Browsing by Subject "lipid metabolism"

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  • Neumann, Hartmut P.; Young, William F.; Krauss, Tobias; Bayley, Jean-Pierre; Schiavi, Francesca; Opocher, Giuseppe; Boedeker, Carsten C.; Tirosh, Amit; Castinetti, Frederic; Ruf, Juri; Beltsevich, Dmitry; Walz, Martin; Groeben, Harald-Thomas; von Dobschuetz, Ernst; Gimm, Oliver; Wohllk, Nelson; Pfeifer, Marija; Lourenco, Delmar M.; Peczkowska, Mariola; Patocs, Attila; Ngeow, Joanne; Makay, Ozer; Shah, Nalini S.; Tischler, Arthur; Leijon, Helena; Pennelli, Gianmaria; Villar Gomez de las Heras, Karina; Links, Thera P.; Bausch, Birke; Eng, Charis (2018)
    Although the authors of the present review have contributed to genetic discoveries in the field of pheochromocytoma research, we can legitimately ask whether these advances have led to improvements in the diagnosis and management of patients with pheochromocytoma. The answer to this question is an emphatic Yes! In the field of molecular genetics, the well-established axiom that familial (genetic) pheochromocytoma represents 10% of all cases has been overturned, with >35% of cases now attributable to germline disease-causing mutations. Furthermore, genetic pheochromocytoma can now be grouped into five different clinical presentation types in the context of the ten known susceptibility genes for pheochromocytoma-associated syndromes. We now have the tools to diagnose patients with genetic pheochromocytoma, identify germline mutation carriers and to offer gene-informed medical management including enhanced surveillance and prevention. Clinically, we now treat an entire family of tumors of the paraganglia, with the exact phenotype varying by specific gene. In terms of detection and classification, simultaneous advances in biochemical detection and imaging localization have taken place, and the histopathology of the paraganglioma tumor family has been revised by immunohistochemical-genetic classification by gene-specific antibody immunohistochemistry. Treatment options have also been substantially enriched by the application of minimally invasive and adrenal-sparing surgery. Finally and most importantly, it is now widely recognized that patients with genetic pheochromocytoma/paraganglioma syndromes should be treated in specialized centers dedicated to the diagnosis, treatment and surveillance of this rare neoplasm.
  • Yetukuri, Laxman; Soderlund, Sanni; Koivuniemi, Artturi; Seppanen-Laakso, Tuulikki; Niemela, Perttu S.; Hyvonen, Marja; Taskinen, Marja-Riitta; Vattulainen, Ilpo Tapio; Jauhiainen, Matti; Oresic, Matej (2010)
  • Hasygar, Kiran; Deniz, Onur; Liu, Ying; Gullmets, Josef; Hynynen, Riikka; Ruhanen, Hanna; Kokki, Krista; Kakela, Reijo; Hietakangas, Ville (2021)
    Energy storage and growth are coordinated in response to nutrient status of animals. How nutrient-regulated signaling pathways control these processes in vivo remains insufficiently understood. Here, we establish an atypical MAP kinase, ERK7, as an inhibitor of adiposity and growth in Drosophila. ERK7 mutant larvae display elevated triacylglycerol (TAG) stores and accelerated growth rate, while overexpressed ERK7 is sufficient to inhibit lipid storage and growth. ERK7 expression is elevated upon fasting and ERK7 mutant larvae display impaired survival during nutrient deprivation. ERK7 acts in the fat body, the insect counterpart of liver and adipose tissue, where it controls the subcellular localization of chromatin-binding protein PWP1, a growth-promoting downstream effector of mTOR. PWP1 maintains the expression of sugarbabe, encoding a lipogenic Gli-similar family transcription factor. Both PWP1 and Sugarbabe are necessary for the increased growth and adiposity phenotypes of ERK7 loss-of-function animals. In conclusion, ERK7 is an anti-anabolic kinase that inhibits lipid storage and growth while promoting survival on fasting conditions.
  • EFSA Panel Dietetic Prod Nut (2018)
    Following an application from Lonza Ltd., submitted for authorisation of a health claim pursuant to Article 13(5) of Regulation (EC) No1924/2006 via the Competent Authority of Germany, the EFSA Panelon Dietetic Products, Nutrition and Allergies (NDA) was asked to deliver an opinion on the scientific substantiation of a health claim related to L-carnitine and normal lipid metabolism. The food that is proposed as the subject of the health claim is L-carnitine. The Panelconsiders that L-carnitine is sufficiently characterised. The claimed effect proposed by the applicant is normal lipid metabolism'. The target population proposed by the applicant is the general population. The Panelconsiders that contribution to normal lipid metabolism is a beneficial physiological effect. The applicant proposes that the claim submitted with this application is based on the essentiality of a nutrient. The Panelconsiders that the evidence provided does not establish that dietary L-carnitine is required to maintain normal lipid metabolism in the target population, for which the claim is intended. The Panelconcludes that a cause and effect relationship has not been established between the consumption of L-carnitine and contribution to normal lipid metabolism in the target population. (c) 2018 European Food Safety Authority. EFSA Journal published by John Wiley and Sons Ltd on behalf of European Food Safety Authority.
  • Tigistu-Sahle, Feven (Helsingin yliopisto, 2017)
    The application of human bone marrow derived mesenchymal stromal cells (hBMSCs) for regenerative or immunomodulatory therapies, e.g. treatment of the graft-versus-host disease, requires in vitro expansion of the cells. The hBMSCs undergo subtle changes during expansion which may compromise their functionality. In order to evaluate these changes lipidomics techniques were applied and the fatty acid (FA) and glycerophospholipid (GPL) profiles of hBMSCs were determined. During the cell passaging, arachidonic acid (20:4n-6) -containing species of phosphatidylcholine (PC) and phosphatidyl-ethanolamine (PE) accumulated while the species containing monounsaturated fatty acids (MUFA) or n-3 polyunsaturated fatty acids (n-3 PUFAs) decreased. The accumulation of 20:4n-6 and deficiency of n-3 PUFAs correlated with the decreased immunosuppressive capacity of the hBMSCs, which suggests that extensive expansion of hBMSCs harmfully modulates membrane GPLs profiles, affects lipid signaling and eventually impairs the functionality of the cells. Experiments, in which hBMSCs were cultured with different PUFA supplements revealed that the cells may limit the proinflammatory 20:4n-6 signaling by elongating this precursor with high biological activity to the less active precursor, 22:4n-6. It was also found that the ability of hBMSCs to produce long chain highly unsaturated fatty acids from C18 PUFA precursors was limited apparently due to the low desaturase activity of the cells. Thus, when the n-3 PUFA precursor, 18:3n-3, had little potency to reduce the GPL 20:4n-6 content, the eicosapentaenoic (20:5n-3) and docosahexaenoic (22:6n-3) acid supplements efficiently displaced the 20:4n-6 acyls, allowing attenuation of inflammatory signaling. These findings call for specifically designed optimal PUFA supplements for the cultures with sufficiently 20:5n-3 and 22:6n-3 but moderately 20:4n-6. Studies on the dynamics of PUFA incorporation into the major GPL classes revealed that the PUFAs in PC are remodeled at first, then those of the PEs and phosphatidylserines (PS). These results demonstrate that not only the type of PUFA administered but also the treatment time largely determines the resulting composition of the membrane GPL species, which serve as PUFA donors for the synthesis of lipid mediators. This thesis work highlights the importance of using lipidomics data to complement genomics or proteomics approaches when aiming at understanding of the therapeutic mechanisms of stem/stromal cells. The work provides tools to develop the protocols of hBMSCs culture and manipulate the functionality of the cells.