scholarly journals The mechanical and biochemical properties of tail tendon in a rat model of obesity: Effect of moderate exercise and prebiotic fibre supplementation

2019 ◽  
Vol 88 ◽  
pp. 148-154 ◽  
Author(s):  
Jaqueline L. Rios ◽  
Loretta Ko ◽  
Venus Joumaa ◽  
Shuyue Liu ◽  
Fernando Diefenthaeler ◽  
...  
2019 ◽  
Vol 27 ◽  
pp. S155
Author(s):  
J.L. Rios ◽  
J.W. Mather ◽  
J. Michaiel ◽  
S.M. Mattiello ◽  
W. Herzog

Author(s):  
Ernst Johannes Menzel ◽  
Roland Reihsner

The biomechanical and biochemical properties of collagen are changed by non-enzymatic glycation culminating in increased cross-linking. We have previously shown that dibasic amino acids such as L-arginine inhibit in vitro the non-enzymatic glycation of soluble proteins and insoluble connective tissue macromolecules. In the present in vitro study we obtained evidence that the nucleophilic hydrazine derivative aminoguanidine and the non-steroidal antirheumatic drug ibuprofen inhibit the formation of fluorescent advanced glycation end products (AGEs) to a comparable extent, while arginine is ineffective as a consequence of its tendency to form AGEs itself. Periodic replacement of glycated arginine in the rat tail tendon system, however, engendered an inhibition of fluorescence similar to that obtained by the other inhibitors. Long-term glycation of rat tail tendons caused a significant increase in Young's modulus, which could also be inhibited by periodically renewed arginine. In contrast to ibuprofen, aminoguanidine and arginine-lysine inhibited the marked increase in maximum contraction force of long-term glycated rat tail tendons. As opposed to other inhibitors, aminoguanidine also reduced the thermal contraction force of native tendons, shifted the maximum contraction temperature to markedly lower values and solubilized a significant part of the rat tail tendon collagen. These findings indicate that the in vitro alterations of rat tail tendon collagen induced by non-enzymatic glycation can be prevented by arginine, arginine-lysine and aminoguanidine. However, collagen structure is seriously affected by aminoguanidine.


Diabetologia ◽  
2016 ◽  
Vol 60 (3) ◽  
pp. 597-606 ◽  
Author(s):  
Takeru Shima ◽  
Takashi Matsui ◽  
Subrina Jesmin ◽  
Masahiro Okamoto ◽  
Mariko Soya ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Gemma Sanguesa ◽  
Montserrat Batlle ◽  
Emma Munoz Moreno ◽  
Guadalupe Soria ◽  
Anna Alcarraz ◽  
...  

Introduction: A U-shaped relationship between exercise load and cardiovascular risk has been demonstrated. In the brain, moderate exercise improves cognitive performance but the consequences of intense exercise remain unknown. We aimed to describe the effects of moderate and intensive exercise load on brain structure and function. Methods: Male Wistar rats were subjected to moderate (MOD, 35 cm/s for 45 min, n=8) or intense (INT, 60 cm/s for 60 min, n=8) exercise for 16 weeks, 5 days/week; sedentary rats (SED, n=10) were used as controls. At 16 weeks, learning and motivation tests, and brain magnetic resonance (MR) were obtained. In MR, structural brain networks were analyzed using fractional anisotropy normalized connectomes, and cerebral blood flow (CBF) was assessed using pulsed arterial spin labelling. BDNF levels were analysed in plasma, hippocampus and frontal cortex samples with ELISA. Results: MOD rats showed a greater motivation than SED rats and enhanced learning capacity than INT rats. In the MR, only moderate exercise increased global and local efficiency and average clustering coefficient. Global CBF was increased by moderate but not intensive exercise (Fig A). CBF was subsequently assessed at specific brain regions. In comparison to SED, MOD rats presented a higher CBF in the right and left cortex, and in the left hippocampus; in INT rats, CBF was higher only in the left cortex compared to SED (Fig B). MOD training induced a significant decrease in BDNF protein levels in the hippocampus compared to both SED and INT groups. No significant differences were found on BDNF levels in plasma and frontal cortex samples among groups. Conclusions: In a rat model, moderate exercise induces brain structural and functional improvements that are not perpetuated with intensive exercise, supporting the existence of a U-shaped relationship between exercise load and brain function.


2014 ◽  
Vol 47 (3) ◽  
pp. 681-686 ◽  
Author(s):  
Armando Diaz Gonzalez ◽  
Maxime A. Gallant ◽  
David B. Burr ◽  
Joseph M. Wallace

2017 ◽  
Vol 25 ◽  
pp. S308
Author(s):  
J.L. Rios ◽  
D.A. Hart ◽  
R.A. Reimer ◽  
K.H. Collins ◽  
R.A. Seerattan ◽  
...  

2016 ◽  
Vol 31 (2) ◽  
pp. 147-156 ◽  
Author(s):  
Delin Ma ◽  
Jeffrey M. Shuler ◽  
Aishwarya Kumar ◽  
Quincy R. Stanford ◽  
Sudheer Tungtur ◽  
...  

Background. The use of exercise in amyotrophic lateral sclerosis (ALS) is controversial. Although moderate exercise appears to be beneficial for limb muscles in ALS, the effects of exercise on bulbar muscles such as the tongue have not been studied. Objective. To determine the effects of tongue force training on bulbar motor function in the SOD1-G93A rat model of ALS. Methods. We compared the effects of tongue force training on bulbar motor function and neuromuscular junction innervation in female SOD1-G93A rats and age-matched female wild-type controls. Half of each group underwent afternoon tongue force training sessions, and all rats were tested under minimal force conditions in the mornings. Results. Tongue force did not differ between the SOD1-G93A rats and healthy controls during the morning testing sessions, nor was it affected by training. Surprisingly, decreases in tongue motility, the number of licks per session, and body weight were greater in the tongue force–trained SOD1-G93A rats. Forelimb grip force, survival, and denervation of the genioglossus (GG) muscle did not differ between the trained and untrained SOD1-G93A rats. GG innervation was correlated with changes in tongue force but not tongue motility in SOD1-G93A rats at end stage. Conclusions. The results indicate a potential deleterious effect of tongue force training on tongue motility in female SOD1-G93A rats. The lack of a relationship between GG innervation and tongue motility suggests that factors other than lower–motor neuron integrity likely accounted for this effect.


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