The effects of epidermal growth factor administration ways on glycogen metabolism and blood glucose levels

1998 ◽  
Vol 5 ◽  
pp. 72
Author(s):  
H. Sayan ◽  
B. Gönül ◽  
A. Türkyýlmaz ◽  
N. Çelebi
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Glycogen Metabolism ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Epidermal Growth

scholarly journals Epidermal growth factor counteracts the glycogenic effect of insulin in parenchymal hepatocyte cultures

1987 ◽  
Vol 247 (2) ◽  
pp. 307-314 ◽  
Author(s):  
M H Chowdhury ◽  
L Agius
Keyword(s):  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Epithelial Cells ◽  
Cyclic Amp ◽  
Glycogen Metabolism ◽  
Metabolic Effects ◽  
Hepatocyte Cultures ◽  
Glucose Incorporation ◽  
Epidermal Growth ◽  
Parenchymal Hepatocytes

Rat parenchymal hepatocytes in monolayer culture were used to study the metabolic effects of epidermal growth factor (EGF) and insulin on ketogenesis, gluconeogenesis and glycogen metabolism. EGF, unlike insulin, did not inhibit ketogenesis from palmitate or gluconeogenesis from pyruvate in hepatocyte cultures. It also had no effect on these pathways in the presence of insulin. In contrast, EGF potently counteracted the stimulation of [14C]pyruvate incorporation into glycogen by insulin, and also glycogen deposition from both gluconeogenic precursors and glucose. The EGF concentration causing half-maximal effect was about 0.1 nM. The anti-glycogenic effect of EGF was observed after both long-term (24 h) and short-term (1 h) exposure to EGF, and was more marked in the presence of insulin than in its absence. EGF did not displace bound insulin, suggesting that it neither competes for the insulin receptor nor affects the affinity of the receptor for insulin. EGF did not alter cellular cyclic AMP; and inhibition of cyclic AMP phosphodiesterase activity did not prevent the anti-glycogenic effect of EGF. In liver-derived dividing epithelial cells, Hep-G2 cells and fibroblasts, which have no capacity for gluconeogenesis, EGF did not counteract the stimulatory effect of insulin on [14C]glucose incorporation into glycogen, and in the epithelial cells EGF increased [14C]glucose incorporation into glycogen. The counter-effect of EGF on the glycogenic action of insulin in parenchymal hepatocytes may be due to a direct effect on glycogen metabolism or to an interaction with the post-receptor events in insulin action.

INSULIN-LIKE GROWTH FACTOR-BINDING PROTEIN-1 MODULATES BLOOD GLUCOSE LEVELS

Endocrinology ◽  
1991 ◽  
Vol 129 (4) ◽  
pp. 2254-2256 ◽  
Author(s):  
Moira S. Lewitt ◽  
Gareth S. Denyerf ◽  
Gregory Cooney J ◽  
Robert C. Baxter
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Glucose Levels ◽  
Blood Glucose Levels

scholarly journals Omeprazole and PGC-Formulated Heparin Binding Epidermal Growth Factor Normalizes Fasting Blood Glucose and Suppresses Insulitis in Multiple Low Dose Streptozotocin Diabetes Model

2013 ◽  
Vol 30 (11) ◽  
pp. 2843-2854 ◽  
Author(s):  
Gerardo M. Castillo ◽  
Akiko Nishimoto-Ashfield ◽  
Aryamitra A. Banerjee ◽  
Jennifer A. Landolfi ◽  
Alexander V. Lyubimov ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Epidermal Growth Factor ◽  
Low Dose ◽  
Fasting Blood Glucose ◽  
Streptozotocin Diabetes ◽  
Heparin Binding ◽  
Diabetes Model ◽  
Epidermal Growth

scholarly journals Liraglutide Suppresses Obesity and Hyperglycemia Associated with Increases in Hepatic Fibroblast Growth Factor 21 Production in KKAyMice

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Katsunori Nonogaki ◽  
Miki Hazama ◽  
Noriko Satoh
Keyword(s):  
Body Weight ◽  
Blood Glucose ◽  
Growth Factor ◽  
Food Intake ◽  
Fibroblast Growth Factor ◽  
Fold Increase ◽  
Systemic Administration ◽  
Fibroblast Growth ◽  
Glucose Levels ◽  
Blood Glucose Levels

Social isolation contributes to the development of obesity and insulin-independent diabetes in KKAymice. Here we show that systemic administration of liraglutide, a long-acting human glucagon-like peptide-1 (GLP-1) analog, significantly decreased food intake, body weight, and blood glucose levels at 24 h after its administration while having no significant effects on plasma insulin and glucagon levels in individually housed KKAymice. In addition, the systemic administration of liraglutide significantly increased plasma fibroblast growth factor (Fgf) 21 levels (1.8-fold increase) associated with increases in the expression of hepaticFgf21(1.9-fold increase) andPparγ(1.8-fold increase), while having no effects on the expression of hepaticPparαandFgf21in white adipose tissue. Moreover, systemic administration of liraglutide over 3 days significantly suppressed food intake, body weight gain, and hyperglycemia in KKAymice. On the other hand, despite remarkably increased plasma active GLP-1 levels (4.2-fold increase), the ingestion of alogliptin, a selective dipeptidyl peptidase-4 inhibitor, over 3 days had no effects on food intake, body weight, blood glucose levels, and plasma Fgf21 levels in KKAymice. These findings suggest that systemic administration of liraglutide induces hepatic Fgf21 production and suppresses the social isolation-induced obesity and diabetes independently of insulin, glucagon, and active GLP-1 in KKAymice.

scholarly journals Oral administration of insulin-like growth factor-I from colostral whey reduces blood glucose in streptozotocin-induced diabetic mice

2011 ◽  
Vol 108 (1) ◽  
pp. 39-45 ◽  
Author(s):  
Kyung-A Hwang ◽  
Yu-Jin Hwang ◽  
Woelkyu Ha ◽  
Young-Kug Choo ◽  
Kisung Ko
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Oral Administration ◽  
Insulin Like Growth Factor ◽  
Diabetic Mice ◽  
Glucose Levels ◽  
Factor I ◽  
Blood Glucose Levels ◽  
Igf I ◽  
Growth Factor I

The aim of the present study was to investigate the effects of oral administration of the insulin-like growth factor-I-rich fraction (IGF-I-RF) from bovine colostral whey on the regulation of blood glucose levels in streptozotocin (STZ)-induced diabetic mice. We obtained a peptide fraction containing IGF-I (10 ng/mg protein) from Holstein colostrum within 24 h after parturition by using ultrafiltration. The blood glucose levels of STZ-induced diabetic mice fed with IGF-I-RF (50 μg/kg per d) were significantly reduced by 11 and 33 % at weeks 2 and 4, respectively (P < 0·05). The body weights of STZ-induced diabetic mice increased following the oral administration of the IGF-I-RF. The kidney weights of STZ-induced diabetic mice decreased significantly (P < 0·05) following the administration of the IGF-I-RF, and the liver weights of STZ-induced diabetic mice decreased significantly (P < 0·05) following the administration of 50 μg/kg per d of the IGF-I-RF. The present results indicate that the IGF-I-RF obtained from Holstein colostrum could be a useful component for an alternative therapeutic modality for the treatment of diabetes in insulin-resistant patients.

scholarly journals RTEF-1 Attenuates Blood Glucose Levels by Regulating Insulin-Like Growth Factor Binding Protein-1 in the Endothelium

2012 ◽  
Vol 111 (8) ◽  
pp. 991-1001 ◽  
Author(s):  
Angela F. Messmer-Blust ◽  
Melissa J. Philbrick ◽  
Shuzhen Guo ◽  
Jiaping Wu ◽  
Ping He ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Growth Factor ◽  
Binding Protein ◽  
Insulin Like Growth Factor ◽  
Factor Binding ◽  
Glucose Levels ◽  
Blood Glucose Levels

scholarly journals Nrf2-Mediated Regulation of Skeletal Muscle Glycogen Metabolism

2016 ◽  
Vol 36 (11) ◽  
pp. 1655-1672 ◽  
Author(s):  
Akira Uruno ◽  
Yoko Yagishita ◽  
Fumiki Katsuoka ◽  
Yasuo Kitajima ◽  
Aki Nunomiya ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Glucose ◽  
Muscle Glycogen ◽  
Glycogen Content ◽  
Glycogen Metabolism ◽  
C2c12 Myotubes ◽  
Branching Enzyme ◽  
Glucose Levels ◽  
Blood Glucose Levels ◽  
Glycogen Branching Enzyme

Nrf2 (NF-E2-related factor 2) contributes to the maintenance of glucose homeostasisin vivo. Nrf2 suppresses blood glucose levels by protecting pancreatic β cells from oxidative stress and improving peripheral tissue glucose utilization. To elucidate the molecular mechanisms by which Nrf2 contributes to the maintenance of glucose homeostasis, we generated skeletal muscle (SkM)-specificKeap1knockout (Keap1MuKO) mice that express abundant Nrf2 in their SkM and then examined Nrf2 target gene expression in that tissue. InKeap1MuKOmice, blood glucose levels were significantly downregulated and the levels of the glycogen branching enzyme (Gbe1) and muscle-type PhKα subunit (Phka1) mRNAs, along with those of the glycogen branching enzyme (GBE) and the phosphorylasebkinase α subunit (PhKα) protein, were significantly upregulated in mouse SkM. Consistent with this result, chemical Nrf2 inducers promotedGbe1andPhka1mRNA expression in both mouse SkM and C2C12 myotubes. Chromatin immunoprecipitation analysis demonstrated that Nrf2 binds theGbe1andPhka1upstream promoter regions. InKeap1MuKOmice, muscle glycogen content was strongly reduced and forced GBE expression in C2C12 myotubes promoted glucose uptake. Therefore, our results demonstrate that Nrf2 induction in SkM increases GBE and PhKα expression and reduces muscle glycogen content, resulting in improved glucose tolerance. Our results also indicate that Nrf2 differentially regulates glycogen metabolism in SkM and the liver.

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