scholarly journals Long chain fatty acids: in vitro cholecystokinin production and in vivo energy intake and body composition alteration

2011 ◽  
Vol 70 (OCE3) ◽  
Author(s):  
C. J. Harden ◽  
A. N. Jones ◽  
T. Maya-Jimenez ◽  
M. E. Barker ◽  
N. J. Hepburn ◽  
...  
2012 ◽  
Vol 108 (4) ◽  
pp. 755-758 ◽  
Author(s):  
Charlotte J. Harden ◽  
Adam N. Jones ◽  
Tannia Maya-Jimenez ◽  
Margo E. Barker ◽  
Natalie J. Hepburn ◽  
...  

Long-chain fatty acids have been shown to suppress appetite and reduce energy intake (EI) by stimulating the release of gastrointestinal hormones such as cholecystokinin (CCK). The effect of NEFA acyl chain length on these parameters is not comprehensively understood. Anin vitroscreen tested the capacity of individual NEFA (C12 to C22) to trigger CCK release. There was a gradient in CCK release with increasing chain length. DHA (C22) stimulated significantly (P < 0·01) more CCK release than all other NEFA tested. Subsequently, we conducted a randomised, controlled, crossover intervention study using healthy males (n18). The effects of no treatment (NT) and oral doses of emulsified DHA-rich (DHA) and oleic acid (OA)-rich oils were compared using 24 h EI as the primary endpoint. Participants reported significantly (P = 0·039) lower total daily EI (29 % reduction) with DHA compared to NT. There were no differences between DHA compared to OA and OA compared to NT. There was no between-treatment difference in the time to, or EI of, the first post-intervention eating occasion. It is concluded that NEFA stimulate CCK release in a chain length-dependent manner up to C22. These effects may be extended to thein vivosetting, as a DHA-based emulsion significantly reduced short-term EI.


1984 ◽  
Vol 67 (7) ◽  
pp. 1439-1444 ◽  
Author(s):  
William Chalupa ◽  
Bonnie Rickabaugh ◽  
D. Kronfeld ◽  
S. David Sklan

2006 ◽  
Vol 5 (12) ◽  
pp. 2047-2061 ◽  
Author(s):  
Jana Klose ◽  
James W. Kronstad

ABSTRACT The transition from yeast-like to filamentous growth in the biotrophic fungal phytopathogen Ustilago maydis is a crucial event for pathogenesis. Previously, we showed that fatty acids induce filamentation in U. maydis and that the resulting hyphal cells resemble the infectious filaments observed in planta. To explore the potential metabolic role of lipids in the morphological transition and in pathogenic development in host tissue, we deleted the mfe2 gene encoding the multifunctional enzyme that catalyzes the second and third reactions in β-oxidation of fatty acids in peroxisomes. The growth of the strains defective in mfe2 was attenuated on long-chain fatty acids and abolished on very-long-chain fatty acids. The mfe2 gene was not generally required for the production of filaments during mating in vitro, but loss of the gene blocked extensive proliferation of fungal filaments in planta. Consistent with this observation, mfe2 mutants exhibited significantly reduced virulence in that only 27% of infected seedlings produced tumors compared to 88% tumor production upon infection by wild-type strains. Similarly, a defect in virulence was observed in developing ears upon infection of mature maize plants. Specifically, the absence of the mfe2 gene delayed the development of teliospores within mature tumor tissue. Overall, these results indicate that the ability to utilize host lipids contributes to the pathogenic development of U. maydis.


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