scholarly journals Remodeling of protein and mRNA expression in Leishmania mexicana induced by deletion of glucose transporter genes

2011 ◽  
Vol 175 (1) ◽  
pp. 39-48 ◽  
Author(s):  
Xiuhong Feng ◽  
Torben Feistel ◽  
Cosmo Buffalo ◽  
Ashley McCormack ◽  
Elizabeth Kruvand ◽  
...  
2020 ◽  
Author(s):  
Ke-ke Qi ◽  
Jie Wu ◽  
Wen-Jun Zhou ◽  
Bo Deng ◽  
Xiao-ming Men ◽  
...  

Abstract Background Intrauterine growth restriction (IUGR) results in abnormal morphology and gastrointestinal function. As a gastrointestinal growth factor, the manner by which the porcine glucagon-like peptide-2 (pGLP-2) microsphere administration catches up with the growth of IUGR piglets was investigated. Methods Fourteen newborn IUGR piglets were assigned into the IUGR and pGLP-2 microsphere groups. The piglets in the pGLP-2 microsphere group were intraperitoneally administered with 100 mg of pGLP-2 microspheres on day 1 of birth. Results From days 15 to 26 of trial, the body weight of the IUGR piglets treated with pGLP-2 microspheres was significantly higher than that in the control group. Importantly, the weaning weight in the pGLP-2 group catches up with the body weight of normal birth weight piglets. IUGR piglets treated with pGLP-2 microspheres significantly showed increased pancreas weight, serum insulin content, and activities of digestive enzymes (lipase, trypsin, chymotrypsin, and amylase). Injection of pGLP-2 microspheres returned the intestinal absorptive capacity by significantly increasing the mRNA expression of sodium-glucose cotransporter 1 in the jejunum, glucose transporter type 2 in the duodenum and jejunum, H + -coupled transporter, and peptide transporter 1 in the jejunum and ileum. It also returned the redox balance by increasing the catalase mRNA expression and decreasing the heat shock protein 70 mRNA expression. In addition, this improvement was associated with the significant increase in gut diameter, length, and weight induced by pGLP-2. Conclusions Injection of pGLP-2 microspheres was a suitable therapeutic strategy for compensatory growth in low birth weight IUGR piglet.


2005 ◽  
Vol 17 (8) ◽  
pp. 775 ◽  
Author(s):  
Hiemke M. Knijn ◽  
Christine Wrenzycki ◽  
Peter J. M. Hendriksen ◽  
Peter L. A. M. Vos ◽  
Elly C. Zeinstra ◽  
...  

Bovine blastocysts produced in vitro differ substantially from their in vivo-derived counterparts with regard to glucose metabolism, level of apoptosis and mRNA expression patterns. Maternal embryonic genomic transition is a critical period in which these changes could be induced. The goals of the present study were twofold: (1) to identify the critical period of culture during which the differences in expression of gene transcripts involved in glucose metabolism are induced; and (2) to identify gene transcripts involved in apoptosis that are differentially expressed in in vitro- and in vivo-produced blastocysts. Relative abundances of transcripts for the glucose transporters Glut-1, Glut-3, Glut-4 and Glut-8, and transcripts involved in the apoptotic cascade, including BAX, BCL-XL, XIAP and HSP 70.1, were analysed by a semiquantitative reverse transcription–polymerase chain reaction assay in single blastocysts produced in vitro or in vivo for specific time intervals, that is, before or after maternal embryonic transition. Whether the culture environment was in vitro or in vivo affected the expression of glucose transporter transcripts Glut-3, Glut-4 and Glut-8. However, the critical period during culture responsible for these changes, before or after maternal embryonic transition, could not be determined. With the exception of XIAP, no effects of culture system on the mRNA expression patterns of BAX, BCL-XL and HSP 70.1 could be observed. These data show that expression of XIAP transcripts in expanded blastocysts is affected by in vitro culture. These findings add to the list of bovine genes aberrantly expressed in culture conditions, but do not support the hypothesis that maternal embryonic transition is critical in inducing the aberrations in gene expression patterns studied here.


2015 ◽  
Vol 2015 ◽  
pp. 1-12 ◽  
Author(s):  
Wenting Lin ◽  
Wenxiang Wang ◽  
Dongdong Liao ◽  
Damiao Chen ◽  
Pingping Zhu ◽  
...  

This study investigated the effects of polysaccharides fromEnteromorpha prolifera(PEP) on glucose metabolism in a rat model of diabetes mellitus (DM). PEP (0, 150, 300, and 600 mg/kg) was administered intragastrically to rats for four weeks. After treatment, fasting blood glucose (FBG) and insulin (INS) levels were measured, and the insulin sensitivity index (ISI) was calculated. The morphopathological changes in the pancreas were observed. Serum samples were collected to measure the oxidant-antioxidant status. The mRNA expression levels of glucokinase (GCK) and insulin receptor (InsR) in liver tissue and glucose transporter type 4 (GLUT-4) and adiponectin (APN) in adipose tissue were determined. Compared with the model group, the FBG and INS levels were lower, the ISI was higher, and the number of isletβ-cells was significantly increased in all the PEP groups. In the medium- and high-dose PEP groups, MDA levels decreased, and the enzymatic activities of SOD and GSH-Px increased. The mRNA expression of InsR and GCK increased in all the PEP groups; APN mRNA expression increased in the high-dose PEP group, and GLUT-4 mRNA expression increased in adipose tissue. These findings suggest that PEP is a potential therapeutic agent that can be utilized to treat DM.


1999 ◽  
Vol 54 (5) ◽  
pp. B183-B188 ◽  
Author(s):  
K. Hotta ◽  
N. L. Bodkin ◽  
T. A. Gustafson ◽  
S. Yoshioka ◽  
H. K. Ortmeyer ◽  
...  

Author(s):  
Katarina Hadova ◽  
Lucia Mesarosova ◽  
Eva Kralova ◽  
Gabriel Doka ◽  
Peter Krenek ◽  
...  

Tyrosine kinases inhibitors (TKIs) may alter glycaemia and may be cardiotoxic with importance in diabetic heart. We investigated the effect of multi-TKI crizotinib after short-term administration on metabolic modulators of the heart of diabetic rats. Experimental diabetes mellitus (DM) was induced by streptozotocin (STZ; 80 mg/kg, i.p.), controls received vehicle (CON). Three days after STZ, crizotinib (STZ+CRI; 25 mg/kg/day p.o.) or vehicle was administered for 7 days. Blood glucose, C-peptide and glucagon were assessed in plasma samples. Receptor tyrosine kinases (RTKs), cardiac glucose transporters and PPARs were determined in rat left ventricle by RT-qPCR method. Crizotinib moderately reduced blood glucose (by 25%, P<0.05) when compared to STZ rats. The drug did not affect levels of C-peptide, an indicator of insulin secretion, suggesting altered tissue glucose utilization. Crizotinib had no impact on cardiac RTKs. However, an mRNA downregulation of insulin-dependent glucose transporter Glut4 in hearts of STZ rats was attenuated after crizotinib treatment. Moreover, crizotinib normalized Ppard and reduced Pparg mRNA expression in diabetic hearts. Crizotinib decreased blood glucose independently of insulin and glucagon. This could be related to changes in regulators of cardiac metabolism such as GLUT4 and PPARs.


2009 ◽  
Vol 23 (6) ◽  
pp. 914-924 ◽  
Author(s):  
Jeffrey S. Davies ◽  
Pia Kotokorpi ◽  
Sinan R. Eccles ◽  
Sarah K. Barnes ◽  
Paweł F. Tokarczuk ◽  
...  

Abstract Circulating ghrelin elevates abdominal adiposity by a mechanism independent of its central orexigenic activity. In this study we tested the hypothesis that peripheral ghrelin induces a depot-specific increase in white adipose tissue (WAT) mass in vivo by GH secretagogue receptor (GHS-R1a)-mediated lipolysis. Chronic iv infusion of acylated ghrelin increased retroperitoneal and inguinal WAT volume in rats without elevating superficial sc fat, food intake, or circulating lipids and glucose. Increased retroperitoneal WAT mass resulted from adipocyte enlargement probably due to reduced lipid export (ATP-binding cassette transporter G1 mRNA expression and circulating free fatty acids were halved by ghrelin infusion). In contrast, ghrelin treatment did not up-regulate biomarkers of adipogenesis (peroxisome proliferator-activated receptor-γ2 or CCAAT/enhancer binding protein-α) or substrate uptake (glucose transporter 4, lipoprotein lipase, or CD36) and although ghrelin elevated sterol-regulatory element-binding protein 1c expression, WAT-specific mediators of lipogenesis (liver X receptor-α and fatty acid synthase) were unchanged. Adiposity was unaffected by infusion of unacylated ghrelin, and the effects of acylated ghrelin were abolished by transcriptional blockade of GHS-R1a, but GHS-R1a mRNA expression was similar in responsive and unresponsive WAT. Microarray analysis suggested that depot-specific sensitivity to ghrelin may arise from differential fine tuning of signal transduction and/or lipid-handling mechanisms. Acylated ghrelin also induced hepatic steatosis, increasing lipid droplet number and triacylglycerol content by a GHS-R1a-dependent mechanism. Our data imply that, during periods of energy insufficiency, exposure to acylated ghrelin may limit energy utilization in specific WAT depots by GHS-R1a-dependent lipid retention.


2010 ◽  
Vol 105 (3) ◽  
pp. 329-338 ◽  
Author(s):  
Alannah D. Maurer ◽  
Raylene A. Reimer

Risk of developing the metabolic syndrome may be influenced by nutritional environment early in life. We examined the effects of high-fibre (HF) and high-protein (HP) diets consumed during pregnancy and lactation on satiety hormones and expression of genes involved in glucose and lipid metabolism in offspring. Wistar dams were fed a control (C), HF or HP diets during pregnancy and lactation. At parturition, litters were culled to ten pups. At 21 d, all pups were weaned onto C diet. At 7, 14, 21, 28 and 35 d after birth, blood was analysed for satiety hormones and tissues for mRNA expression in offspring. No differences were observed in litter size or birth weight. At 21 d, offspring of HF dams had greater adjusted intestinal mass and lower liver weight than those of C but not of HP dams. Plasma glucose at 28 d and amylin at 7, 14 and 28 d were lower in HF v. C and HP offspring. Glucagon-like peptide-1 was higher in HP offspring than in HF offspring at 7 d but was higher in HF v. C offspring at 21 d. Offspring of HF dams had higher glucose transporter (GLUT2 and Na+-dependent glucose/galactose transporter) mRNA expression at 21 d v. C and HP offspring. In brown adipose tissue, HF and HP up-regulated uncoupling protein-1 and PPAR-γ coactivator. HP was associated with increased resistin and IL-6 mRNA expression. The present study demonstrates that maternal diet composition differentially regulates circulating satiety hormones and genes involved in glucose transport and energy metabolism in offspring. These early changes could have long-term consequences for obesity risk.


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