer new insights into the aetiology of metabolic disease. This thesis provides novel work in hyperinsulinaemia and is broadly divided into four parts. Part 1 comprises a collation of the literature to show the aetiology and pathologies of hyperinsulinaemia, and to critically review the current diagnostic methods. The aetiology of hyperinsulinaemia is not yet fully elucidated, but is likely to include excessive carbohydrate ingestion, excessive cortisol or uric acid production, and/or medications. Subsequent pathologies include: cardio-, cerebro-, and peripheral- vascular disorders; type 2 diabetes; inflammation; and certain cancers or dementias. This is the first review to comprehensively link hyperinsulinaemia to such a wide range of metabolic disorders. Except for fasting insulin levels being considered unreliable, there was no consensus regarding diagnostic criteria. This means that diagnostic criteria needs to be determined prior to further research. Part 2 examined the prevalence of hyperinsulinaemia in the Kraft database. This important database comprises a large sample of oral glucose tolerance tests with insulin assays collected over 20 years in Chicago, USA. From the 15 000 available tests, those involving men aged ≥ 20 years and women ≥ 45 years, with a BMI > 18kg/m2 were included (n = 7750).
    [Show full text]
  • Cardiovascular Adipobiology: a Novel
    UDK 616.13-004.6-02 / Ser J Exp Clin Res 2008; 9 (3): 81 – 88 CARDIOVASCULAR ADIPOBIOLOGY: A NOVEL HEART-ASSOCIATED ADIPOSE TISSUE IN CARDIOVASCULAR DISEASE ABSTRACT 81 This article provides a conceptual framework for the possible role of myocardium. The present review highlights the possibility for tunica (i) periadventitial adipose tissue, and (ii) epicardial adipose tissue in adiposa and epicardial adipose tissue to play an important role in the pathogenesis of cardiovascular disease. Traditional concepts of an “outside-in” signaling in the development of atherosclerosis and atherogenesis are focused on luminal surface, where “inside-out” in- cardiomyopathy. In effect, adipose-targeted pharmacology and non- flammatory events trigger the extravasation of immune cells and the invasive measures might provide novel clinical insights into cardio- accumulation of lipids, smooth muscle cells and matrix components vascular adipobiology. Data of adipose-derived adipokines, including leading to atherosclerotic plaque formation. However, increasing evi- neurotrophic factors and neuropeptides, are also presented, raising a dence supports a new concept of an “outside-in” responses, involving hypothesis of neuroendocrine potential of adipose tissue; it may also periadventitial adipose tissue, herein referred to as tunica adiposa, be instrumental in the pathogenesis of cardiovascular disease. and epicardial adipose tissue, these two adipose loci functioning as Key words: adipokines, atherosclerosis, epicarial adipose tissue, secretory tissues. Thus, a paracrine signals originated from these tis- neurotrophic factors, neuropeptides, periadventitial adipose tissue sues could be transmitted into both the coronary artery intima and the INTRODUCTION “Ask yourself for each of your thoughts: is it a new one?” Carl Gustav Jung (1875-1961) Contemporary human lifestyle related to feeding and ered as the common denominators of the development physical activity can lead to an increasing accumula- of cardiovascular disease (1-4).
    [Show full text]
  • Fructose-Induced Inflammation and Increased Cortisol
    Progress in Cardiovascular Diseases xxx (2017) xxx–xxx Contents lists available at ScienceDirect Progress in Cardiovascular Diseases journal homepage: www.onlinepcd.com Fructose-induced inflammation and increased cortisol: A new mechanism for how sugar induces visceral adiposity James J. DiNicolantonio a,⁎, Varshil Mehta b, Neema Onkaramurthy c, James H. O'Keefe a a Saint Luke's Mid America Heart Institute, United States b MGM Medical College, Navi Mumbai, India c Kempegowda Institute of Medical Sciences, Bangalore, India article info abstract Available online xxxx Traditionally, the leading hypothesis regarding the development of obesity involves caloric imbalance, whereby Keywords: the amount of calories consumed exceeds the amount of calories burned which causes obesity. Another hypoth- Fructose esis for why we get fat has surfaced in the last decade which is the idea that the overconsumption of added sugars Sugar and refined carbohydrates induce insulin resistance and high insulin levels causing obesity. While insulin is a fat- Inflammation storing hormone, this hypothesis does not explain visceral adiposity, or why certain people are found to have fat Cortisol stored in and around their organs. We propose a new mechanism for body fattening, particular visceral adiposity. Visceral adiposity fl Fat This hypothesis involves the overconsumption of fructose, which leads to in ammation in all cells that metabo- Obesity lize it rapidly. When fructose is metabolized in subcutaneous adipocytes, the subsequent inflammation leads to an increase in intracellular cortisol in order to help squelch the inflammation. Unfortunately, the increase in in- tracellular cortisol leads to an increased flux of fatty acids out of the subcutaneous adipocytes allowing more sub- strate for fat storage into visceral fat tissue.
    [Show full text]
  • The Other Pandemic: Obesity Anastasia Economou Introduction
    The other pandemic: Obesity Anastasia Economou Introduction Obesity is defined as “abnormal or excessive fat accumulation that presents a risk to health” (World Health Organisation, [WHO], 2020). The Body Mass Index (BMI), weight is divided by height squared, is used to screen for obesity: a person ≥30 kg/m2 is ‘obese’; between 25 kg/m2 and 30 kg/m2 is ‘overweight’. In 2016, 1.6 billion adults (18 years +), were overweight, of which 650 million were obese. Obesity is a major burden of disease (WHO, 2020) not only in high-income countries, but also in low-income (e.g. Eritrea) and middle income countries (e.g. India) (Malik, Willett & Hu, 2013). Obesity has become a pandemic with projections pointing to 38% of Earth’s population becoming overweight and 20% obese by 2030 (Anekwe et al., 2020). Obesity in the UK is also on the rise: it affects 1 in 4 adults, 1 in 10 children aged 4-5, and 1 in 5 children aged 10-11 (NHS, 2020). 63% of adults and 33% of children leaving primary school are above a healthy weight (Public Health England, [PHE], 2020). Obesity is linked to a number of chronic and debilitating conditions like cardio- metabolic risk (CMR) (i.e. metabolic syndrome, diabetes, hypertension, dyslipidaemia, cardiovascular disease or stroke) and to conditions such as depression which can impact on an individual’s lifecycle. This paper will explore these links and further look at food insecurity and how it could contribute to obesity as well as how socioeconomic inequalities impact on this. It will then seek to evaluate the latest policy of the UK government on ‘Tackling Obesity: empowering adults and children to live healthier lives’ (UK Government, 2020) with a view to exploring whether this policy is appropriate in addressing food insecurity to prevent obesity.
    [Show full text]
  • The Importance of Diet Quality. Analysis of MAGNETIC Cohort
    Osadnik et al. Nutrition Journal (2020) 19:19 https://doi.org/10.1186/s12937-020-00532-0 RESEARCH Open Access Metabolically healthy obese and metabolic syndrome of the lean: the importance of diet quality. Analysis of MAGNETIC cohort Kamila Osadnik1, Tadeusz Osadnik1,2* , Marta Lonnie3, Mateusz Lejawa1, Rafał Reguła4, Martyna Fronczek5, Marcin Gawlita5,6, Lidia Wądołowska3, Mariusz Gąsior4 and Natalia Pawlas1 Abstract Background: Obesity is considered as an indispensable component of metabolic health assessment and metabolic syndrome diagnosis. The associations between diet quality and metabolic health in lean, young adults have not been yet established whilst data addressing this issue in overweight and obese subjects is scarce. Our analysis aimed to establish the link between diet quality (measured with data-driven dietary patterns and diet quality scores) and metabolic syndrome (MS) in young adults, regardless of their adiposity status. Methods: A total of 797 participants aged 18–35 years old were included in the study. Participants were assigned into metabolic syndrome (MS) group if at least two abnormalities within the following parameters were present: blood pressure, triglycerides, total cholesterol, HDL cholesterol, blood glucose. Participants with one or none abnormalities were considered as metabolically healthy subjects (MH), Diet quality was assessed with two approaches: 1) a posteriori by drawing dietary patterns (DPs) with principal component analysis (PCA) and 2) a priori by establishing diet quality scores and the adherence to pro-Healthy-Diet-Index (pHDI) and non-Healthy-Diet- Index (nHDI). Logistic regression with backward selection based on Akaike information criterion was carried out, to identify factors independently associated with metabolic health.
    [Show full text]
  • Metabolomic Signatures for Visceral Adiposity and Dysglycaemia in Asian Chinese and Caucasian European Adults: the Cross‑Sectional TOFI Asia Study Zhanxuan E
    Wu et al. Nutr Metab (Lond) (2020) 17:95 https://doi.org/10.1186/s12986-020-00518-z RESEARCH Open Access Metabolomic signatures for visceral adiposity and dysglycaemia in Asian Chinese and Caucasian European adults: the cross-sectional TOFI_Asia study Zhanxuan E. Wu1,2,3, Karl Fraser1,3,4* , Marlena C. Kruger2,4, Ivana R. Sequeira3,5, Wilson Yip3,5, Louise W. Lu3,5, Lindsay D. Plank6, Rinki Murphy3,7, Garth J. S. Cooper7,8, Jean‑Charles Martin9 and Sally D. Poppitt3,4,5,7 Abstract Background: Asian Chinese are more susceptible to deposition of visceral adipose tissue (VAT) and type 2 diabetes (T2D) development than European Caucasians when matched for gender, age and body mass index (BMI). Our aims were: (i) characterise the ethnicity‑specifc metabolomic signature of visceral adiposity measured by dual energy X‑ray absorptiometry (DXA) and fasting plasma glucose (FPG), and (ii) identify individuals susceptible to worse metabolic health outcomes. Methods: Fasting plasma samples from normoglycaemic (n 274) and prediabetic (n 83) participants were analysed with liquid chromatography–mass spectrometry using= untargeted metabolomics.= Multiple linear regression adjusting for age, gender and BMI was performed to identify metabolites associated with FPG and VAT calculated as percentage of total body fat (%VATTBF) in each ethnic group. Metabolic risk groups in each ethnicity were stratifed based on the joint metabolomic signature for FPG and %VATTBF and clinically characterised using partial least squares‑ discriminant analysis (PLS‑DA) and t‑tests. Results: FPG was correlated with 40 and 110 metabolites in Caucasians and Chinese respectively, with diglyceride DG(38:5) (adjusted β 0.29, p 3.00E 05) in Caucasians and triglyceride TG(54:4) (adjusted β 0.28, p 2.02E 07) in = = − = = − Chinese being the most signifcantly correlated metabolite based on the p‑value.
    [Show full text]
  • Westminsterresearch Phenotyping Ethnic Differences in Body Fat
    WestminsterResearch http://www.westminster.ac.uk/westminsterresearch Phenotyping Ethnic Differences in Body Fat Depots Alenaini, W. This is an electronic version of a PhD thesis awarded by the University of Westminster. © Ms Wareed Alenaini, 2019. The WestminsterResearch online digital archive at the University of Westminster aims to make the research output of the University available to a wider audience. Copyright and Moral Rights remain with the authors and/or copyright owners. Phenotyping Ethnic Differences in Body Fat Depots Wareed H. Alenaini A thesis submitted in partial fulfilment of the requirements of the University of Westminster for the degree of Doctor of Philosophy January 2019 1 Declaration of Originality The thesis has not previously been presented in any form to the University for assessment. I declare that all the materials contained in this thesis are my own work and any specific contribution or assistance is fully explained and appropriately referenced. 2 ABSTRACT There are remarkable ethnic differences in the incidence of metabolic syndrome associated features; including insulin resistance, type 2 diabetes, hypertension and cardiovascular diseases. Studies have suggested that South Asians (SA) present an unfavourable body fat phenotype, which includes a pattern of elevated visceral adipose tissue (VAT), and liver fat content; depots strongly associated with the progression of metabolic dysregulation. However, there are a limited number of studies examining body fat composition by ethnicity. The purpose of this thesis was to comprehensively phenotype VAT, abdominal subcutaneous adipose tissue (ASAT) and liver fat content in Caucasian (Cau), SA and Black African (BA) individuals from a large number of distinct populations. Here, I include data from three adult cohorts: the UK Biobank (n=9533) of mixed ethnicities, the DIRECT cohort (n=1553) of Cau pre-diabetic individuals and The West London Observation (TWLO) cohort (n=747) of mixed ethnicities.
    [Show full text]
  • Study Protocol
    Protocol Summary: HVN_Prediabetic Asian and Caucasian_TOFI_metabolomics Version FINAL_v4 Date: 03-Aug-2017 Author: Prof. SD Poppitt Page 1 of 23 High Value Nutrition – Priority Program Peak Nutrition for Metabolic Health [PANaMAH] CHARACTERISING THE PRE-DIABETIC ASIAN AND CAUCASIAN PHENOTYPE: THE ‘TOFI’ PROFILE identifying biomarkers of diabetic susceptibility and resilience using a metabolomics platform Sally Poppitt1, Karl Fraser2, Rinki Murphy1, Justin O’Sullivan1, John Ingram3 University of Auckland1, AgResearch2 and Plant & Food Research Ltd3 New Zealand In collaboration with Professor Garth Cooper, CADET, University of Manchester, UK; A/Prof Lindsay Plank, Department of Surgery Body Composition Unit, University of Auckland Study protocol Protocol Summary: HVN_Prediabetic Asian and Caucasian_TOFI_metabolomics Version FINAL_v4 Date: 03-Aug-2017 Author: Prof. SD Poppitt Page 2 of 23 PRINCIPAL INVESTIGATORS PROF. SALLY POPPITT PHD Professor of Human Nutrition Director, Human Nutrition Unit (HNU) School of Biological Sciences & Institute for Innovation in Biotechnology University of Auckland [email protected] DR KARL FRASER PHD Senior Research Scientist AgResearch Grasslands, Palmerston North [email protected] ASSOCIATE INVESTIGATORS DR RINKI MURPHY MBCHB, PHD Consultant endocrinologist, diabetes specialist Senior Lecturer, Department of Medicine University of Auckland & Auckland City Hospital [email protected] DR JUSTIN O’SULLIVAN PHD Research Fellow Liggins Institute University of Auckland [email protected]
    [Show full text]
  • Global Obesity Epidemic?
    WEIGHT IS NOT EVERYTHING Global obesity epidemic? The condition of obesity is the result of complex interactions between genetic and environmental factors. The diagnosis is based on the body mass index (BMI) de됍ned as the weight of the individual divided by the square of the height (kg/m2 ). The World Health Organization (WHO) in 2016 estimated that 39% of adults in the world are overweight (1.9 billion people with BMI between 20 and 25 kg / m2) while 13% are obese (650 million people with BMI greater than 30 kg / m2 ) . GLOBESITY is the term used to describe this global obesity epidemic. Furthermore, if we consider that a pregnant woman, if in a situation of overweight or obesity, can de됍ne the metabolic programming and the behavior that the unborn child will have towards food, we can easily realize the dimensions of GLOBESITY in the years to come. In 2019, the WHO estimated that 38 million children under the age of 5 are obese. Beyond the body mass index (BMI) Using only the body mass index, we can divide Using only the body mass index, we can divide the population into three large groups *: people of normal weight (BMI between 18.5 and 24.9 kg / m2), people who are overweight (BMI between 25 and 29.9 kg / m2) ) and obesity (BMI equal to or greater than 30 kg / m2). However, this index of measurement of fat mass, coined 150 years ago, does not take into account the real state of health and does not accurately de됍ne the degree of risk factor for the individual.
    [Show full text]