Rudolph Leibel

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Rudolph Leibel
Rudolph Leibel, MD.jpg
Rudolph Leibel, 2012
Born1942 (age 81–82)
United States of America
Citizenship United States
Alma mater Colgate University, Albert Einstein College of Medicine
Known forCo-Discovery of Leptin, Advancing the Understanding of Obesity
SpouseLulu Leibel
Awards National Academy of Sciences Institute of Medicine Member; TOPS Scientific Achievement Award; NIH/HHS Intragency Committee on Human Nutrition Research; New York State Science, Technology and Academic Research (NYSTAR) Distinguished Professor; Albert Einstein College of Medicine Distinguished Alumnus Award; Berthold Medal of the European Society of Endocrinology, Federation Award for Biomedical Research of the Federation of Medical Scientific Societies of the Netherlands, Leiden University; National Institute of Diabetes and Digestive and Kidney Diseases Federal Advisory Council Member; The Christopher J. Murphy Professorship of Diabetes Research at Columbia University; Honoris Causa Doctorate, Louisiana State University
Scientific career
Fields Molecular Genetics, Obesity, Diabetes Mellitus, Pediatrics
Institutions Boston Children's Hospital, Cambridge Hospital, Massachusetts General Hospital, Rockefeller University, Columbia University

Rudolph Leibel (born 1942) is the Christopher J. Murphy Professor of Diabetes Research, Professor of Pediatrics and Medicine at Columbia University Medical Center, [1] and Director of the Division of Molecular Genetics in the Department of Pediatrics. [2] He is also co-director of the Naomi Berrie Diabetes Center [3] and executive director of the Russell and Angelica Berrie Program in Cellular Therapy, [4] Co-director of the New York Obesity Research Center [5] and the Columbia University Diabetes and Endocrinology Research Center. [6]

Contents

Leibel's co-discovery at Rockefeller University of the hormone leptin, and cloning of the leptin and leptin receptor genes, has had a major role in the area of understanding human obesity. [7] [8] Leibel has published hundreds of scientific papers on obesity, and has authored and co-authored 70 scientific papers on the topic of leptin specifically.

Research on the "obesity gene": Leptin

Having encountered obesity in children as a medical doctor in the 1970s, Leibel believed that biology played a stronger role than "willpower" in human obesity and joined Jules Hirsch in theorizing about the psychobiology of obesity - a belief that body weight was the result of complex interactions between genes and the environment rather than a simple matter of free will. [9] In 1978, based on his theory that genetics played a major role in determining body weight regulation in humans, Leibel left Harvard University to join Jules Hirsch at Rockefeller University with the goal of finding the factor that drove eating. In collaboration with Douglas Coleman, Leibel determined that a mutation of the ob gene resulted in mice that were unable to manufacture a working satiety-signaling protein and that a db mutation resulted in mice that had the protein, but lacked the ability to detect the signal. [7] [8]

Leibel and Hirsch began a series of scientific investigations aimed at determining any connections between genetics and obesity. Over the course of eight years, Leibel's work ranged from studies of glycerol to the development of a radioisotopic technique for analysis of free fatty acid re-esterification in human adipose tissue to the metabolic characterization of obesity. [10] [11] After concluding that the tools of molecular genetics were key to moving his research forward and finding the obesity gene, [12] Leibel initiated a collaboration with Rockefeller University faculty member and molecular biologist Jeffrey Friedman in 1986, and began to assemble a team of researchers including Streamson C. Chua, Nathan Bahary, Don Siegel, Yiying Zhang, Ricardo Proenca and others. Leibel obtained ongoing funding from the National Institutes of Health and other sources, allowing the team to develop and utilize new techniques in their research such as chromosome microdissection.

As their research progressed, Leibel at al published a series of papers in scientific journals that reported the mapping of the ob gene, the first of these being a 1990 paper in World Review of Nutrition and Dietetics entitled "Genetic Variation and Nutrition in Obesity: Approaches to the Molecular Genetics of Obesity", [13] and another 1990 paper in the Proceedings of the National Academy of Sciences entitled "Molecular Mapping of the Mouse db Mutation". [14]

Among numerous additional papers published on the topic between 1991 and 1994, Leibel was the lead author of a paper entitled "Strategies for the Molecular Genetic Analysis of Obesity in Humans" in 1993. [15] In 1994, Friedman published a scientific paper that discovered and isolated the ob gene. Leibel was not a co-author of this paper, however, although Leibel was acknowledged in fine print at the end of the paper as an "important contributor to the early phases of this work". [16] Leibel was bitter about not being included as a full co-author and being relegated to a section of special thanks that included Friedman's fiancée, who was not a scientist; various theories surrounding the omission of Leibel as co-author of this important paper are presented in Ellen Ruppel Shell 's 2002 book The Hungry Gene . [7] [8]

Leibel continued to author and co-author numerous papers on the connection between genetics and obesity. In 1997, he published a paper in the scientific journal Nature Genetics titled "And Finally, Genes for Human Obesity". [17] Leibel and others involved with the discovery of the obesity gene eventually left Rockefeller University to establish a research base at Columbia University where Leibel became the head of the Division of Molecular Genetics.

Biography and academic background

Leibel obtained an A.B. from Colgate University in 1963 and an MD in 1967 from Albert Einstein College of Medicine. He was an Intern and Junior Resident in Pediatrics at Massachusetts General Hospital from 1967 to 1969, after which he served as a Major in the United States Army Medical Corps from 1969 to 1971.

Medical training

After serving as a Senior Resident in Medicine at Boston Children's Hospital from 1971 to 1972, Leibel became an NIH Clinical and Research Fellow in Pediatric Endocrinology-Metabolism at Massachusetts General Hospital from 1972 to 1974. He was a Research Associate in the Department of Nutrition and Food Science at the Massachusetts Institute of Technology from 1975 to 1978 and joined Rockefeller University from 1978 to 1981 as a Rockefeller Scholar in Clinical Science. Leibel completed his training as an Established Investigator at the American Heart Association from 1985 to 1989.

Scientific career

Leibel's seminal contributions to the field of obesity research, and childhood obesity specifically, were highlighted in Okie's 2005 book Fed Up!: Winning the War Against Childhood Obesity. [18] He has authored or co-authored over 300 peer-reviewed scientific papers, which have been cited over 13,000 times in the world scientific literature. [19] He also serves on the editorial boards of the Journal of Clinical Investigation, International Journal of Obesity, and Obesity Research, and has received numerous awards for scientific and pioneering work in medical research.

In recognition of his scientific work, Leibel was elected as a member of the Institute of Medicine of the National Academy of Sciences in 1998 [20] and serves as a member of the National Institute of Diabetes and Digestive and Kidney Diseases (NIDDK) Federal Advisory Council. His research is funded by the National Institutes of Health, the American Diabetes Association, the New York State Stem Cell Science Program, the Russell Berrie Foundation and the Leona M. and Harry B. Helmsley Charitable Trust, as well as Astra Zeneca. Leibel also serves as one of four Scientific Steering Committee members of the Type 1 Diabetes Research Consortium, a multi-institutional collaborative program of The Leona M. and Harry B. Helmsley Charitable Trust, that was established in 2009 to better understand the causes of type 1 diabetes and explore potential therapies. As of 2012, the consortium encompassed 11 institutions and 45 investigators through 28 grants totaling $21.8 million.

Leibel is the Chairman of the Selection Committee for the Pollin Prize for Pediatric Research and is the co-director of the NIH Diabetes and Endocrinology Research Center (DERC), at Columbia University.

Research focus

Leibel's initial research was focused on adrenergic receptor-mediated effects on lipolysis, and on the control of fatty acid re-esterification in human adipose tissue. Being among the first investigators to describe anatomic site-related differences in alpha 2 and beta 1 adrenoceptor activity in human adipose tissue, Leibel was also one of the first scientists to assess the role of alpha 2 and beta 1 adrenoceptor in determining the sexual dimorphism in human adipose tissue distribution. [21] [22]

In addition to cloning the mouse mahoganoid mutation that modifies the obesity of Yellow mice, Leibel also developed a microassay system for quantifying the re-esterification pathway in human adipose tissue. This invention has led to elucidation of the control mechanisms involved with circulating free fatty acids in humans.

After Leibel's co-discovery of the leptin gene in 1994, which involved a reverse genetic/positional cloning strategy to clone ob and db, Leibel, working with collaborators at Millennium Pharmaceuticals and colleague Streamson Chua, confirmed cloning of the leptin receptor by demonstrating that an apparent leptin receptor cloned from a choroid plexus library using leptin as ligand, mapped to a physical map that included db and fa. [23]

The efforts of the Leibel laboratory at Columbia University focus on the genetics of obesity and non-insulin dependent diabetes, or diabetes mellitus type 2. The laboratory has mapped, cloned and identified mutations in the obese and fatty genes in humans, rats, and mice and focuses on defining the physiological basis by which signaling networks regulate body size and composition. The Leibel laboratory is also working to isolate additional human and rodent genes that influence body weight and the susceptibility to diabetes mellitus type 2 in the context of obesity.

Press and media

Leibel was featured throughout HBO's The Weight of the Nation series in 2012 as a key scientific commentator. [24] He has been featured on numerous television news shows such as Charlie Rose , [25] and is often featured in the popular press. [26]

Honors and awards

Some awards have been granted to Leibel include:

  1. Phi Beta Kappa
  2. Alpha Omega Alpha
  3. Austen-Colgate Scholar
  4. NIH Postdoctoral Fellowship
  5. Rockefeller Scholar in Clinical Science
  6. Established Investigator, American Heart Association
  7. Eliot Hochstein Award for excellence in teaching, Cornell University Medical College
  8. Senior List for excellence in teaching, Cornell University Medical College
  9. TOPS Scientific Achievement Award (NAASO - 1996)
  10. NIH/HHS Intragency Committee on Human Nutrition Research (1997)
  11. Member, Institute of Medicine, National Academy of Sciences
  12. New York State Science, Technology and Academic Research (NYSTAR) Distinguished Professor (2002)
  13. Distinguished Alumnus Award, Albert Einstein College of Medicine (2005)
  14. Berthold Medal of the European Society of Endocrinology (2008)
  15. Federation Award for Biomedical Research of the Federation of Medical Scientific Societies of the Netherlands, Leiden University. (2008) [27]
  16. Member, National Institute of Diabetes and Digestive and Kidney Diseases Federal Advisory Council
  17. The Christopher J. Murphy Professorship of Diabetes Research (2011)
  18. Louisiana State University/Pennington Biomedical Research Honoris Causa Doctorate (2012)

Selected articles

Related Research Articles

<span class="mw-page-title-main">Leptin</span> Hormone that inhibits hunger

Leptin is a protein hormone predominantly made by adipocytes and its primary role is likely to regulate long-term energy balance.

<span class="mw-page-title-main">Adipose tissue</span> Loose connective tissue composed mostly by adipocytes

Adipose tissue (also known as body fat, or simply fat) is a loose connective tissue composed mostly of adipocytes. In addition to adipocytes, adipose tissue contains the stromal vascular fraction(SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and a variety of immune cells such as adipose tissue macrophages. Adipose tissue is derived from preadipocytes. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body. Far from being hormonally inert, adipose tissue has, in recent years, been recognized as a major endocrine organ, as it produces hormones such as leptin, estrogen, resistin, and cytokines (especially TNFα). In obesity, adipose tissue is also implicated in the chronic release of pro-inflammatory markers known as adipokines, which are responsible for the development of metabolic syndrome, a constellation of diseases, including type 2 diabetes, cardiovascular disease and atherosclerosis. The two types of adipose tissue are white adipose tissue (WAT), which stores energy, and brown adipose tissue (BAT), which generates body heat. The formation of adipose tissue appears to be controlled in part by the adipose gene. Adipose tissue – more specifically brown adipose tissue – was first identified by the Swiss naturalist Conrad Gessner in 1551.

<span class="mw-page-title-main">Adipocyte</span> Cells that primarily compose adipose tissue, specialized in storing energy as fat

Adipocytes, also known as lipocytes and fat cells, are the cells that primarily compose adipose tissue, specialized in storing energy as fat. Adipocytes are derived from mesenchymal stem cells which give rise to adipocytes through adipogenesis. In cell culture, adipocyte progenitors can also form osteoblasts, myocytes and other cell types.

<span class="mw-page-title-main">Adiponectin</span> Mammalian protein found in Homo sapiens

Adiponectin is a protein hormone and adipokine, which is involved in regulating glucose levels and fatty acid breakdown. In humans, it is encoded by the ADIPOQ gene and is produced primarily in adipose tissue, but also in muscle and even in the brain.

<span class="mw-page-title-main">Resistin</span> Mammalian protein found in Homo sapiens

Resistin also known as adipose tissue-specific secretory factor (ADSF) or C/EBP-epsilon-regulated myeloid-specific secreted cysteine-rich protein (XCP1) is a cysteine-rich peptide hormone derived from adipose tissue that in humans is encoded by the RETN gene.

<span class="mw-page-title-main">Perilipin-1</span> Protein in humans

Perilipin, also known as lipid droplet-associated protein, perilipin 1, or PLIN, is a protein that, in humans, is encoded by the PLIN gene. The perilipins are a family of proteins that associate with the surface of lipid droplets. Phosphorylation of perilipin is essential for the mobilization of fats in adipose tissue.

<span class="mw-page-title-main">Jeffrey M. Friedman</span>

Jeffrey M. Friedman is a molecular geneticist at New York City's Rockefeller University and an Investigator of the Howard Hughes Medical Institute. His discovery of the hormone leptin and its role in regulating body weight has had a major role in the area of human obesity. Friedman is a physician scientist studying the genetic mechanisms that regulate body weight. His research on various aspects of obesity received national attention in late 1994, when it was announced that he and his colleagues had isolated the mouse ob gene and its human homologue. They subsequently found that injections of the encoded protein, leptin, decreases body weight of mice by reducing food intake and increasing energy expenditure. Current research is aimed at understanding the genetic basis of obesity in human and the mechanisms by which leptin transmits its weight-reducing signal.

<span class="mw-page-title-main">White adipose tissue</span> Fatty tissue composed of white adipocytes

White adipose tissue or white fat is one of the two types of adipose tissue found in mammals. The other kind is brown adipose tissue. White adipose tissue is composed of monolocular adipocytes.

<span class="mw-page-title-main">Fatty acid-binding protein</span>

The fatty-acid-binding proteins (FABPs) are a family of transport proteins for fatty acids and other lipophilic substances such as eicosanoids and retinoids. These proteins are thought to facilitate the transfer of fatty acids between extra- and intracellular membranes. Some family members are also believed to transport lipophilic molecules from outer cell membrane to certain intracellular receptors such as PPAR. The FABPs are intracellular carriers that “solubilize” the endocannabinoid anandamide (AEA), transporting AEA to the breakdown by FAAH, and compounds that bind to FABPs block AEA breakdown, raising its level. The cannabinoids are also discovered to bind human FABPs that function as intracellular carriers, as THC and CBD inhibit the cellular uptake and catabolism of AEA by targeting FABPs. Competition for FABPs may in part or wholly explain the increased circulating levels of endocannabinoids reported after consumption of cannabinoids. Levels of fatty-acid-binding protein have been shown to decline with ageing in the mouse brain, possibly contributing to age-associated decline in synaptic activity.

<span class="mw-page-title-main">Stearoyl-CoA 9-desaturase</span> Class of enzymes

Stearoyl-CoA desaturase (Δ-9-desaturase) is an endoplasmic reticulum enzyme that catalyzes the rate-limiting step in the formation of monounsaturated fatty acids (MUFAs), specifically oleate and palmitoleate from stearoyl-CoA and palmitoyl-CoA. Oleate and palmitoleate are major components of membrane phospholipids, cholesterol esters and alkyl-diacylglycerol. In humans, the enzyme is encoded by the SCD gene.

<span class="mw-page-title-main">UCP3</span> Protein-coding gene in the species Homo sapiens

Mitochondrial uncoupling protein 3 is a protein that in humans is encoded by the UCP3 gene. The gene is located in chromosome (11q13.4) with an exon count of 7 and is expressed on the inner mitochondrial membrane. Uncoupling proteins transfer anions from the inner mitochondrial membrane to the outer mitochondrial membrane, thereby separating oxidative phosphorylation from synthesis of ATP, and dissipating energy stored in the mitochondrial membrane potential as heat. Uncoupling proteins also reduce generation of reactive oxygen species.

<span class="mw-page-title-main">Leptin receptor</span> Type I cytokine receptor

Leptin receptor, also known as LEP-R or OB-R, is a type I cytokine receptor, a protein that in humans is encoded by the LEPR gene. LEP-R functions as a receptor for the fat cell-specific hormone leptin. LEP-R has also been designated as CD295. Its location is the cell membrane, and it has extracellular, trans-membrane and intracellular sections.

<span class="mw-page-title-main">Free fatty acid receptor 3</span> Protein-coding gene in the species Homo sapiens

Free fatty acid receptor 3 protein is a G protein coupled receptor that in humans is encoded by the FFAR3 gene. GPRs reside on cell surfaces, bind specific signaling molecules, and thereby are activated to trigger certain functional responses in their parent cells. FFAR3 is a member of the free fatty acid receptor group of GPRs that includes FFAR1, FFAR2, and FFAR4. All of these FFARs are activated by fatty acids. FFAR3 and FFAR2 are activated by certain short-chain fatty acids (SC-FAs), i.e., fatty acids consisting of 2 to 6 carbon atoms whereas FFFAR1 and FFAR4 are activated by certain fatty acids that are 6 to more than 21 carbon atoms long. Hydroxycarboxylic acid receptor 2 is also activated by a SC-FA that activate FFAR3, i.e., butyric acid.

<span class="mw-page-title-main">Aquaporin-7</span> Protein-coding gene in the species Homo sapiens

Aquaporin-7 (AQP-7) is a protein that in humans is encoded by the AQP7 gene.

ob/ob mouse

The ob/ob or obese mouse is a mutant mouse that eats excessively due to mutations in the gene responsible for the production of leptin and becomes profoundly obese. It is an animal model of type II diabetes. Identification of the gene mutated in ob led to the discovery of the hormone leptin, which is important in the control of appetite.

Adipose tissue is an endocrine organ that secretes numerous protein hormones, including leptin, adiponectin, and resistin. These hormones generally influence energy metabolism, which is of great interest to the understanding and treatment of type 2 diabetes and obesity.

Douglas L. Coleman was a scientist and professor emeritus at the Jackson Laboratory, in Bar Harbor, Maine. His work predicted that there exists a hormone that can cause mice to feel full, and that a mutation in the gene encoding this hormone can lead to obesity. The gene and corresponding hormone were discovered about 20 years later by Jeffrey M. Friedman, Rudolph Leibel, and their research teams at Rockefeller University, which Friedman named leptin.

<span class="mw-page-title-main">Lipotoxicity</span> Metabolic syndrome

Lipotoxicity is a metabolic syndrome that results from the accumulation of lipid intermediates in non-adipose tissue, leading to cellular dysfunction and death. The tissues normally affected include the kidneys, liver, heart and skeletal muscle. Lipotoxicity is believed to have a role in heart failure, obesity, and diabetes, and is estimated to affect approximately 25% of the adult American population.

Adipose tissue macrophages (ATMs) comprise tissue resident macrophages present in adipose tissue. Adipose tissue apart from adipocytes is composed of the stromal vascular fraction (SVF) of cells including preadipocytes, fibroblasts, vascular endothelial cells and variety of immune cells. The latter ones are composed of mast cells, eosinophils, B cells, T cells and macrophages. The number of macrophages within adipose tissue differs depending on the metabolic status. As discovered by Rudolph Leibel and Anthony Ferrante et al. in 2003 at Columbia University, the percentage of macrophages within adipose tissue ranges from 10% in lean mice and humans up to 50% in extremely obese, leptin deficient mice and almost 40% in obese humans. Increased number of adipose tissue macrophages correlates with increased adipose tissue production of proinflammatory molecules and might therefore contribute to the pathophysiological consequences of obesity.

<span class="mw-page-title-main">Pathophysiology of obesity</span>

Pathophysiology of obesity is the study of disordered physiological processes that cause, result from, or are otherwise associated with obesity. A number of possible pathophysiological mechanisms have been identified which may contribute in the development and maintenance of obesity.

References

  1. ↑ "Rudolph L. Leibel, MD". Archived from the original on 2014-04-19. Retrieved 2013-03-09.
  2. ↑ "Faculty - Department of Pediatrics - Columbia University College of Physicians & Surgeons". www.cumc.columbia.edu. 29 October 2018.
  3. ↑ "Our Research Faculty | Naomi Berrie Diabetes Center". Archived from the original on 2014-04-19. Retrieved 2013-03-09.
  4. ↑ "The Russell Berrie Foundation - Diabetes and Medical Innovation". Archived from the original on 2014-04-19. Retrieved 2013-03-09.
  5. ↑ "Co-Director". www.nyorc.org. Archived from the original on 24 August 2011. Retrieved 13 January 2022.
  6. ↑ "Diabetes Research Center". Diabetes Research Center.
  7. 1 2 3 Shell E (January 1, 2002). "Chapter 4: On the Cutting Edge". The Hungry Gene: The Inside Story of the Obesity Industry. Atlantic Monthly Press. ISBN   978-1422352434.
  8. 1 2 3 Shell E (January 1, 2002). "Chapter 5: Hunger". The Hungry Gene: The Inside Story of the Obesity Industry. Atlantic Monthly Press. ISBN   978-1422352434.
  9. ↑ Hirsch J, Leibel RL (January 1984). "What constitutes a sufficient psychobiologic explanation for obesity?". Res Publ Assoc Res Nerv Ment Dis. 62 (1): 121–30. PMID   6695109.
  10. ↑ Leibel RL, Drewnowski A, Hirsch J (December 1980). "Effect of glycerol on weight loss and hunger in obese patients". Metabolism. 29 (12): 1234–6. doi:10.1016/0026-0495(80)90150-x. PMID   7453567.
  11. ↑ Leibel RL, Hirsch J (January 1985). "A radioisotopic technique for analysis of free fatty acid reesterification in human adipose tissue". Am J Physiol. 248 (1): E140-7. doi:10.1152/ajpendo.1985.248.1.e140. PMID   3881046.
  12. ↑ Hirsch J, Leibel RL (February 1988). "New light on obesity". The New England Journal of Medicine. 318 (8): 509–10. doi:10.1056/NEJM198802253180808. PMID   3340130.
  13. ↑ Leibel RL, Bahary N, Friedman JM (January 1990). "Genetic variation and nutrition in obesity: approaches to the molecular genetics of obesity". World Rev Nutr Diet. World Review of Nutrition and Dietetics. 63 (1): 90–101. doi:10.1159/000418501. ISBN   978-3-8055-5126-7. PMID   1973864.
  14. ↑ Bahary N, Leibel RL, Joseph L, Friedman JM (November 1990). "Molecular mapping of the mouse db mutation". Proc Natl Acad Sci U S A. 87 (21): 8642–6. doi: 10.1073/pnas.87.21.8642 . PMC   55013 . PMID   1978328.
  15. ↑ Leibel RL, Bahary N, Friedman JM (January 1993). "Strategies for the molecular genetic analysis of obesity in humans". Crit Rev Food Sci Nutr. 33 (4–5): 351–58. doi:10.1080/10408399309527632. PMID   8357496.
  16. ↑ Zhang, Y, Proenca, R, Maffei, M, Barone, M, Leopold, L, and Friedman, JM. Positional cloning of the mouse obese gene and its human homologue" Nature 1994, 372: 425-432.
  17. ↑ Leibel RL (July 1997). "And finally, genes for human obesity". Nat. Genet. 16 (3): 218–20. doi:10.1038/ng0797-218. PMID   9207782. S2CID   44421686.
  18. ↑ Okie S (February 11, 2005). "Chapter 2: Obese Twins and Thrifty Genes". Fed Up!: Winning the War Against Childhood Obesity. Joseph Henry Press, an imprint of the National Academies Press. ISBN   978-0309101981.
  19. ↑ "Pennington Biomedical Research Center". www.pbrc.edu.
  20. ↑ "Rudolph Leibel - Institute of Medicine". Archived from the original on 2013-04-09.
  21. ↑ Rosenbaum M; Nicolson M; Hirsch J; Heymsfield SB; Gallagher D; Chu F; Leibel RL. (September 1996). "Effects of gender, body composition, and menopause on plasma concentrations of leptin". J Clin Endocrinol Metab. 81 (9): 3424–7. doi: 10.1210/jcem.81.9.8784109 . PMID   8784109.
  22. ↑ Rosenbaum M, Pietrobelli A, Vasselli JR, Heymsfield SB, Leibel RL (September 2001). "Sexual dimorphism in circulating leptin concentrations is not accounted for by differences in adipose tissue distribution". Int J Obes Relat Metab Disord. 25 (9): 1365–71. doi:10.1038/sj.ijo.0801730. PMID   11571601. S2CID   21353177.
  23. ↑ Leibel RL (Dec 2008). "Molecular physiology of weight regulation in mice and humans". Int J Obes. 32 (S7): S98-108. doi:10.1038/ijo.2008.245. PMC   2682360 . PMID   19136999.
  24. ↑ "Documentaries". HBO.
  25. ↑ "Charlie Rose - Rudy Leibel". Archived from the original on 2013-03-28. Retrieved 2013-03-08.
  26. ↑
  27. ↑ "Activiteiten FMWV - Federa". www.federa.org.
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