scholarly journals Dietary apple polyphenols increase skeletal muscle capillaries in Wistar rats

2018 ◽  
Vol 6 (18) ◽  
pp. e13866 ◽  
Author(s):  
Yuki Yoshida ◽  
Arata Tsutaki ◽  
Yuki Tamura ◽  
Karina Kouzaki ◽  
Koichi Sashihara ◽  
...  
2019 ◽  
Author(s):  
Ian M Williams ◽  
P Mason McClatchey ◽  
Deanna P Bracy ◽  
Jeffrey S Bonner ◽  
Francisco A Valenzuela ◽  
...  

ABSTRACTDelivery of insulin to the surface of myocytes is required for skeletal muscle (SkM) insulin action. Previous studies have shown that SkM insulin delivery is reduced in the setting of obesity and insulin resistance (IR). The key variables that control SkM insulin delivery are 1) microvascular perfusion and 2) the rate at which insulin moves across the continuous endothelium of SkM capillaries. Obesity and IR are associated with reduced insulin-stimulated SkM perfusion. Whether an impairment in trans-endothelial insulin transport (EIT) contributes to SkM IR, however, is unknown. We hypothesized that EIT would be delayed in a mouse model of diet-induced obesity (DIO) and IR. Using intravital insulin imaging, we found that DIO male mice have a ~15% reduction in EIT compared to their lean counterparts. This impairment in EIT is associated with a 45% reduction in the density of endothelial vesicles. Despite impaired EIT, hyperinsulinemia sustained delivery of insulin to the interstitial space in DIO male mice. Even with maintained interstitial insulin delivery DIO male mice still showed SkM IR, indicating severe myocyellular IR in this model. Interestingly, there was no difference in EIT, endothelial ultrastructure or SkM insulin sensitivity between lean and high fat diet-fed female mice. These results suggest that, in male mice, obesity results in damage to the capillary endothelium which limits the capacity for EIT.


1977 ◽  
Vol 150 (1) ◽  
pp. 213-218 ◽  
Author(s):  
Ralph V. McKinney ◽  
Baldev B. Singh ◽  
Phyllis D. Brewer

2020 ◽  
Vol 21 (13) ◽  
pp. 4815 ◽  
Author(s):  
Ekaterina P. Mochalova ◽  
Svetlana P. Belova ◽  
Tatiana Y. Kostrominova ◽  
Boris S. Shenkman ◽  
Tatiana L. Nemirovskaya

Unloading leads to skeletal muscle atrophy via the upregulation of MuRF-1 and MAFbx E3-ligases expression. Reportedly, histone deacetylases (HDACs) 4 and 5 may regulate the expression of MuRF1 and MAFbx. To examine the HDAC-dependent mechanisms involved in the control of E3-ubiquitin ligases expression at the early stages of muscle unloading we used HDACs 4 and 5 inhibitor LMK-235 and HDAC 4 inhibitor Tasqinimod (Tq). Male Wistar rats were divided into four groups (eight rats per group): nontreated control (C), three days of unloading/hindlimb suspension (HS) and three days HS with HDACs inhibitor LMK-235 (HSLMK) or Tq (HSTq). Treatment with LMK-235 diminished unloading-induced of MAFbx, myogenin (MYOG), ubiquitin and calpain-1 mRNA expression (p < 0.05). Tq administration had no effect on the expression of E3-ligases. The mRNA expression of MuRF1 and MAFbx was significantly increased in both HS and HSTq groups (1.5 and 4.0 folds, respectively; p < 0.05) when compared with the C group. It is concluded that during three days of muscle unloading: (1) the HDACs 4 and 5 participate in the regulation of MAFbx expression as well as the expression of MYOG, ubiquitin and calpain-1; (2) the inhibition of HDAC 4 has no effect on MAFbx expression. Therefore, HDAC 5 is perhaps more important for the regulation of MAFbx expression than HDAC 4.


2015 ◽  
Vol 36 (3) ◽  
pp. 428-433 ◽  
Author(s):  
Nathalia Trasmonte da Silva ◽  
Hananiah Tardivo Quintana ◽  
Jeferson André Bortolin ◽  
Daniel Araki Ribeiro ◽  
Flavia de Oliveira

2016 ◽  
Vol 34 (5) ◽  
pp. 187-193 ◽  
Author(s):  
Mayna Adabbo ◽  
Fernanda Rossi Paolillo ◽  
Paulo Sérgio Bossini ◽  
Natalia Camargo Rodrigues ◽  
Vanderlei Salvador Bagnato ◽  
...  

2016 ◽  
Vol 218 (2) ◽  
pp. 98-111 ◽  
Author(s):  
M. Bigler ◽  
D. Koutsantonis ◽  
A. Odriozola ◽  
S. Halm ◽  
S. A. Tschanz ◽  
...  

1928 ◽  
Vol 47 (2) ◽  
pp. 273-290 ◽  
Author(s):  
Joseph T. Wearn ◽  

By means of injections made into the coronary arteries of beating hearts it has been possible to determine the number of capillaries in the normal heart muscle. This study has shown a very rich blood supply with an average of approximately one capillary for each muscle fibre in the ventricular walls and papillary muscles, and a less abundant supply in the auricular muscle and Purkinje system. The number of capillaries per sq. mm. of ventricular wall or papillary muscle is about twice that found by Krogh in skeletal muscle. Capillaries were not found constantly in the valves of hearts in which there was apparently a complete injection of the capillary bed. The method described for injecting the capillaries of the heart also provides a means of studying the blood supply to the muscle, valves and aortic wall in pathological hearts.


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