Jeffrey M. Friedman

Last updated
Jeffrey Friedman
Jeffrey Friedman Royal Society.jpg
Jeffrey Friedman at the Royal Society admissions day in London, July 2018
Born (1954-07-20) July 20, 1954 (age 69)
Alma mater Rockefeller University (PhD)
Known fordiscovery of the hormone leptin and its role in regulating body weight
Awards
Scientific career
Fields Molecular genetics
Institutions Rockefeller University
Thesis Regulation of liver gene expression  (1986)
Website www.rockefeller.edu/our-scientists/heads-of-laboratories/1163-jeffrey-m-friedman/

Jeffrey M. Friedman (born July 20, 1954) 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. [1] 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.

Contents

Education

Friedman was born in Orlando, Florida on July 20, 1954, and grew up in North Woodmere, New York, graduating from Hewlett High School in the Class of 1971. [2] As a young man he aspired to becoming a physician. He entered a six-year medical program out of high school and received his M.D. at the age of 22. But after a year-long fellowship working in the laboratory of Mary Jeanne Kreek, he fell in love with the science life. "As a doctor, you're trained to absorb the facts you're given and accept them," says Friedman. "Science is almost the opposite. It's a frontier of discovery that's always moving. And I decided I wanted to do research." Friedman started his affiliation with the Rockefeller University in 1980, [3] where he was awarded a Ph.D. degree in 1986. Friedman received a BS from Rensselaer Polytechnic Institute in 1973 and M.D. degree from Albany Medical College in 1977 and completed a medical residency at Albany Medical College in 1980. [4] From 1980 to 1981, he also served as a postgraduate fellow at Cornell University Medical College. [5]

Career and research

Friedman was appointed Assistant Investigator with the Howard Hughes Medical Institute at The Rockefeller University in 1986, promoted to Associate Investigator in 1991, and Investigator in 1996 and received the Marilyn M. Simpson professorship in 1998.

When Friedman started his own laboratory at The Rockefeller University, he turned his attention to the question of weight regulation. Working with a special strain of mice, he set out to identify the hormone that normal animals use to control their appetite - a molecule that was missing in the plump rodents. After eight years—on May 8, 1994, at 5:30 a.m.—he found what he was looking for: evidence that he'd located the gene that produces the hormone he later dubbed "leptin", after the Greek word for "thin" (λεπτός leptos). [4] "It was astonishingly beautiful", he says of the x-ray film that nailed the gene, a piece of data that now hangs on his office wall.[ citation needed ]

Numerous lines of evidence have suggested that energy balance in animals and humans is tightly controlled.[ citation needed ] With the identification of leptin and its receptors by Friedman's laboratory, two of the molecular components of a system that maintains constant weight were identified. Leptin is a hormone secreted by the adipose (fat) tissue in proportion to its mass that in turn modulates food intake relative to energy expenditure. Increased fat mass increases leptin levels, which in turn reduces body weight; decreased fat mass leads to a decrease in leptin] levels and an increase in body weight.[ citation needed ] By this mechanism, weight is maintained within a relatively narrow range. Defects in the leptin gene are associated with severe obesity in animals and in humans. Leptin acts on sets of neurons in brain centers that control energy balance.[ citation needed ] Leptin also plays a general role in regulating many of the physiologic responses that are observed with changes in nutritional state, with clear effects on female reproduction, immune function and the function of many other hormones, including insulin.[ citation needed ]

Leptin feeds into the circuit of neurons in the brain that controls eating and energy expenditure.[ citation needed ] When an animal loses weight, leptin concentrations fall. This dip in leptin levels instructs the body to search for food.[ citation needed ] In studies of obese mice, Friedman has found that leptin actually restructures the brain, rewiring the neural circuit that controls feeding.[ citation needed ] The hormone reinforces the nerve cells that encourage the body to slenderize and prunes the neurons that compel eating.[ citation needed ]

Friedman has published over one hundred and fifty publications and over ten book chapters.

He is also involved in the research [6] related to the 1st inbred rat model of obesity [7] and aging, [8] also known as WNIN/Ob obese rats developed in National Institute of Nutrition, Hyderabad, India.

Awards and honors

Friedman's work in the area of obesity and the leptin gene has led to Friedman receiving many prestigious awards:

His work on leptin also garnered him much television time, including an appearance on the PBS show Scientific American Frontiers in a long interview with host Alan Alda. [15]

Personal life

Friedman lives in New York City with his wife, Lily Safani, and his twin daughters, Alexandra and Nathalie. [16] [17]

Related Research Articles

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

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

A maternal effect is a situation where the phenotype of an organism is determined not only by the environment it experiences and its genotype, but also by the environment and genotype of its mother. In genetics, maternal effects occur when an organism shows the phenotype expected from the genotype of the mother, irrespective of its own genotype, often due to the mother supplying messenger RNA or proteins to the egg. Maternal effects can also be caused by the maternal environment independent of genotype, sometimes controlling the size, sex, or behaviour of the offspring. These adaptive maternal effects lead to phenotypes of offspring that increase their fitness. Further, it introduces the concept of phenotypic plasticity, an important evolutionary concept. It has been proposed that maternal effects are important for the evolution of adaptive responses to environmental heterogeneity.

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

Adipose tissue is a loose connective tissue composed mostly of adipocytes. It also 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. Its main role is to store energy in the form of lipids, although it also cushions and insulates the body.

Pathophysiology is a branch of study, at the intersection of pathology and physiology, concerning disordered physiological processes that cause, result from, or are otherwise associated with a disease or injury. Pathology is the medical discipline that describes conditions typically observed during a disease state, whereas physiology is the biological discipline that describes processes or mechanisms operating within an organism. Pathology describes the abnormal or undesired condition, whereas pathophysiology seeks to explain the functional changes that are occurring within an individual due to a disease or pathologic state.

<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">Neuropeptide Y</span> Mammalian protein found in Homo sapiens

Neuropeptide Y (NPY) is a 36 amino-acid neuropeptide that is involved in various physiological and homeostatic processes in both the central and peripheral nervous systems. It is secreted alongside other neurotransmitters such as GABA and glutamate. 

Ronald Mark Evans is an American Biologist, Professor and Head of the Salk’s Gene Expression Laboratory, and the March of Dimes Chair in Molecular and Developmental Biology at the Salk Institute for Biological Studies in La Jolla, California and a Howard Hughes Medical Institute Investigator. Dr. Ronald M. Evans is known for his original discoveries of nuclear hormone receptors (NR), a special class of transcriptional factor, and the elucidation of their universal mechanism of action, a process that governs how lipophilic hormones and drugs regulate virtually every developmental and metabolic pathway in animals and humans. Nowadays, NRs are among the most widely investigated group of pharmaceutical targets in the world, already yielding benefits in drug discovery for cancer, muscular dystrophies, osteoporosis, type II diabetes, obesity, and cardiovascular diseases. His current research focuses on the function of nuclear hormone signaling and their function in metabolism and cancer.

Albany Medical College (AMC) is a private medical school in Albany, New York. It was founded in 1839 by Alden March and James H. Armsby and is one of the oldest medical schools in the nation. The college is part of the Albany Medical Center, which includes the Albany Medical Center Hospital. Along with Albany College of Pharmacy, Albany Law School, the Dudley Observatory, and Union College, it is one of the constituent entities of Union University.

<span class="mw-page-title-main">Peptide YY</span> Peptide released from cells in the ileum and colon in response to feeding

Peptide YY (PYY), also known as peptide tyrosine tyrosine, is a peptide that in humans is encoded by the PYY gene. Peptide YY is a short peptide released from cells in the ileum and colon in response to feeding. In the blood, gut, and other elements of periphery, PYY acts to reduce appetite; similarly, when injected directly into the central nervous system, PYY is also anorexigenic, i.e., it reduces appetite.

<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.

ob/ob mouse Mutant mouse that eats excessively and becomes profoundly obese

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.

In biology, energy homeostasis, or the homeostatic control of energy balance, is a biological process that involves the coordinated homeostatic regulation of food intake and energy expenditure. The human brain, particularly the hypothalamus, plays a central role in regulating energy homeostasis and generating the sense of hunger by integrating a number of biochemical signals that transmit information about energy balance. Fifty percent of the energy from glucose metabolism is immediately converted to heat.

Michael Cowley FTSE is an Australian physiologist. He is best known for his mapping of the neural circuits involved in metabolism and obesity and diabetes treatment. He is a professor in the Department of Physiology at Monash University in the Faculty of Biomedical and Psychological Sciences. He is also a director of the Australian diabetes drug development company, Verva Inc, and director of the Monash Obesity & Diabetes Institute] (modi).

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.

Sleep is important in regulating metabolism. Mammalian sleep can be sub-divided into two distinct phases - REM and non-REM (NREM) sleep. In humans and cats, NREM sleep has four stages, where the third and fourth stages are considered slow-wave sleep (SWS). SWS is considered deep sleep, when metabolism is least active.

<span class="mw-page-title-main">Rudolph Leibel</span>

Rudolph Leibel is the Christopher J. Murphy Professor of Diabetes Research, Professor of Pediatrics and Medicine at Columbia University Medical Center, and Director of the Division of Molecular Genetics in the Department of Pediatrics. He is also co-director of the Naomi Berrie Diabetes Center and executive director of the Russell and Angelica Berrie Program in Cellular Therapy, Co-director of the New York Obesity Research Center and the Columbia University Diabetes and Endocrinology Research Center.

<span class="mw-page-title-main">Jose F. Caro</span> American physician

José F. Caro is an American physician, scientist, and educator most notable for his research in obesity and diabetes. The Institute for Scientific Information listed him the third most cited investigator in the world in the field of obesity research during the 1991-2000 period for his work on Leptin. Caro is an artist and a signature member of the Pastel Society of America.

<span class="mw-page-title-main">Sadaf Farooqi</span> British consultant physician

Ismaa Sadaf Farooqi is a Wellcome Trust Senior Research fellow in Clinical Science, professor of Metabolism and Medicine at the University of Cambridge and a consultant physician at Addenbrooke's Hospital in Cambridge, UK.

<span class="mw-page-title-main">Ana Domingos</span> Portuguese neuroscientist

Ana I. Domingos is a Portuguese neuroscientist specialising in the treatment of obesity independently of food intake. Domingos is a full Professor of Neuroscience at the Department of Physiology, Anatomy and Genetics of the University of Oxford in the United Kingdom. Domingos is also a fellow, tutor and the director of studies in medicine at Lady Margaret Hall, Oxford.

References

  1. Zhang, Y; Proenca, R; Maffei, M; Barone, M; Leopold, L; Friedman, JM (December 1994). "Positional cloning of the mouse obese gene and its human homologue". Nature. 1994 (372): 425–432. Bibcode:1994Natur.372..425Z. doi:10.1038/372425a0. PMID   7984236. S2CID   4359725.
  2. Katz, Debra M. (February 5, 1995). "Long Island Q&A;: Jeffrey M. Friedman; Finding the Gene That Makes Mice, and Maybe Others, Fat". The New York Times. Retrieved 17 May 2021.
  3. 1 2 "Jeffrey M. Friedman - Nobel Conference 46 | Nobel Conference - 2010". gustavus.edu. Retrieved 13 December 2021.
  4. 1 2 "The Rockefeller University » Hospital Centennial". centennial.rucares.org. Retrieved 13 December 2021.
  5. "Jeffrey Friedman, discoverer of leptin, receives Gairdner, Passano awards".
  6. Kalashikam, R. R.; Battula, K. K.; Kirlampalli, V.; Friedman, J. M.; Nappanveettil, G. (2013). "Obese Locus in WNIN/Obese Rat Maps on Chromosome 5 Upstream of Leptin Receptor". PLOS ONE. 8 (10): 10. Bibcode:2013PLoSO...877679K. doi: 10.1371/journal.pone.0077679 . PMC   3804619 . PMID   24204914.
  7. Giridharan, N V (1998). "Animal models of obesity & their usefulness in molecular approach to obesity". Indian J Med Res. 108: 225–42. PMID   9863278.
  8. Sinha, Jitendra Kumar; Ghosh, Shampa; Swain, Umakanta; Giridharan, Nappan Veethil; Raghunath, Manchala (2014). "Increased macromolecular damage due to oxidative stress in the neocortex and hippocampus of WNIN/Ob, a novel rat model of premature aging". Neuroscience. 269: 256–64. doi:10.1016/j.neuroscience.2014.03.040. PMID   24709042. S2CID   9934178.
  9. "All Gairdner Awards Laureates". Gairdner Foundation. Retrieved 25 June 2020.
  10. "About the Jessie Stevenson Kovalenko Medal". National Academy of Sciences. Retrieved 25 June 2020.
  11. "Jeffrey Friedman, 2007 awardee". Danone Institute. Retrieved 25 June 2020.
  12. "Wolf Prize laureates announced". The Jerusalem Post | JPost.com. 16 January 2019. Retrieved 13 December 2021.
  13. "Breakthrough Prize – Winners Of The 2020 Breakthrough Prize In Life Sciences, Fundamental Physics And Mathematics Announced". breakthroughprize.org. Retrieved 13 December 2021.
  14. Princess of Asturias Awards 2024
  15. "Jeffrey M. Friedman, on season 14 , episode 1". Scientific American Frontiers . Chedd-Angier Production Company. 2004. PBS. Archived from the original on 2006-01-01.
  16. "Lily Safani". New York BIO. Archived from the original on 11 May 2021. Retrieved 25 June 2020.
  17. Ruppel Shell, Ellen (2002). The Hungry Gene: The Inside Story of the Obesity Industry. Grove Press. ISBN   0-8021-4033-5 . Retrieved 25 June 2020.