Role of Potassium in Protein Metabolism in Plants

MOLECULAR ASPECTS OF SARCOPENIA PATHOGENESIS IN CHRONOC KIDNEY DISEASE: INTEGRATED ROLE OF mTOR

Nephrology (Saint-Petersburg) ◽

10.24884/1561-6274-2018-22-5-9-16 ◽

2018 ◽

Vol 22 (5) ◽

pp. 9-16 ◽

Cited By ~ 3

Author(s):

M. Z. Gasanov

Keyword(s):

Kidney Disease ◽

Muscle Mass ◽

Protein Metabolism ◽

Mammalian Target Of Rapamycin ◽

Healthy Person ◽

Scientific Review ◽

Cytoskeleton Organization ◽

Molecular Aspects ◽

End Stage

In recent decades, the main pathogenetic mechanisms for maintaining muscle mass and strength have been discovered. Most of the scientific papers on the molecular aspects of the pathogenesis of sarcopenia were focused on the Akt-signaling pathway. The subject of the study were people of elderly and senile age, immobilized patients, patients with CKD 1-4 stages, animals. However, recently more attention has been paid to the role of protein – the mammalian target of rapamycin mTOR. It seems to be a key link in the control of muscle mass and is a promising marker in understanding the mechanisms of the pathogenesis of sarcopenia. Its importance in protein metabolism in patients with end stage kidney disease is not studied and requires further research. The presented scientific review contains information on the role of mTOR and its components – mTORC1 and mTORC2 in maintaining muscle mass and strength in a healthy person and in the formation of sarcopenia in patients with CKD. The general aid of mTORC1 complex is regulation of protein production which is necessary for cell growth and differentiation. mTORC2 complex functions are not enough studied. It is established that it plays important role in such biological processes as cytoskeleton organization, intracellular homeostasis maintaining, so it provides cell resistance and cell survivability in negative external and internal impulses. mTOR protein can be considered as promising molecular marker in diagnostics of protein metabolism early disturbances in patients with CKD and also as additory factor of sarcopenia severity assessment.

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The role of striated muscle Pik3r1 in glucose and protein metabolism following chronic glucocorticoid exposure

Journal of Biological Chemistry ◽

10.1016/j.jbc.2021.100395 ◽

2021 ◽

Vol 296 ◽

pp. 100395

Author(s):

Tzu-Chieh Chen ◽

Taiyi Kuo ◽

Mohamad Dandan ◽

Rebecca A. Lee ◽

Maggie Chang ◽

...

Keyword(s):

Protein Metabolism ◽

Striated Muscle

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Role of insulin and branched-chain amino acids in regulating protein metabolism during fasting

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1990.258.6.e907 ◽

1990 ◽

Vol 258 (6) ◽

pp. E907-E917 ◽

Cited By ~ 2

Author(s):

M. Frexes-Steed ◽

M. L. Warner ◽

N. Bulus ◽

P. Flakoll ◽

N. N. Abumrad

Keyword(s):

Amino Acids ◽

Protein Metabolism ◽

Insulin Dose ◽

Group Iii ◽

Group I ◽

Tissue Sensitivity ◽

Branched Chain ◽

Independent Effects ◽

Dose Dependent

This study examines the independent effects of insulin and amino acids on protein metabolism after a 12-h and 4-day fast in healthy volunteers. Leucine (Leu) kinetics were examined during sequential insulin infusions of 0 (group I) or 0.0125 (groups II and III), 1.2, and 10 mU.kg-1.min-1. Plasma Leu was maintained at 12-h fasted levels in groups I and II and at 84-h fasted levels in group III. Four-day fast (vs. 1 day, P less than 0.01) was associated with a 79% drop in plasma insulin and elevations in plasma Leu (122%), Leu rates of appearance (Ra) (21%), and Leu oxidation (56%), and no change in nonoxidative rates of disappearance (Rd). Insulin resulted in a dose-dependent suppression of endogenous Leu Ra with group III = I greater than II. Leu oxidation rose 1.7-fold in group III at the highest insulin dose but remained stable in the two other groups. In conclusion, 4-day fasting is associated with enhanced proteolysis and Leu oxidation with no change in nonoxidative Rd (protein synthesis). Elevated branched-chain (and other) amino acids were required to restore tissue sensitivity and specificity to the effects of insulin on protein metabolism after 4 days of fasting.

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Pentoxifylline decreases body weight loss and muscle protein wasting characteristics of sepsis

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.1993.265.4.e660 ◽

1993 ◽

Vol 265 (4) ◽

pp. E660-E666 ◽

Cited By ~ 9

Author(s):

D. Breuille ◽

M. C. Farge ◽

F. Rose ◽

M. Arnal ◽

D. Attaix ◽

...

Keyword(s):

Body Weight ◽

Protein Synthesis ◽

Acute Phase ◽

Protein Metabolism ◽

Muscle Wasting ◽

Acute Phase Protein ◽

Muscle Protein ◽

Liver Protein ◽

Phase Protein

Sepsis induces metabolic disorders that include loss of body weight, muscle wasting, and acute-phase protein synthesis in liver. Cytokines are generally recognized as active mediators of these disorders, and the implication of tumor necrosis factor (TNF) has been frequently discussed in the recent past. However, the identity of the active agent in alterations of protein metabolism is still controversial. To improve our understanding of the role of cytokines in mediating muscle wasting observed in sepsis, we investigated muscle and liver protein metabolism in the following three groups of rats: infected control rats (INF-C); infected rats pretreated with pentoxifylline (PTX-INF), which is a potent inhibitor of TNF secretion; and pair-fed rats for the PTX-INF group pretreated with pentoxifylline. Pentoxifylline nearly completely suppressed TNF secretion but did not influence the transient fall in rectal temperature, the decreased hematocrit, and the increased liver protein mass and synthesis observed in INF-C rats. Pentoxifylline decreased the anorexia, the loss of body weight and muscle protein observed in INF-C animals, and partially prevented the decrease in muscle protein synthesis induced by infection. The overall data indicate that pentoxifylline is an effective agent in mitigating the characteristic muscle protein wasting induced by sepsis and confirm the limited role of TNF in the mediation of the acute-phase protein synthesis. Our results suggest a probable implication of TNF in the regulation of protein balance in muscle but do not allow discarding possible implication of other mediators that would be inhibited by pentoxifylline.

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