Effects of dietary carbohydrate levels on growth, glucose tolerance, glucose homeostasis and GLUT4 gene expression in Tilapia nilotica

2018 ◽  
Vol 49 (12) ◽  
pp. 3735-3745 ◽  
Author(s):  
Hong-Yu Liu ◽  
Qiang Chen ◽  
Bei-Ping Tan ◽  
Xiao-Hui Dong ◽  
Shu-Yan Chi ◽  
...  
2004 ◽  
Vol 36 (Supplement) ◽  
pp. S327
Author(s):  
Yi Hung Liao ◽  
Chia Hua Kuo ◽  
Henrich Cheng ◽  
Yu Min Cho ◽  
Hui Wen Hsieh ◽  
...  

2004 ◽  
Vol 36 (Supplement) ◽  
pp. S327
Author(s):  
Yi Hung Liao ◽  
Chia Hua Kuo ◽  
Henrich Cheng ◽  
Yu Min Cho ◽  
Hui Wen Hsieh ◽  
...  

2013 ◽  
Vol 218 (1) ◽  
pp. 85-97 ◽  
Author(s):  
Thin Xuan Vo ◽  
Andrew Revesz ◽  
Gurjeev Sohi ◽  
Noelle Ma ◽  
Daniel B Hardy

Epidemiological studies demonstrate that the link between impaired fetal development and glucose intolerance in later life is exacerbated by postnatal catch-up growth. Maternal protein restriction (MPR) during pregnancy and lactation in the rat has been previously demonstrated to lead to impaired glucose tolerance in adulthood, however the effects of protein restoration during weaning on glucose homeostasis are largely unknown. Recentin vitrostudies have identified that the liver X receptor α (LXRα) maintains glucose homeostasis by inhibiting critical genes involved in gluconeogenesis includingG6pase(G6pc),11β-Hsd1(Hsd11b1) andPepck(Pck1). Therefore, we hypothesized that MPR with postnatal catch-up growth would impair LXRαin vivo, which in turn would lead to augmented gluconeogenic LXRα-target gene expression and glucose intolerance. To examine this hypothesis, pregnant Wistar rats were fed a control (20%) protein diet (C) or a low (8%) protein diet during pregnancy and switched to a control diet at birth (LP). At 4 months, the LP offspring had impaired glucose tolerance. In addition, LP offspring had decreased LXRα expression, while hepatic expression of 11β-HSD1 and G6Pase was significantly higher. This was concomitant with decreased binding of LXRα to the putative LXRE on11β-Hsd1andG6pase. Finally, we demonstrated that the acetylation of histone H3 (K9,14) surrounding the transcriptional start site of hepaticLxrα(Nr1h3) was decreased in LP offspring, suggesting MPR-induced epigenetic silencing of theLxrαpromoter. In summary, our study demonstrates for the first time the important role of LXRα in mediating enhanced hepatic gluconeogenic gene expression and consequent glucose intolerance in adult MPR offspring.


Endocrinology ◽  
2010 ◽  
Vol 151 (11) ◽  
pp. 5174-5184 ◽  
Author(s):  
Camella G. Wilson ◽  
Michael Schupp ◽  
Brant R. Burkhardt ◽  
Jianmei Wu ◽  
Robert A. Young ◽  
...  

The pancreas-derived hormones, insulin and glucagon, are the two main regulators of glucose homeostasis. However, their actions can be modulated by the presence of other circulating factors including cytokines. Pancreatic-derived factor (PANDER) is a novel cytokine-like molecule secreted from the endocrine pancreas, but its biological function is currently unknown. To address this, we employed adenoviral gene delivery to develop a novel murine model of PANDER overexpression, which we used to study PANDER’s effect on glucose homeostasis. Although serum metabolites in fed mice were unaffected by PANDER overexpression, fasting glucose, insulin, and corticosterone levels were significantly elevated. Additionally, PANDER-overexpressing mice displayed elevated glucose and insulin levels during a glucose tolerance test, indicating that glucose tolerance was impaired. However, there were no defects in glucose-stimulated insulin secretion or peripheral insulin sensitivity. Elevated transcription of hepatic gluconeogenic genes, PEPCK and G6Pase accompanied the fasting hyperglycemia observed in PANDER-overexpressing animals. Similarly, treatment of primary hepatocytes with PANDER-expressing adenovirus or PANDER-enriched conditioned medium elevated gluconeogenic gene expression and glucose output. PANDER treatment also resulted in higher levels of Ser133-phosphorylated cAMP-response element-binding protein in hepatocytes stimulated with 8-bromo-cAMP and dexamethasone and higher levels of intracellular cAMP upon stimulation with forskolin. In summary, we provide the first report that identifies PANDER as a regulator of hepatic glucose metabolism, where it serves as a novel factor that amplifies hepatic cAMP and cAMP-response element-binding protein signaling to induce gluconeogenic gene expression and glucose output.


2009 ◽  
Vol 33 (2) ◽  
pp. 289-295 ◽  
Author(s):  
Yi HU ◽  
Bei-Ping TAN ◽  
Kang-Sen MAI ◽  
Qing-Hui AI ◽  
Shi-Xuan ZHENG ◽  
...  

Diabetologia ◽  
1993 ◽  
Vol 36 (6) ◽  
pp. 503-509 ◽  
Author(s):  
J. Maury ◽  
T. Issad ◽  
D. Perdereau ◽  
B. Gouhot ◽  
P. Ferré ◽  
...  

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