Väitös (farmakologia): MSc Keshav Thapa
Aika
13.12.2024 klo 12.00 - 16.00
MSc Keshav Thapa esittää väitöskirjansa ”THE ROLE OF MELANOCORTIN 1 RECEPTOR IN THE REGULATION OF CHOLESTEROL AND FATTY ACID METABOLISM IN THE LIVER” julkisesti tarkastettavaksi Turun yliopistossa perjantaina 13.12.2024 klo 12.00 (Turun yliopisto, Medisiina C, Osmo Järvi -sali, Kiinamyllynkatu 10, Turku).
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://utu.zoom.us/j/69413690910 (meeting ID: 694 1369 0910, passcode: 2574929, kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Jukka Hakkola (Oulun yliopisto) ja kustoksena professori Eriika Savontaus (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on farmakologia.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9964-4 (kopioi linkki selaimeen).
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Tiivistelmä väitöstutkimuksesta:
My research focused on exploring the role of the melanocortin 1 receptor (MC1R) signaling pathways in the liver and its broader implications for metabolic health. Melanocortins, a family of hormones, are known to regulate various physiological functions, including skin pigmentation, energy regulation, and immune responses. While MC1R is primarily recognized for its role in skin pigmentation, its function in the liver and adipose (fat) tissues had remained largely unexplored - until now.
In this study, I demonstrated that MC1R is active in the liver cells and that its activity diminishes under metabolic stress, such as in conditions like metabolic dysfunction-associated steatotic liver disease (MASLD). By employing both genetic and pharmacological approaches, I investigated the consequences of either blocking or activating signaling in the liver. The findings were striking: mice lacking MC1R developed clear symptoms of liver disease, including increased liver weights, elevated cholesterol levels, and impaired fat metabolism. On the other hand, pharmacologically activating MC1R signaling not only reduced cholesterol levels but also enhanced the uptake of lipoprotein particles, underscoring MC1R’s essential role in maintaining lipid balance and metabolic homeostasis.
These results reveal MC1R as a key regulator of cholesterol and fat metabolism in the liver, directly influencing overall metabolic health. By uncovering this previously unrecognized role of MC1R, my research not only advances our understanding of liver function but also suggests that targeting MC1R could provide novel therapeutic strategies for combating the growing prevalence of metabolic disorders. In conclusion, this research offers valuable insights that could lead to improved treatments and better quality of life for individuals affected by metabolic conditions.
Yleisön on mahdollista osallistua väitökseen myös etäyhteyden kautta: https://utu.zoom.us/j/69413690910 (meeting ID: 694 1369 0910, passcode: 2574929, kopioi linkki selaimeen).
Vastaväittäjänä toimii professori Jukka Hakkola (Oulun yliopisto) ja kustoksena professori Eriika Savontaus (Turun yliopisto). Tilaisuus on englanninkielinen. Väitöksen alana on farmakologia.
Väitöskirja yliopiston julkaisuarkistossa: https://urn.fi/URN:ISBN:978-951-29-9964-4 (kopioi linkki selaimeen).
***
Tiivistelmä väitöstutkimuksesta:
My research focused on exploring the role of the melanocortin 1 receptor (MC1R) signaling pathways in the liver and its broader implications for metabolic health. Melanocortins, a family of hormones, are known to regulate various physiological functions, including skin pigmentation, energy regulation, and immune responses. While MC1R is primarily recognized for its role in skin pigmentation, its function in the liver and adipose (fat) tissues had remained largely unexplored - until now.
In this study, I demonstrated that MC1R is active in the liver cells and that its activity diminishes under metabolic stress, such as in conditions like metabolic dysfunction-associated steatotic liver disease (MASLD). By employing both genetic and pharmacological approaches, I investigated the consequences of either blocking or activating signaling in the liver. The findings were striking: mice lacking MC1R developed clear symptoms of liver disease, including increased liver weights, elevated cholesterol levels, and impaired fat metabolism. On the other hand, pharmacologically activating MC1R signaling not only reduced cholesterol levels but also enhanced the uptake of lipoprotein particles, underscoring MC1R’s essential role in maintaining lipid balance and metabolic homeostasis.
These results reveal MC1R as a key regulator of cholesterol and fat metabolism in the liver, directly influencing overall metabolic health. By uncovering this previously unrecognized role of MC1R, my research not only advances our understanding of liver function but also suggests that targeting MC1R could provide novel therapeutic strategies for combating the growing prevalence of metabolic disorders. In conclusion, this research offers valuable insights that could lead to improved treatments and better quality of life for individuals affected by metabolic conditions.
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