Research Topics
Genomes and Genes
| I Sadaf FarooqiSummaryAffiliation: University of Cambridge Country: UK Publications
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Detail Information
Publications
Genetics of obesityI Sadaf Farooqi
Department of Medicine, University of Cambridge, Addenbrooke's Hospital, UK
Philos Trans R Soc Lond B Biol Sci 361:1095-105. 2006..At the risk of oversimplification, it seems that from an aetiological/genetic standpoint, human obesity appears less a metabolic than a neuro-behavioural disease...
The severely obese patient--a genetic work-upI Sadaf Farooqi
University Department of Medicine, Addenbrooke s Hospital, Cambridge, UK
Nat Clin Pract Endocrinol Metab 2:172-7; quiz following 177. 2006..The family history was suggestive of a dominantly inherited condition, because the boy's father had been hospitalized in early childhood for the management of his obesity...- Heterozygosity for a POMC-null mutation and increased obesity risk in humansI Sadaf Farooqi
University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke's Hospital, Cambridge, CB2 2XY, UK
Diabetes 55:2549-53. 2006..191. We conclude that loss of one copy of the POMC gene predisposes to obesity in humans. Thus, genetic variants having relatively subtle effects on POMC expression and function could influence susceptibility to obesity... - Is leptin an important physiological regulator of CRP?I Sadaf Farooqi
Nat Med 13:16-7; author reply 19-21. 2007 
Insights from the genetics of severe childhood obesitySadaf Farooqi
Department of Medicine, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
Horm Res 68:5-7. 2007....- Mutations in ligands and receptors of the leptin-melanocortin pathway that lead to obesityI Sadaf Farooqi
University of Cambridge Metabolic Research Laboratories, Addenbrooke s Hospital, Cambridge, UK
Nat Clin Pract Endocrinol Metab 4:569-77. 2008..The genes affected in these monogenic disorders all encode ligands and receptors of the highly conserved leptin-melanocortin pathway, which is critical for the regulation of food intake and body weight... - Genetic aspects of severe childhood obesityI Sadaf Farooqi
University Department of Medicine, Addenbrooke s Hospital, Cambridge, United Kingdom
Pediatr Endocrinol Rev 3:528-36. 2006.... - Clinical and molecular genetic spectrum of congenital deficiency of the leptin receptorI Sadaf Farooqi
Cambridge Institute for Medical Research, University Department of Clinical Biochemistry, Addenbrooke s Hospital, Cambridge, United Kingdom
N Engl J Med 356:237-47. 2007..A single family has been described in which obesity results from a mutation in the leptin-receptor gene (LEPR), but the prevalence of such mutations in severe, early-onset obesity has not been systematically examined... - Monogenic human obesityI Sadaf Farooqi
Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
Front Horm Res 36:1-11. 2008.... - Leptin: a pivotal regulator of human energy homeostasisI Sadaf Farooqi
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Box 289, Addenbrooke s Hospital, Cambridge CB2 0QQ, United Kingdom
Am J Clin Nutr 89:980S-984S. 2009.... - Obesity genes-it's all about the parents!Sadaf Farooqi
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge, UK
Cell Metab 9:487-8. 2009..In this issue, Chen et al. (2009) have generated mice with brain specific deletion of either the maternal or paternal allele to trace the origin of the phenotype... - Leptin regulates striatal regions and human eating behaviorI Sadaf Farooqi
University Department of Medicine and Department of Clinical Biochemistry, Addenbrooke s Hospital, University of Cambridge, Cambridge CB2 2QQ, UK
Science 317:1355. 2007.... - Genetic, molecular and physiological insights into human obesityI Sadaf Farooqi
Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
Eur J Clin Invest 41:451-5. 2011.... - Obesity due to melanocortin 4 receptor (MC4R) deficiency is associated with increased linear growth and final height, fasting hyperinsulinemia, and incompletely suppressed growth hormone secretionCarlos E Martinelli
Department of Pediatrics, Hospital das Clinicas, University of Sao Paulo, Ribeirao Preto, Sao Paulo, Brazil
J Clin Endocrinol Metab 96:E181-8. 2011..Melanocortin receptor 4 (MC4R) deficiency is characterized by increased linear growth greater than expected for the degree of obesity... - Clinical spectrum of obesity and mutations in the melanocortin 4 receptor geneI Sadaf Farooqi
University Department of Medicine, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge, United Kingdom
N Engl J Med 348:1085-95. 2003..However, the clinical spectrum and mode of inheritance have not been defined, pathophysiological mechanisms leading to obesity are poorly understood, and there is little information regarding genotype-phenotype correlations... - A POMC variant implicates beta-melanocyte-stimulating hormone in the control of human energy balanceYung Seng Lee
University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge, CB2 2XY, United Kingdom
Cell Metab 3:135-40. 2006..Obese children carrying the Tyr221Cys variant were hyperphagic and showed increased linear growth, both of which are features of MC4R deficiency. These studies support a role for beta-MSH in the control of human energy homeostasis... - A de novo mutation affecting human TrkB associated with severe obesity and developmental delayGiles S H Yeo
University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge CB2 2XY, UK
Nat Neurosci 7:1187-9. 2004..The associated impairment in memory, learning and nociception seen in the proband reflects the crucial role of TrkB in the human nervous system... - Hyperphagia and early-onset obesity due to a novel homozygous missense mutation in prohormone convertase 1/3I Sadaf Farooqi
University Department of Clinical Biochemistry, Addenbrooke s Hospital, Cambridge CB2 2XY, United Kingdom
J Clin Endocrinol Metab 92:3369-73. 2007..To date, only two unrelated subjects with this disorder have been reported. Research.. - Studies of the peptide YY and neuropeptide Y2 receptor genes in relation to human obesity and obesity-related traitsChiao Chien Connie Hung
University Department of Clinical Biochemistry, Addenbrookes Hospital, Cambridge, CB2 2QQ, UK
Diabetes 53:2461-6. 2004..01). In conclusion, mutations in PYY and Y2R are not commonly found in humans with severe early-onset obesity. The relationship between common variants in Y2R and obesity-related traits deserves further exploration in other populations... - Large, rare chromosomal deletions associated with severe early-onset obesityElena G Bochukova
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge CB2 0QQ, UK
Nature 463:666-70. 2010..Deletion carriers exhibited hyperphagia and severe insulin resistance disproportionate for the degree of obesity. We show that copy number variation contributes significantly to the genetic architecture of human obesity... - Sequence variants in the melatonin-related receptor gene (GPR50) associate with circulating triglyceride and HDL levelsSumit Bhattacharyya
Department of Medicine, University of Cambridge, Cambridge, UK
J Lipid Res 47:761-6. 2006..39 mM) than wild-type subjects (1.47 mM) (P < 0.01). These findings suggest a previously unexpected role for this orphan receptor in the regulation of lipid metabolism that warrants further investigation... - Does physical activity energy expenditure explain the between-individual variation in plasma leptin concentrations after adjusting for differences in body composition?Paul W Franks
University of Cambridge, Department of Public Health and Primary Care, Cambridge, United Kingdom
J Clin Endocrinol Metab 88:3258-63. 2003..28, P = 0.005; women: beta = -0.23, P = 0.01; combined: beta = -0.26, P = 0.00008). These data suggest the existence in this population of an independent inverse association between PAEE and fasting plasma leptin level... - Modulation of blood pressure by central melanocortinergic pathwaysJerry R Greenfield
University of Cambridge Metabolic Research Laboratories, Addenbrooke s Hospital, Cambridge, United Kingdom
N Engl J Med 360:44-52. 2009..Central melanocortinergic signaling is implicated in the control of energy balance and blood pressure in rodents, but there is no information regarding such an association with blood pressure in humans... - Monogenic obesity in humansI Sadaf Farooqi
Departments of Medicine and Clinical Biochemistry, Cambridge University, Addenbrooke's Hospital, Cambridge CB2 2QQ, UK
Annu Rev Med 56:443-58. 2005..Practical implications of these findings for genetic counseling, prognostication, and even therapy have already emerged... - Functional characterization and structural modeling of obesity associated mutations in the melanocortin 4 receptorKaren Tan
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Box 289, Hills Road, Cambridge CB2 2QQ, United Kingdom
Endocrinology 150:114-25. 2009..The combination of functional studies and structural modeling of naturally occurring pathogenic mutations in MC4R can provide valuable information regarding the molecular mechanism of MC4R activation and its dysfunction in human disease... - Leptin regulates peripheral lipid metabolism primarily through central effects on food intakeXavier Prieur
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge CB2 OQQ, United Kingdom
Endocrinology 149:5432-9. 2008..Whereas we cannot exclude direct peripheral effects of leptin on certain aspects of lipid metabolism, we were unable to detect any such effects on the parameters measured in this study... - Studies of the neuromedin U-2 receptor gene in human obesity: evidence for the existence of two ancestral forms of the receptorSumit Bhattacharyya
University of Cambridge, Department of Medicine, Box 232, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, UK
J Endocrinol 183:115-20. 2004..Further investigation of the pharmacogenomic consequences of NMU2R variation in humans is warranted... - Congenital leptin deficiency due to homozygosity for the Delta133G mutation: report of another case and evaluation of response to four years of leptin therapyWilliam T Gibson
University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge, United Kingdom CB2 2XY
J Clin Endocrinol Metab 89:4821-6. 2004.... - Beneficial effects of leptin on obesity, T cell hyporesponsiveness, and neuroendocrine/metabolic dysfunction of human congenital leptin deficiencyI Sadaf Farooqi
University Department of Medicine, Department of Clinical Biochemistry, Addenbrooke s Hospital, Cambridge, United Kingdom
J Clin Invest 110:1093-103. 2002..The subcutaneous administration of recombinant human leptin has major and sustained beneficial effects on the multiple phenotypic abnormalities associated with congenital human leptin deficiency... - Functional characterization of naturally occurring pathogenic mutations in the human leptin receptorWendy Kimber
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge CB2 0QQ, United Kingdom
Endocrinology 149:6043-52. 2008..Naturally occurring mutations associated with human obesity are valuable tools with which to explore structure/function relationships within the LR... - Postprandial total ghrelin suppression is modulated by melanocortin signaling in humansAgatha A van der Klaauw
University of Cambridge, Metabolic Research Laboratories Box 289, Addenbrookes Hospital, Hills Road, Cambridge CB2 0QQ, United Kingdom
J Clin Endocrinol Metab 98:E288-92. 2013..09). Conclusions: These findings are consistent with a role for central melanocortinergic signaling in modulating meal-related total ghrelin suppression... - Mutational analysis of the serotonin receptor 5HT2c in severe early-onset human obesityWilliam T Gibson
Department of Clinical Biochemistry and Cambridge Institute for Medical Research, Addenbrooke s Hospital, UK
Can J Physiol Pharmacol 82:426-9. 2004..9%, respectively. In conclusion, mutations in 5HT2c are unlikely to be a common cause of severe early-onset human obesity. The identification of several novel polymorphisms at this locus may aid future genetic epidemiological studies... - Minireview: human obesity-lessons from monogenic disordersStephen O'Rahilly
University Department of Medicine, Cambridge Institute of Medical Research, Addenbrooke s Hospital, Cambridge CB2 2QQ, United Kingdom
Endocrinology 144:3757-64. 2003.... - Contribution of variants in the small heterodimer partner gene to birthweight, adiposity, and insulin levels: mutational analysis and association studies in multiple populationsChiao Chien Connie Hung
University Departments of Medicine and Clinical Biochemistry, Cambridge Institute for Medical Research, Cambridge, U K
Diabetes 52:1288-91. 2003..03). In conclusion, although mutations in SHP are not a common cause of severe human obesity, genetic variation in the SHP locus may influence birth weight and have effects on BMI, possibly through effects on insulin secretion... - Mutations in the human melanocortin-4 receptor gene associated with severe familial obesity disrupts receptor function through multiple molecular mechanismsGiles S H Yeo
Cambridge Institute for Medical Research, University of Cambridge, Addenbrooke s Hospital, Cambridge CB2 2XY, UK
Hum Mol Genet 12:561-74. 2003.... - Genetic and hereditary aspects of childhood obesityI Sadaf Farooqi
University Departments of Medicine and Clinical Biochemistry, Box 232, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
Best Pract Res Clin Endocrinol Metab 19:359-74. 2005.... - Association of polymorphisms in GPR10, the gene encoding the prolactin-releasing peptide receptor with blood pressure, but not obesity, in a U.K. Caucasian populationSumit Bhattacharyya
Department of Medicine, University of Cambridge, Addenbrooke s Hospital, Hills Road, Cambridge CB2 2QQ, U K
Diabetes 52:1296-9. 2003..The alteration in signaling properties of the receptor produced by P305L may provide a functional basis for this association... - A mutation in the thyroid hormone receptor alpha geneElena Bochukova
University of Cambridge Metabolic Research Laboratories and National Institute for Health Research Cambridge Biomedical Research Centre, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge, United Kingdom
N Engl J Med 366:243-9. 2012..Our observations are consistent with defective human TRα-mediated thyroid hormone resistance and substantiate the concept of hormone action through distinct receptor subtypes in different target tissues... - Genetic approaches to understanding human obesityShwetha Ramachandrappa
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge, United Kingdom
J Clin Invest 121:2080-6. 2011..We anticipate that future studies will provide the framework for the development of a more rational targeted approach to the prevention and treatment of genetically susceptible individuals... - Hyperphagia, severe obesity, impaired cognitive function, and hyperactivity associated with functional loss of one copy of the brain-derived neurotrophic factor (BDNF) geneJuliette Gray
University Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge, CB2 2XY, U K
Diabetes 55:3366-71. 2006..These findings provide direct evidence for the role of the neurotrophin BDNF in human energy homeostasis, as well as in cognitive function, memory, and behavior... - Distinct modulatory effects of satiety and sibutramine on brain responses to food images in humans: a double dissociation across hypothalamus, amygdala, and ventral striatumPaul C Fletcher
Department of Psychiatry, University of Cambridge, GlaxoSmithKline Clinical Unit Cambridge, Addenbrooke s Centre for Clinical Investigations, Addenbrooke s Hospital, Cambridge CB2 2QQ, United Kingdom
J Neurosci 30:14346-55. 2010..Furthermore, they support a regionally specific effect on brain function through which sibutramine exerts its clinical effect... - FTO and Obesity: The Missing LinkI Sadaf Farooqi
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
Cell Metab 13:7-8. 2011..A recent study in Nature Genetics (Church et al., 2010) demonstrates that mice overexpressing fto exhibit a dose-dependent increase in body weight, confirming a role for FTO in the development of obesity... - A missense mutation disrupting a dibasic prohormone processing site in pro-opiomelanocortin (POMC) increases susceptibility to early-onset obesity through a novel molecular mechanismBenjamin G Challis
University Department of Medicine, Addenbrooke s Hospital, Cambridge CB2 2QQ, UK
Hum Mol Genet 11:1997-2004. 2002..These results suggest that the R236G mutation may confer an inherited susceptibility to obesity through the production of an aberrant fusion protein that has the capacity to interfere with central melanocortin signalling... - Leptin and the onset of puberty: insights from rodent and human geneticsI Sadaf Farooqi
University Department of Medicine, Addenbrooke's Hospital, Cambridge, United Kingdom
Semin Reprod Med 20:139-44. 2002..This work suggests that leptin is a metabolic gate for the onset of puberty in humans. Leptin's actions may be mediated by central pathways and by direct action on peripheral organs... - Oral glutamine increases circulating glucagon-like peptide 1, glucagon, and insulin concentrations in lean, obese, and type 2 diabetic subjectsJerry R Greenfield
Cambridge Institute for Medical Research and Department of Clinical Biochemistry, University of Cambridge, Cambridge, UK
Am J Clin Nutr 89:106-13. 2009..We previously demonstrated that glutamine is a potent stimulus of GLP-1 secretion in vitro... - Obesity and the brain: how convincing is the addiction model?Hisham Ziauddeen
Department of Psychiatry, University of Cambridge, Herchel Smith Building, Addenbrooke s Hospital, Cambridge CB2 0SZ, UK
Nat Rev Neurosci 13:279-86. 2012.... - Resistance to thyroid hormone is associated with raised energy expenditure, muscle mitochondrial uncoupling, and hyperphagiaCatherine S Mitchell
University of Cambridge Metabolic Research Laboratories, Institute of Metabolic Science, Addenbrooke s Hospital, Cambridge, United Kingdom
J Clin Invest 120:1345-54. 2010.... - The hormonal control of food intakeAnthony P Coll
Department of Clinical Biochemistry, Cambridge Institute for Medical Research, Addenbrooke s Hospital, Cambridge CB2 2XY, United Kingdom
Cell 129:251-62. 2007..These hormones come from three major sites-fat cells, the gastrointestinal tract, and the pancreas. In this Review we provide a synthesis of recent evidence concerning the actions of these hormones on food intake... - Melanocortin receptors as targets in the treatment of obesityDaniel D Lam
Department of Clinical Biochemistry, Addenbrooke s Hospital, University of Cambridge, Cambridge, UK
Curr Top Med Chem 7:1085-1097. 2007..However, various promising strategies are being pursued to overcome these limitations, including the synthesis of more selective and potent melanocortin analogs... - Prevalence of melanocortin-4 receptor deficiency in Europeans and their age-dependent penetrance in multigenerational pedigreesFanny Stutzmann
Centre National de la Recherche Scientifique 8090, Institute of Biology, Pasteur Institute, Lille, France
Diabetes 57:2511-8. 2008..However, there is uncertainty regarding the degree of penetrance of this condition, and the putative impact of the environment on the development of obesity in MC4R mutation carriers is unknown... - Leptin predicts a worsening of the features of the metabolic syndrome independently of obesityPaul W Franks
Phoenix Epidemiology and Clinical Research Branch, National Institute of Diabetes and Digestive and Kidney Diseases, NIH, Phoenix, AZ 85014, USA
Obes Res 13:1476-84. 2005..Our goal was to test the hypothesis that leptin predicts the development of the features of MS independently of obesity... - Rapid-onset obesity with hypothalamic dysfunction, hypoventilation, and autonomic dysregulation presenting in childhoodDiego Ize Ludlow
Department of Pediatrics, University of Pittsburgh, Pittsburgh, Pennsylvania, USA
Pediatrics 120:e179-88. 2007..The goal was to characterize the phenotype and potential candidate genes responsible for the syndrome of late-onset central hypoventilation with hypothalamic dysfunction... - Influence of leptin on arterial distensibility: a novel link between obesity and cardiovascular disease?Atul Singhal
MRC Childhood Nutrition Research Center, Institute of Child Health, London, UK
Circulation 106:1919-24. 2002..Therefore, we tested the hypothesis that high leptin concentrations are associated with lower arterial distensibility, an index of circulatory function relevant to the atherosclerotic process... - Serum ghrelin levels are inversely correlated with body mass index, age, and insulin concentrations in normal children and are markedly increased in Prader-Willi syndromeAndrea M Haqq
Division of Endocrinology, Department of Pediatrics, Oregon Health and Science University, Portland, Oregon 97201, USA
J Clin Endocrinol Metab 88:174-8. 2003..Elevation of serum ghrelin levels to the degree documented in this study may play a role as an orexigenic factor driving the insatiable appetite and obesity found in PWS... - The central melanocortin system directly controls peripheral lipid metabolismRuben Nogueiras
Obesity Research Center, Department of Psychiatry, University of Cincinnati, Cincinnati, Ohio 45237, USA
J Clin Invest 117:3475-88. 2007..We also reveal molecular underpinnings for direct control of the CNS-Mcr over lipid metabolism. These results suggest ways to design more efficient pharmacological methods for controlling adiposity... - Proopiomelanocortin and energy balance: insights from human and murine geneticsAnthony P Coll
University Departments of Medicine and Clinical Biochemistry, Cambridge Institute of Medical Research, Addenbrooke's Hospital, Cambridge, United Kingdom CB2 2QQ
J Clin Endocrinol Metab 89:2557-62. 2004.... - Obesity associated genetic variation in FTO is associated with diminished satietyJane Wardle
Health Behavior Research Centre, University College London, Gower Street, London WC1E 6BT, United Kingdom
J Clin Endocrinol Metab 93:3640-3. 2008..However, to date, it is not known whether the association between genetic variation in FTO and obesity is mediated through effects on energy intake or energy expenditure... - Melanocortin receptors weigh inGiles S H Yeo
Nat Med 10:351-2. 2004 - Small-intestinal dysfunction accompanies the complex endocrinopathy of human proprotein convertase 1 deficiencyRobert S Jackson
Chemical Pathology Department, East Surrey Hospital, Surrey, United Kingdom
J Clin Invest 112:1550-60. 2003.... - Early nutrition and leptin concentrations in later lifeAtul Singhal
MRC Childhood Nutrition Research Center, Institute of Child Health, London, United Kingdom
Am J Clin Nutr 75:993-9. 2002..Because obesity is associated with high leptin concentrations relative to fat mass, programming of leptin concentrations may be one mechanism by which early nutrition influences later obesity... - The obesity-associated FTO gene encodes a 2-oxoglutarate-dependent nucleic acid demethylaseThomas Gerken
Chemistry Research Laboratory and Oxford Centre for Integrative Systems Biology, University of Oxford, 12 Mansfield Road, Oxford, Oxon OX1 3TA, UK
Science 318:1469-72. 2007..Studies can now be directed toward determining the physiologically relevant FTO substrate and how nucleic acid methylation status is linked to increased fat mass... - Screening the human prepro-orexin gene in a single-centre narcolepsy cohortTimothy G Quinnell
Respiratory Support and Sleep Centre, Papworth Hospital, Papworth Everard, Cambridgeshire, UK
Sleep Med 8:498-502. 2007..In this study, we examined the prepro-orexin gene for mutations in a cohort of unrelated patients with narcolepsy from a national UK referral centre... - Evaluation of Prader-Willi Syndrome gene MAGEL2 in severe childhood-onset obesityI Sadaf Farooqi
Department of Medical Genetics, 8-42 Medical Science Building, University of Alberta, Edmonton, Alberta, Canada T6G 2H7
Obes Res 13:1841-2. 2005..Although no mutations likely to affect gene function were identified, we identified three variant alleles. We conclude that severe childhood-onset obesity is not commonly caused by MAGEL2 mutations... - Molecular genetic analysis of normosmic hypogonadotropic hypogonadism in a Turkish population: identification and detailed functional characterization of a novel mutation in the gonadotropin-releasing hormone receptor geneA Kemal Topaloglu
Division of Paediatric Endocrinology and Metabolism, Cukurova University, Faculty of Medicine, Adana, Turkey
Neuroendocrinology 84:301-8. 2006..Currently known mutations account for less than 15% of cases with normosmic hypogonadotropic hypogonadism (nIHH). The objective of the study was to identify novel hereditary associations in the pathogenesis of nIHH... - A quantitative trait locus on chromosome 18q for physical activity and dietary intake in Hispanic childrenGuowen Cai
U S Department of Agriculture Agricultural Research Service, Children s Nutrition Research Center, Baylor College of Medicine, Houston, Texas 77030, USA
Obesity (Silver Spring) 14:1596-604. 2006..Genome scans were performed to identify chromosomal regions contributing to physical activity and dietary intake traits in Hispanic children participating in the VIVA LA FAMILIA Study... - Melanin-concentrating hormone receptor mutations and human obesity: functional analysisWilliam T Gibson
University Department of Clinical Biochemistry, Cambridge Institute of Medical Research, Cambridge United Kingdom
Obes Res 12:743-9. 2004..Clarification of the relationship of these variants to obesity must await study in other populations and/or in genetically modified mice...