scholarly journals Faculty Opinions recommendation of Suramin exposure alters cellular metabolism and mitochondrial energy production in African trypanosomes.

Author(s):  
Markus Engstler ◽  
Brooke Morriswood
2017 ◽  
Vol 158 (11) ◽  
pp. 409-417
Author(s):  
Kornél Simon ◽  
István Wittmann

Abstract: In clinical recommendations the normalized blood glucose level is declared as the main target in therapy of diabetes mellitus, i.e. the achievement of euglycemia is the main therapeutic goal. This approach suggests, that the normal blood glucose value is the marker of the normal carbohydrate metabolism (eumetabolism), and vice versa: hyperglycemia is associated with abnormal metabolism (dysmetabolism). However the question arises, whether identical blood glucose values do reflect the same intracellular biochemical mechanisms? On the basis of data published in the literature authors try to answer these questions by studying the relations between the short/longterm blood glucose level and the cellular metabolism in different clinical settings characterized by divergent pathophysiological parameters. The correlations between blood glucose level and cellular metabolism in development of micro-, and macroangiopathy, in the breakthrough phenomenon, as well as during administration of metabolic promoters, the discrepancies of relation between blood glucose values and cellular metabolism in type 1, and type 2 diabetes mellitus, furthermore association between blood glucose value and myocardial metabolism in acute and chronic stress were analyzed. Authors conclude, that the actual blood glucose values reveal the actual cellular metabolism in a very variable manner: neither euglycemia does mandatorily indicate eumetabolism (balance of cellular energy production), nor hyperglycemia is necessarily a marker of abnormal metabolic state (dept of cellular energy production). Moreover, at the same actual blood glucose level both the metabolic efficacy of the same organ may sharply vary, and the intracellular biochemical machinery could also be very different. In case of the very same longterm blood glucose level the metabolic state of the different organs could be very variable: some organs show an energetically balanced metabolism, while others produce a significant deficit. These inconsistencies between blood glucose level and cellular metabolism can be explained by the fact, that blood glucose value is a transport parameter, reflecting the actual steady state of glucose transport from the carbohydrate pools into the blood, and that from the blood into the tissues. Without knowing the speed of these transports of opposite direction, the blood glucose value per se can not reveal the quantitative and qualitative characteristics of cellular metabolism. Orv. Hetil., 2017, 158(11), 409–417.


Author(s):  
Majd AlGhatrif ◽  
Ariel Zane ◽  
Matt Oberdier ◽  
Marco Canepa ◽  
Stephanie Studenski ◽  
...  

2006 ◽  
Vol 44 (6) ◽  
pp. 519-525 ◽  
Author(s):  
S. Prabhu ◽  
Mallika Jainu ◽  
K.E. Sabitha ◽  
C.S. Shyamala Devi

Molecules ◽  
2020 ◽  
Vol 25 (12) ◽  
pp. 2876
Author(s):  
Poh-Shiow Yeh ◽  
Jui-Tai Chen ◽  
Yih-Giun Cherng ◽  
Shun-Tai Yang ◽  
Yu-Ting Tai ◽  
...  

An estrogen deficiency is the main cause of osteoporosis in postmenopausal women. In bone remodeling, estrogen receptors (ERs) can mediate estrogen-transducing signals. Methylpiperidinopyrazole (MPP) is a highly specific antagonist of ER-alpha (ERα). This study was designed to evaluate the effects of MPP on estrogen-induced energy production, subsequent osteoblast maturation, and the possible mechanisms. Exposure of primary osteoblasts isolated from neonatal rat calvarias to MPP did not affect cell morphology or survival. Estradiol can induce translocation of ERα into mitochondria from the cytoplasm. Interestingly, pretreatment of rat calvarial osteoblasts with MPP lowered estrogen-induced ERα translocation. Sequentially, estrogen-triggered expressions of mitochondrial energy production-linked cytochrome c oxidase (COX) I and COX II messenger (m)RNAs were inhibited following pretreatment with MPP. Consequently, MPP caused decreases in estrogen-triggered augmentation of the activities of mitochondrial respiratory complex enzymes and levels of cellular adenosine phosphate (ATP). During progression of osteoblast maturation, estrogen induced bone morphogenetic protein (BMP)-6 and type I collagen mRNA expressions, but MPP treatment inhibited such induction. Consequently, estrogen-induced osteoblast activation and mineralization were attenuated after exposure to MPP. Taken together, MPP suppressed estrogen-induced osteoblast maturation through decreasing chromosomal osteogenesis-related BMP-6 and type I collagen mRNA expressions and mitochondrial ATP synthesis due to inhibiting energy production-linked COX I and II mRNA expressions. MPP can appropriately be applied to evaluate estrogen-involved bioenergetics and osteoblast maturation.


Author(s):  
Patrick Ritz ◽  
Jean-François Dumas ◽  
Pierre-Henri Ducluzeau ◽  
Gilles Simard

2014 ◽  
Vol 16 (6) ◽  
pp. 511-511 ◽  
Author(s):  
Christina Karlsson Rosenthal

PLoS Biology ◽  
2015 ◽  
Vol 13 (7) ◽  
pp. e1002197 ◽  
Author(s):  
Manish Jaiswal ◽  
Nele A. Haelterman ◽  
Hector Sandoval ◽  
Bo Xiong ◽  
Taraka Donti ◽  
...  

2011 ◽  
Vol 71 (16) ◽  
pp. 5588-5597 ◽  
Author(s):  
Renée F. Johnson ◽  
Ini-Isabée Witzel ◽  
Neil D. Perkins

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