Effect of fescue toxicosis on whole body energy and nitrogen balance, in situ degradation and ruminal passage rates in Holstein steers

2015 ◽  
Vol 55 (8) ◽  
pp. 988 ◽  
Author(s):  
A. F. Koontz ◽  
D. H. Kim ◽  
K. R. McLeod ◽  
J. L. Klotz ◽  
D. L. Harmon

This study was designed to examine alteration of ruminal kinetics, as well as N and energy balance during fescue toxicosis. Six ruminally cannulated Holstein steers (bodyweight (BW) = 217 ± 7 kg) were weight matched into pairs and pair fed throughout a crossover design experiment with a 2×2 factorial treatment structure. Factors were endophyte (infected, E+ vs. uninfected, E−) and feeding level (1100 (L) or 1800 (H) kJ/kG BW.75). During each period, after 8 days of feeding level adaptation, animals were ruminally dosed twice daily with ground fescue seed for the remainder of the period. One steer per pair was dosed with ground endophyte infected fescue seed (E+), the other with ground endophyte free fescue seed. In situ degradation of ground alfalfa was determined on Days 13–16. Total faecal and urinary collections were performed on Days 17–21, with animals placed into indirect calorimetry head-boxes during Days 20 and 21. Heat production (HP) was calculated using the Brower equation. Retained energy (RE) was calculated as intakeE – (faecalE + urinaryE + gaseousE + HP). Liquid and particulate passage rates were evaluated using Cr:EDTA and iADF respectively on Days 22 and 23. There was no difference (P > 0.9) in dry matter intake (DMI)/kg.75 between endophyte treatments, and DMI/kg.75 was different (P < 0.01) between H and L intake by design. Animals on H feeding had higher (P < 0.01) water, N and energy intakes. Energy and N excretion, as well as retained DE, ME, RE, and HP were higher (P < 0.03) for H versus L. There was no difference in retained N, DE, ME, or HP (P > 0.15) between endophyte treatments. Neither rate nor extent of in situ degradation was altered by intake level or endophyte treatment (P > 0.3). DM percentage and DM weight of rumen contents were increased (P < 0.01) by E+ dosing. Particulate passage increased (P = 0.0002) during H intake and decreased (P = 0.02) with E+ dosing. Ruminal liquid passage decreased (P < 0.03) with H feeding, while liquid flow rate tended to be reduced (P < 0.14) with E+ dosing. Total VFA concentration increased with both H feeding (P < 0.01) and E+ dosing (P < 0.0001). Despite these differences, the N and energy balance data indicate that the reductions in weight gain and productivity seen during fescue toxicosis are primarily due to reduced intake.

2013 ◽  
Vol 37 (7) ◽  
pp. 1033-1047 ◽  
Author(s):  
Mardi S. Byerly ◽  
Muhannad Al Salayta ◽  
Roy D. Swanson ◽  
Kiwook Kwon ◽  
Jonathan M. Peterson ◽  
...  

PLoS ONE ◽  
2012 ◽  
Vol 7 (8) ◽  
pp. e43962 ◽  
Author(s):  
Su-Hyoun Chon ◽  
John D. Douglass ◽  
Yin Xiu Zhou ◽  
Nashmia Malik ◽  
Joseph L. Dixon ◽  
...  

2016 ◽  
Vol 12 (7) ◽  
pp. 421-432 ◽  
Author(s):  
Miguel López ◽  
Rubén Nogueiras ◽  
Manuel Tena-Sempere ◽  
Carlos Diéguez

2011 ◽  
Vol 12 (3) ◽  
pp. 127-140 ◽  
Author(s):  
Pablo Blanco Martínez de Morentin ◽  
Carmen R. González ◽  
Asisk K. Saha ◽  
Luís Martins ◽  
Carlos Diéguez ◽  
...  

2016 ◽  
Vol 104 (4) ◽  
pp. 398-411 ◽  
Author(s):  
Ismael González-García ◽  
Johan Fernø ◽  
Carlos Diéguez ◽  
Rubén Nogueiras ◽  
Miguel López

2011 ◽  
Vol 10 (1) ◽  
pp. 99 ◽  
Author(s):  
Mandy So ◽  
Mandeep P Gaidhu ◽  
Babak Maghdoori ◽  
Rolando B Ceddia

2013 ◽  
Vol 14 (4) ◽  
pp. 377-386 ◽  
Author(s):  
Min-Seon Kim ◽  
Wenying Quan ◽  
Myung-Shik Lee

Author(s):  
Natalie Burchat ◽  
Priyanka Sharma ◽  
Hong Ye ◽  
Sai Santosh Babu Komakula ◽  
Agnieszka Dobrzyn ◽  
...  

Obesity and related metabolic disorders are pressing public health concerns, raising the risk for a multitude of chronic diseases. Obesity is multi-factorial disease, with both diet and lifestyle, as well as genetic and developmental factors leading to alterations in energy balance. In this regard, a novel role for DNA repair glycosylases in modulating risk for obesity has been previously established. Global deletion of either of two different glycosylases with varying substrate specificities, Nei-like endonuclease 1 (NEIL1) or 8-oxoguanine DNA glycosylase-1 (OGG1), both predispose mice to diet-induced obesity (DIO). Conversely, enhanced expression of the human OGG1 gene renders mice resistant to obesity and adiposity. This resistance to DIO is mediated through increases in whole body energy expenditure and increased respiration in adipose tissue. Here, we report that hOGG1 expression also confers resistance to genetically-induced obesity. While Agouti obese (Ay/a) mice are hyperphagic and consequently develop obesity on a chow diet, hOGG1 expression in Ay/a mice (Ay/aTg) prevents increased body weight, without reducing food intake. Instead, obesity resistance in Ay/aTg mice is accompanied by increased whole body energy expenditure and tissue mitochondrial content. We also report for the first time that OGG1-mediated obesity resistance in both the Ay/a model and DIO model requires maternal transmission of the hOGG1 transgene. Maternal, but not paternal, transmission of the hOGG1 transgene is associated with obesity resistance and increased mitochondrial content in adipose tissue. These data demonstrate a critical role for OGG1 in modulating energy balance through changes in adipose tissue function. They also demonstrate the importance of OGG1 in modulating developmental programming of mitochondrial content and quality, thereby determining metabolic outcomes in offspring.


2019 ◽  
Vol 47 (2) ◽  
pp. 733-741 ◽  
Author(s):  
Ana Laura de Souza Almeida Matos ◽  
Jonathan S. Oakhill ◽  
José Moreira ◽  
Kim Loh ◽  
Sandra Galic ◽  
...  

Abstract The AMP (adenosine 5′-monophosphate)-activated protein kinase (AMPK) is a key regulator of cellular and whole-body energy homeostasis that co-ordinates metabolic processes to ensure energy supply meets demand. At the cellular level, AMPK is activated by metabolic stresses that increase AMP or adenosine 5′-diphosphate (ADP) coupled with falling adenosine 5′-triphosphate (ATP) and acts to restore energy balance by choreographing a shift in metabolism in favour of energy-producing catabolic pathways while inhibiting non-essential anabolic processes. AMPK also regulates systemic energy balance and is activated by hormones and nutritional signals in the hypothalamus to control appetite and body weight. Failure to maintain energy balance plays an important role in chronic diseases such as obesity, type 2 diabetes and inflammatory disorders, which has prompted a major drive to develop pharmacological activators of AMPK. An array of small-molecule allosteric activators has now been developed, several of which can activate AMPK by direct allosteric activation, independently of Thr172 phosphorylation, which was previously regarded as indispensable for AMPK activity. In this review, we summarise the state-of-the-art regarding our understanding of the molecular mechanisms that govern direct allosteric activation of AMPK by adenylate nucleotides and small-molecule drugs.


2011 ◽  
Vol 20 (13) ◽  
pp. 2571-2584 ◽  
Author(s):  
Santiago Vernia ◽  
Miguel Heredia ◽  
Olga Criado ◽  
Santiago Rodriguez de Cordoba ◽  
Pablo M. Garcia-Roves ◽  
...  

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