Defect in insulin action on expression of the muscle/adipose tissue glucose transporter gene in skeletal muscle of type 1 diabetic patients

1992 ◽  
Vol 75 (3) ◽  
pp. 795-799 ◽  
Author(s):  
H. Yki-Jarvinen
Keyword(s):  
Skeletal Muscle ◽  
Adipose Tissue ◽  
Insulin Action ◽  
Glucose Transporter ◽  
Diabetic Patients ◽  
Transporter Gene ◽  
Type 1 Diabetic Patients

Insulin signal transduction in human skeletal muscle: identifying the defects in Type II diabetes

2005 ◽  
Vol 33 (2) ◽  
pp. 354-357 ◽  
Author(s):  
M. Björnholm ◽  
J.R. Zierath
Keyword(s):  
Skeletal Muscle ◽  
Type Ii Diabetes ◽  
Insulin Action ◽  
Glucose Transporter ◽  
Whole Body ◽  
Diabetic Patients ◽  
Type Ii ◽  
Peripheral Tissues ◽  
Glucose Homoeostasis ◽  
Insulin Receptor Signalling

Type II diabetes is characterized by defects in insulin action on peripheral tissues, such as skeletal muscle, adipose tissue and liver and pancreatic β-cell defects. Since the skeletal muscle accounts for approx. 75% of whole body insulin-stimulated glucose uptake, defects in this tissue play a major role in the impaired glucose homoeostasis in Type II diabetic patients. Thus identifying defective steps in this process may reveal attractive targets for drug development to combat insulin resistance and Type II diabetes. This review will describe the effects of insulin on glucose transport and other metabolic events in skeletal muscle that are mediated by intracellular signalling cascades. Evidence for impaired activation of the insulin receptor signalling cascade and defective glucose transporter 4 translocation in the skeletal muscle from Type II diabetic patients will be presented. Through the identification of the intracellular defects in insulin action that control glucose homoeostasis, a better understanding of the disease pathogenesis can be gained and strategies for intervention may be developed.

scholarly journals Skeletal muscle gene transcript changes in type 1 diabetic patients following insulin deprivation

2007 ◽  
Vol 21 (5) ◽  
Author(s):  
Helen Karakelides ◽  
Yan Asmann ◽  
Maureen Bigelow ◽  
Kevin R Short ◽  
Ketan Dhatariya ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Diabetic Patients ◽  
Gene Transcript ◽  
Muscle Gene ◽  
Type 1 Diabetic Patients

C-peptide improves adenosine-induced myocardial vasodilation in type 1 diabetes patients

2004 ◽  
Vol 286 (1) ◽  
pp. E14-E19 ◽  
Author(s):  
Bo-Lennart Johansson ◽  
Jan Sundell ◽  
Karin Ekberg ◽  
Cathrine Jonsson ◽  
Marko Seppänen ◽  
...  
Keyword(s):  
Skeletal Muscle ◽  
Blood Flow ◽  
Type 1 Diabetes ◽  
Muscle Blood Flow ◽  
Left Ventricular ◽  
Diabetic Patients ◽  
Skeletal Muscle Blood Flow ◽  
C Peptide ◽  
Type 1 Diabetic Patients

Patients with type 1 (insulin-dependent) diabetes show reduced skeletal muscle blood flow and coronary vasodilatory function despite intensive insulin therapy and good metabolic control. Administration of proinsulin C-peptide increases skeletal muscle blood flow in these patients, but a possible influence of C-peptide on myocardial vasodilatory function in type 1 diabetes has not been investigated. Ten otherwise healthy young male type 1 diabetic patients (Hb A1c 6.6%, range 5.7-7.9%) were studied on two consecutive days during normoinsulinemia and euglycemia in a double-blind, randomized, crossover design, receiving intravenous infusion of C-peptide (5 pmol·kg-1·min-1) for 120 min on one day and saline infusion on the other day. Myocardial blood flow (MBF) was measured at rest and during adenosine administration (140 μg·kg-1·min-1) both before and during the C-peptide or saline infusions by use of positron emission tomography and [15O]H2O administration. Basal MBF was not significantly different in the patients compared with an age-matched control group, but adenosine-induced myocardial vasodilation was 30% lower ( P < 0.05) in the patients. During C-peptide administration, adenosine-stimulated MBF increased on average 35% more than during saline infusion ( P < 0.02) and reached values similar to those for the healthy controls. Moreover, as evaluated from transthoracal echocardiographic measurements, C-peptide infusion resulted in significant increases in both left ventricular ejection fraction (+5%, P < 0.05) and stroke volume (+7%, P < 0.05). It is concluded that short-term C-peptide infusion in physiological amounts increases the hyperemic MBF and left-ventricular function in type 1 diabetic patients.

Exercise reduces muscle glucose transport protein (GLUT-4) mRNA in type 1 diabetic patients

1993 ◽  
Vol 74 (4) ◽  
pp. 1755-1760 ◽  
Author(s):  
V. A. Koivisto ◽  
R. E. Bourey ◽  
H. Vuorinen-Markkola ◽  
L. Koranyi
Keyword(s):  
Acute Exercise ◽  
Glucose Transporter ◽  
Glycosylated Hemoglobin ◽  
Insulin Dose ◽  
Diabetic Patients ◽  
Control Subjects ◽  
Glut 4 ◽  
Ergometer Exercise ◽  
Type 1 Diabetic Patients

We examined the effect of acute exercise on muscle glucose transporter (GLUT-4) protein and mRNA concentrations in nine male type 1 diabetic patients (age 31 +/- 3 yr, body mass index 23.6 +/- 0.7 kg/m2, insulin dose 44 +/- 4 U/day, glycosylated hemoglobin 7.8 +/- 0.4%) and in nine healthy control subjects (34 +/- 1 yr, 25.3 +/- 0.8 kg/m2). Three hours of cycle ergometer exercise was performed after an overnight fast. A needle biopsy (100–150 mg) was taken from the quadriceps femoris 40 min before and immediately after the end of exercise. During exercise, plasma glucose, insulin, cortisol, and growth hormone concentrations were higher in the diabetic patients than in the control subjects. In the basal state, GLUT-4 protein and mRNA concentrations were similar in the two groups. During exercise, GLUT-4 mRNA concentration decreased by 30–45% in the diabetic patients but remained unchanged in the control subjects. GLUT-4 protein content remained unchanged in both groups. These data suggest an abnormal GLUT-4 mRNA production or degradation or both in type 1 diabetic patients during physical exercise.

scholarly journals Taurine Transporter Gene Expression in Mononuclear Blood Cells of Type 1 Diabetes Patients

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Zaleida Napoli ◽  
Giuseppe Seghieri ◽  
Loria Bianchi ◽  
Roberto Anichini ◽  
Alessandra De Bellis ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Plasma Homocysteine ◽  
Diabetic Patients ◽  
Transporter Gene ◽  
Taurine Transporter ◽  
Markers Of Oxidative Stress ◽  
Type 1 Diabetic Patients ◽  
Diabetes Patients

Background. Taurine transporter gene expression (RNA-TauT) has a role in retinal cell function and is modulatedin vitroandin vivoby hyperglycemia and/or oxidative stress. This study was aimed at testing whether RNA-TauT gene expression is modified in blood mononuclear peripheral cells (MPCs) of type 1 diabetic patients, is related to plasma markers of oxidative stress or endothelial dysfunction, or, finally, is related to presence of retinopathy.Methods. RNA-TauT was measured in MPCs by real-time PCR-analysis in 35 type 1 diabetic patients and in 33 age- and sex-matched controls, additionally measuring plasma and cell taurine and markers of oxidative stress and endothelial dysfunction.Results. RNA-TauT, expressed as2-ΔΔCt, was significantly higher in MPCs of type 1 diabetic patients than in controls [median (interquartile range): 1.32(0.31) versus 1.00(0.15);P=0.01]. In diabetic patients RNA-TauT was related to HbA1c (r=0.42;P=0.01) and inversely to plasma homocysteine (r=-0.39;P=0.02) being additionally significantly higher in MPCs of patients without retinopathy [(n=22); 1.36(0.34)] compared to those with retinopathy [(n=13); 1.16(0.20)], independently from HbA1c or diabetes duration.Conclusions. RNA-TauT gene expression is significantly upregulated in MPCs of type 1 diabetes patients and is related to HbA1c levels and inversely to plasma homocysteine. Finally, in diabetes patients, RNA-TauT upregulation seems to be blunted in patients with retinopathy independently of their metabolic control or longer diabetes duration.

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