Walter Wahli

Last updated
Walter Wahli
Born (1946-05-23) 23 May 1946 (age 78)
Moutier, Switzerland
CitizenshipSwiss
Alma mater
Known forWork on Peroxisome Proliferator-Activated Receptors
Awards
  • Otto Naegeli Prize (2002); European Federation of Lipid Research Award (2002); Hartmann Müller Prize (2008); Life Time Achievement Award (2011); Chaire d’Excellence Pierre de Fermat (2013) [1]
Scientific career
FieldsNuclear Hormone Receptors and gene expression; Energy metabolism
Institutions Nanyang Technological University University of Lausanne

Walter Wahli, born on 23 May 1946 in Moutier, Switzerland, is a distinguished biologist and professor. He has held academic positions at the University of Lausanne and at Nanyang Technological University of Singapore. [2] Wahli's research has contributed to the understanding of metabolic regulation through gene expression. He is particularly recognized for his work on nuclear receptors, specifically the Peroxisome proliferator-activated Receptors (PPARs), which play a crucial role in regulating the body's energy balance. [3]

Contents

Education

Wahli received his Ph.D. in Biological Sciences from the University of Bern in Switzerland. He then worked as a post-doctoral researcher at the Department of Embryology, Carnegie Institution of Washington in Baltimore, and as a visiting fellow and a visiting associate at the National Institutes of Health (NIH), National Cancer Institute, Bethesda, Maryland, US. [4]

Research and career

In 1980, Wahli became full professor and the director of the Institute of Animal Biology at the University of Lausanne where he completed several mandates, such as vice-rector for research, postgraduate and continuing education and founding director of the Center for Integrative Genomics. He then served as a professor of metabolic disease at the Lee Kong Chian School of Medicine, a joint medical school of Nanyang Technological University Singapore and Imperial College London, in Singapore. Since 2019, he is a visiting professor at this school. [5] [6] [7]

Wahli has a long-standing interest in nuclear receptors found within cell nuclei which are responsible for sensing steroid hormones, fatty acids and other lipophilic molecules. Upon activation by these ligands, the receptors regulate the expression of specific genes, thereby controlling key biological processes, such embryonic development, homeostasis, and metabolism of the vertebrates. [8] Since 1977, Wahli reported several discoveries related to the molecular mechanism of action of the estrogen receptor and then of the fatty acid-activated peroxisome proliferator-activated receptors (PPARs), [9] for which he was the co-discoverer, in their functions of regulating lipid and glucose metabolism, inflammation, wound-healing, and cell differentiation processes. He also investigated the role of PPARs in the liver disease known as non-alcoholic fatty liver disease (NAFLD). [10] He underscored the potential of PPARs as drug targets for NAFLD that is often associated to metabolic syndrome and type 2 diabetes. [11] Wahli obtained patents for his inventions. His patents include "Composition for regulating lipid metabolism" (2013) [12] and "Composition for enhancing immunity" (2019). [13]

Honors

Publications

Related Research Articles

<span class="mw-page-title-main">Fibrate</span> Class of chemical compounds

In pharmacology, the fibrates are a class of amphipathic carboxylic acids and esters. They are derivatives of fibric acid. They are used for a range of metabolic disorders, mainly hypercholesterolemia, and are therefore hypolipidemic agents.

<span class="mw-page-title-main">Peroxisome proliferator-activated receptor</span> Group of nuclear receptor proteins

In the field of molecular biology, the peroxisome proliferator–activated receptors (PPARs) are a group of nuclear receptor proteins that function as transcription factors regulating the expression of genes. PPARs play essential roles in the regulation of cellular differentiation, development, and metabolism, and tumorigenesis of higher organisms.

Phytanic acid is a branched chain fatty acid that humans can obtain through the consumption of dairy products, ruminant animal fats, and certain fish. Western diets are estimated to provide 50–100 mg of phytanic acid per day. In a study conducted in Oxford, individuals who consumed meat had, on average, a 6.7-fold higher geometric mean plasma phytanic acid concentration than did vegans.

<span class="mw-page-title-main">Liver X receptor</span> Nuclear receptor

The liver X receptor (LXR) is a member of the nuclear receptor family of transcription factors and is closely related to nuclear receptors such as the PPARs, FXR and RXR. Liver X receptors (LXRs) are important regulators of cholesterol, fatty acid, and glucose homeostasis. LXRs were earlier classified as orphan nuclear receptors, however, upon discovery of endogenous oxysterols as ligands they were subsequently deorphanized.

<span class="mw-page-title-main">Acyl-CoA</span> Group of coenzymes that metabolize fatty acids

Acyl-CoA is a group of CoA-based coenzymes that metabolize carboxylic acids. Fatty acyl-CoA's are susceptible to beta oxidation, forming, ultimately, acetyl-CoA. The acetyl-CoA enters the citric acid cycle, eventually forming several equivalents of ATP. In this way, fats are converted to ATP, the common biochemical energy carrier.

<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">Peroxisome proliferator-activated receptor gamma</span> Nuclear receptor protein found in humans

Peroxisome proliferator-activated receptor gamma, also known as the glitazone reverse insulin resistance receptor, or NR1C3 is a type II nuclear receptor functioning as a transcription factor that in humans is encoded by the PPARG gene.

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

Rev-Erb alpha (Rev-Erbɑ), also known as nuclear receptor subfamily 1 group D member 1 (NR1D1), is one of two Rev-Erb proteins in the nuclear receptor (NR) family of intracellular transcription factors. In humans, REV-ERBɑ is encoded by the NR1D1 gene, which is highly conserved across animal species.

<span class="mw-page-title-main">Obesogen</span> Foreign chemical compound that disrupts lipid balance causing obseity

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<span class="mw-page-title-main">Peroxisome proliferator-activated receptor alpha</span> Nuclear receptor protein found in humans

Peroxisome proliferator-activated receptor alpha (PPAR-α), also known as NR1C1, is a nuclear receptor protein functioning as a transcription factor that in humans is encoded by the PPARA gene. Together with peroxisome proliferator-activated receptor delta and peroxisome proliferator-activated receptor gamma, PPAR-alpha is part of the subfamily of peroxisome proliferator-activated receptors. It was the first member of the PPAR family to be cloned in 1990 by Stephen Green and has been identified as the nuclear receptor for a diverse class of rodent hepatocarcinogens that causes proliferation of peroxisomes.

<span class="mw-page-title-main">Liver X receptor alpha</span> Nuclear receptor protein found in humans

Liver X receptor alpha (LXR-alpha) is a nuclear receptor protein that in humans is encoded by the NR1H3 gene.

<span class="mw-page-title-main">Peroxisome proliferator-activated receptor delta</span> Nuclear receptor protein found in humans

Peroxisome proliferator-activated receptor delta(PPAR-delta), or (PPAR-beta), also known as Nuclear hormone receptor 1(NUC1) is a nuclear receptor that in humans is encoded by the PPARD gene.

<span class="mw-page-title-main">Oleoylethanolamide</span> Chemical compound

Oleoylethanolamide (OEA) is an endogenous peroxisome proliferator-activated receptor alpha (PPAR-α) agonist. It is a naturally occurring ethanolamide lipid that regulates feeding and body weight in vertebrates ranging from mice to pythons.

<span class="mw-page-title-main">GW501516</span> PPAR β/δ receptor agonist compound

GW501516 is a PPARδ receptor agonist that was invented in a collaboration between Ligand Pharmaceuticals and GlaxoSmithKline in the 1990s. It entered into clinical development as a drug candidate for metabolic and cardiovascular diseases, but was abandoned in 2007 because animal testing showed that the drug caused cancer to develop rapidly in several organs.

<span class="mw-page-title-main">PPAR agonist</span> Drug

PPAR agonists are drugs which act upon the peroxisome proliferator-activated receptor. They are used for the treatment of symptoms of the metabolic syndrome, mainly for lowering triglycerides and blood sugar.

Palmitoylethanolamide (PEA) is an endogenous fatty acid amide, and lipid modulator.

<span class="mw-page-title-main">Pirinixic acid</span> Chemical compound

Pirinixic acid is a peroxisome proliferator-activated receptor alpha (PPARα) agonist that is under experimental investigation for prevention of severe cardiac dysfunction, cardiomyopathy and heart failure as a result of lipid accumulation within cardiac myocytes. Treatment is primarily aimed at individuals with an adipose triglyceride lipase (ATGL) enzyme deficiency or mutation because of the essential PPAR protein interactions with free fatty acid monomers derived from the ATGL catalyzed lipid oxidation reaction. It was discovered as WY-14,643 in 1974.

<span class="mw-page-title-main">Saroglitazar</span> Chemical compound

Saroglitazar is a drug for the treatment of type 2 diabetes mellitus, dyslipidemia, NASH and NAFLD It is approved for use in India by the Drug Controller General of India. Saroglitazar is indicated for the treatment of diabetic dyslipidemia and hypertriglyceridemia with type 2 diabetes mellitus not controlled by statin therapy. In clinical studies, saroglitazar has demonstrated reduction of triglycerides (TG), LDL cholesterol, VLDL cholesterol, non-HDL cholesterol and an increase in HDL cholesterol a characteristic hallmark of atherogenic diabetic dyslipidemia (ADD). It has also shown anti-diabetic medication properties by reducing the fasting plasma glucose and HBA1c in diabetes patients.

A selective PPAR modulator (SPPARM) is a selective receptor modulator of the peroxisome proliferator-activated receptor (PPAR). Examples include SPPARMs of the PPARγ, BADGE, EPI-001, INT-131, MK-0533, and S26948.

References

  1. ↑ "Walter". genomyx.ch.
  2. ↑ "Walter Wahli | Metabolomics Congress 2017 | Conferenceseries". www.metabolomicsconference.com. 8 May 2017. Retrieved 2019-10-24.
  3. ↑ "FBM Awardees 2011". www.genomyx.ch. Retrieved 2019-10-24.
  4. ↑ "Prof. Dr. Walter Wahli". www.swir.ch. Retrieved 2019-10-24.
  5. ↑ "Unisciences – UNIL – Walter Wahli". applicationspub.unil.ch. Retrieved 2019-10-24.
  6. ↑ "About". www.unil.ch. Retrieved 2019-10-24.
  7. ↑ "Prof. Wahli". www.unil.ch. Retrieved 2019-10-24.
  8. ↑ Wahli, W; Martinez, E (1991-06-01). "Superfamily of steroid nuclear receptors: positive and negative regulators of gene expression". The FASEB Journal. 5 (9): 2243–2249. doi: 10.1096/fasebj.5.9.1860615 . ISSN   0892-6638. PMID   1860615. S2CID   1464261.
  9. ↑ Wahli, Walter (2002). "Peroxisome proliferator-activated receptors (PPARs): from metabolic control to epidermal wound healing". Swiss Medical Weekly . 132 (7–8): 83–91. doi: 10.4414/smw.2002.09939 . ISSN   1424-7860. PMID   11971202. S2CID   33386091.
  10. ↑ Chen, Jiapeng; Montagner, Alexandra; Tan, Nguan Soon; Wahli, Walter (2018). "Insights into the Role of PPARß/d in NAFLD". International Journal of Molecular Sciences. 19 (7): 1893. doi: 10.3390/ijms19071893 . PMC   6073272 . PMID   29954129.
  11. ↑ Desvergne, Béatrice; Wahli, Walter (1999-10-01). "Peroxisome Proliferator-Activated Receptors: Nuclear Control of Metabolism". Endocrine Reviews. 20 (5): 649–688. doi: 10.1210/edrv.20.5.0380 . ISSN   0163-769X. PMID   10529898.
  12. ↑ US 8518459,Wahli, Walter; Bourgeois-Lugand, Marie Françoise Yvonne& Husson-Robert, Bernadetteet al.,"Composition for regulating lipid metabolism",published 2013-08-27, assigned to Actigenomics SA
  13. ↑ EP 3027056,Bourgeois, Marie Françoise; Cefaï, Daniel& Wahli, Walteret al.,"Composition for enhancing immunity",published 2019-12-04, assigned to Actigenomics SA
  14. ↑ "Find people in the EMBO Communities". people.embo.org. Retrieved 2021-04-07.
  15. ↑ "DNA Tests for Personalized Beauty, Health & Wellness | Imagene Labs" . Retrieved 2019-10-24.
  16. ↑ "ICPI website" (PDF).
  17. ↑ "Prof. Wahli". www.unil.ch. Retrieved 2019-10-24.
  18. ↑ "The Open Nutrition Journal – Editorial Board". opennutritionjournal.com. Retrieved 2019-10-24.
  19. ↑ The Journal of Steroid Biochemistry and Molecular Biology Editorial Board.
  20. ↑ "Cell & Bioscience". Cell & Bioscience. Retrieved 2019-10-24.
  21. ↑ "FBM Awardees 2011". www.genomyx.ch. Retrieved 2019-10-24.
  22. ↑ "Prof. Dr. Walter Wahli". www.swir.ch. Retrieved 2019-10-24.
  23. ↑ "toulouse infra".
  24. ↑ "International Journal of Molecular Sciences". www.mdpi.com. Retrieved 2019-10-24.
  25. ↑ Desvergne, B.; Wahli, W. (1999). "Peroxisome proliferator-activated receptors: nuclear control of metabolism". Endocrine Reviews. 20 (5): 649–688. doi: 10.1210/edrv.20.5.0380 . ISSN   0163-769X. PMID   10529898.
  26. ↑ Braissant, O.; Foufelle, F.; Scotto, C.; Dauça, M.; Wahli, W. (1996-01-01). "Differential expression of peroxisome proliferator-activated receptors (PPARs): tissue distribution of PPAR-alpha, -beta, and -gamma in the adult rat". Endocrinology. 137 (1): 354–366. doi: 10.1210/endo.137.1.8536636 . ISSN   0013-7227. PMID   8536636.
  27. ↑ Kliewer, Steven A.; Sundseth, Scott S.; Jones, Stacey A.; Brown, Peter J.; Wisely, G. Bruce; Koble, Cecilia S.; Devchand, Pallavi; Wahli, Walter; Willson, Timothy M.; Lenhard, James M.; Lehmann, Jürgen M. (1997-04-29). "Fatty acids and eicosanoids regulate gene expression through direct interactions with peroxisome proliferator-activated receptors α and γ". Proceedings of the National Academy of Sciences. 94 (9): 4318–4323. Bibcode:1997PNAS...94.4318K. doi: 10.1073/pnas.94.9.4318 . ISSN   0027-8424. PMC   20720 . PMID   9113987.
  28. ↑ Kersten, Sander; Desvergne, Béatrice; Wahli, Walter (2000). "Roles of PPARs in health and disease". Nature. 405 (6785): 421–424. Bibcode:2000Natur.405..421K. doi:10.1038/35013000. ISSN   1476-4687. PMID   10839530. S2CID   4373446.
  29. ↑ Kersten, Sander; Seydoux, Josiane; Peters, Jeffrey M.; Gonzalez, Frank J.; Desvergne, Béatrice; Wahli, Walter (1999-06-01). "Peroxisome proliferator–activated receptor α mediates the adaptive response to fasting". The Journal of Clinical Investigation. 103 (11): 1489–1498. doi:10.1172/JCI6223. ISSN   0021-9738. PMC   408372 . PMID   10359558.
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