Leaf Responses of Micropropagated Apple Plants to Water Stress: Changes in Endogenous Hormones and Their Influence on Carbohydrate Metabolism

2007 ◽  
Vol 6 (1) ◽  
pp. 58-67 ◽  
Author(s):  
Tian-hong LI ◽  
Shao-hua LI
2008 ◽  
Vol 47 (3) ◽  
pp. 407-416 ◽  
Author(s):  
C. Saint Pierre ◽  
C.J. Peterson ◽  
A.S. Ross ◽  
J.B. Ohm ◽  
M.C. Verhoeven ◽  
...  

2016 ◽  
Vol 59 (2) ◽  
pp. 121-132 ◽  
Author(s):  
Yuanyuan Miao ◽  
Zaibiao Zhu ◽  
Qiaosheng Guo ◽  
Xiaohua Yang ◽  
Li Liu ◽  
...  

2011 ◽  
Vol 72 (8) ◽  
pp. 723-729 ◽  
Author(s):  
Eva Sánchez-Rodríguez ◽  
Diego A. Moreno ◽  
Federico Ferreres ◽  
María del Mar Rubio-Wilhelmi ◽  
Juan Manuel Ruiz

2020 ◽  
Vol 49 (4) ◽  
pp. 42-50
Author(s):  
N. B. Gubergrits ◽  
N. V. Byelyayeva ◽  
T. L. Mozhyna

Non-alcoholic fatty liver disease (NAFLD) and non-alcoholic fatty pancreatic disease (NAFPD) develop against the background of metabolic syndrome, systemic insulin resistance, oxidative stress, changes in lipid and carbohydrate metabolism. There are a number of similarities between NAFLD and NAFPD: the natural course of diseases proceeds from steatosis through inflammation to fibrosis and cancer, one of the etiopathogenetic factors is the disbalance of bile acids synthesis and low expression of farnesoid receptor X (FXR). One of the possible methods of treatment NAFLD and NAFPD is a correction of the biosynthesis of bile acids and increase FXR expression with FXR agonists. Ursodeoxycholic acid (UDCA) is a selective FXR agonist. It has a multipled spectrum of actions: anticholestatic, anti-apoptic, antioxidant, cytoprotective, antifibrotic, hypocholesterolemic, immunomodulatory, hepatoprotective. The ability of UDCA correct lipid and carbohydrate metabolism in combination with anti-inflammatory and antiapoptic effects may be of great importance for the treatment of NAFLD and NAFPD. The article reviews the results of clinical and experimental studies describing the efficacy of UDCA in NAFLD and some pancreatic diseases. It has been suggested that the therapy of UDCA can reduce the severity of NAFLD and NAFPDand improve the functional activity of hepatocytes and β cells. The need for randomized clinical trials was emphasized in order to make an informed decision on the expediency of including UDCA in the treatment of NAFLD and NAFPD.


2005 ◽  
Vol 32 (11) ◽  
pp. 1033 ◽  
Author(s):  
Dorthe Villadsen ◽  
Jesper Henrik Rung ◽  
Tom Hamborg Nielsen

Carbohydrate metabolism was investigated in barley leaves subjected to drought or osmotic stress induced by sorbitol incubation. Both drought and osmotic stress resulted in accumulation of hexoses, depletion of sucrose and starch, and 5–10-fold increase in the level of the regulatory metabolite fructose-2,6-bisphosphate (Fru-2,6-P2). These changes were paralleled by an increased activity ratio of fructose-6-phosphate,2-kinase / fructose-2,6-bisphosphatase (F2KP). The drought-induced changes in carbohydrate content and Fru-2,6-P2 metabolism were reversed upon re-watering. This reveals a reversible mechanism for modification of the F2KP enzyme activity. This suggests that F2KP might be involved in altering carbohydrate metabolism during osmotic stress. However, labelling with [14C]-CO2 showed that sucrose synthesis was not inhibited, despite the increased Fru-2,6-P2 levels, and demonstrated that increased flux into the hexose pools probably derived from sucrose hydrolysis. Similar effects of osmotic stress were observed in leaf sections incubated in the dark, showing that the changes did not result from altered rates of photosynthesis. Metabolism of [14C]-sucrose in the dark also revealed increased flux into hexoses and reduced flux into starch in response to osmotic stress. The activities of a range of enzymes catalysing reactions of carbohydrate metabolism in general showed only a marginal decrease during osmotic stress. Therefore, the observed changes in metabolic flux do not rely on a change in the activity of the analysed enzymes. Fructose-2,6-bisphosphate metabolism responds strongly to drought stress and this response involves modification of the F2KP activity. However, the data also suggests that the sugar accumulation observed during osmotic stress is mainly regulated by another, as yet unidentified mechanism.


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