scholarly journals Insulin resistance and hyperinsulinaemia in mild to moderate progressive chronic renal failure and its association with aerobic work capacity

Diabetologia ◽  
1995 ◽  
Vol 38 (5) ◽  
pp. 565-572 ◽  
Author(s):  
I. Eidemak ◽  
B. Feldt-Rasmussen ◽  
I. -L. Kanstrup ◽  
S. L. Nielsen ◽  
O. Schmitz ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Work Capacity ◽  
Aerobic Work Capacity

scholarly journals Insulin resistance and hyperinsulinaemia in mild to moderate progressive chronic renal failure and its association with aerobic work capacity

Diabetologia ◽  
1995 ◽  
Vol 38 (5) ◽  
pp. 565-572 ◽  
Author(s):  
I. Eidemak ◽  
B. Feldt-Rasmussen ◽  
I.-L. Kanstrup ◽  
S. L. Nielsen ◽  
O. Schmitz ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Work Capacity ◽  
Aerobic Work Capacity

Brief Review Insulin Resistance in Chronic Renal Failure

1985 ◽  
Vol 11 (1-2) ◽  
pp. 113-125 ◽  
Author(s):  
M. L. Mccalebeb ◽  
J. B. Wish ◽  
D. H. Lockwood
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure

Doxazosin, but not amlodipine decreases insulin resistance in patients with chronic renal failure: a prospective, randomized-controlled study

2002 ◽  
Vol 58 (12) ◽  
pp. 405-410 ◽  
Author(s):  
A. Yildiz ◽  
M. Hursit ◽  
A.V. Çelik ◽  
S.M. Kayacan ◽  
H.Yazici ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Randomized Controlled Study ◽  
Controlled Study ◽  
Randomized Controlled

Activity of insulin receptor kinase and glycogen synthase in skeletal muscle from patients with chronic renal failure

1989 ◽  
Vol 121 (5) ◽  
pp. 744-750 ◽  
Author(s):  
Jens F. Bak ◽  
Ole Schmitz ◽  
Søren S. Sørensen ◽  
Jens Frøkjær ◽  
Torben Kjær ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Insulin Receptor ◽  
Glycogen Synthase ◽  
Insulin Receptors ◽  
Receptor Function ◽  
Uremic Patients ◽  
Glycogen Synthase Activity

Abstract. To examine subcellular mechanisms behind the pathogenesis of peripheral insulin resistance in chronic uremic patients, insulin receptor function and glycogen synthase activity were studied in biopsies of skeletal muscle obtained during renal transplant surgery in 9 non-diabetic uremic patients. The results were compared with values obtained in an age- and sex-matched group of subjects with normal renal function, undergoing surgery for urological or gynecological diseases. The recovery of solubilized, wheat germ agglutinin-purified insulin receptors from skeletal muscle was increased among the uremic patients: 49.3 ± 6.1 vs 31.4 ± 2.8 fmol/100 mg muscle in healthy controls (p < 0.03). Basal as well as insulin-stimulated kinase activities of the insulin receptors, expressed as phosphorylation of the synthetic peptide poly(Glu-Tyr(4:1)) were similar. In addition, the maximal activity of the glycogen synthase was enhanced in uremic muscle: 26.6 ± 2.8 vs 19.5 ± 1.8 nmol · (mg protein)−1 · min−1 (p < 0.05), whereas the half-maximal activation constant for glucose-6-phosphate was identical in the two groups. Likewise, the muscle glycogen concentrations were similar in the uremic patients and the normal controls. In conclusion, our data suggest that neither impaired insulin receptor function nor a reduced maximal glycogen synthase activity of skeletal muscle are involved in the pathogenesis of the insulin resistance of patients with chronic renal failure.

scholarly journals Urea-induced ROS generation causes insulin resistance in mice with chronic renal failure

2010 ◽  
Vol 120 (3) ◽  
pp. 932-932 ◽  
Author(s):  
Maria D’Apolito ◽  
Xueliang Du ◽  
Haihong Zong ◽  
Alessandra Catucci ◽  
Luigi Maiuri ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Ros Generation

scholarly journals Valsartan Alleviates Insulin Resistance in Skeletal Muscle of Chronic Renal Failure Rats

2018 ◽  
Vol 24 ◽  
pp. 2413-2419 ◽  
Author(s):  
Yang Wang ◽  
Ri-bao Wei ◽  
Yue Yang ◽  
Ting-Yu Su ◽  
Meng-Jie Huang ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Skeletal Muscle ◽  
Renal Failure ◽  
Chronic Renal Failure

Insulin-mediated changes in PD and glucose uptake after correction of acidosis in humans with CRF

1995 ◽  
Vol 268 (1) ◽  
pp. E121-E126 ◽  
Author(s):  
D. Reaich ◽  
K. A. Graham ◽  
S. M. Channon ◽  
C. Hetherington ◽  
C. M. Scrimgeour ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Renal Failure ◽  
Chronic Renal Failure ◽  
Insulin Sensitivity ◽  
Protein Degradation ◽  
Continuous Infusion ◽  
Glucose Uptake ◽  
Infusion Rate ◽  
Euglycemic Clamp ◽  
Kinetics Of

To test the hypothesis that acidosis contributes to the insulin resistance of chronic renal failure (CRF) and impairs the action of insulin to decrease protein degradation, eight CRF patients were studied using the combined L-[1–13C]leucine-euglycemic clamp technique before (acid) and after (NaHCO3) 4 wk treatment with NaHCO3 (pH: acid 7.29 +/- 0.01 vs. NaHCO3 7.36 +/- 0.01, P < 0.001). Protein degradation (PD) was estimated sequentially from the kinetics of a primed continuous infusion of L-[1–13C]leucine in the basal state and during a hyperinsulinemic euglycemic clamp. Insulin sensitivity was measured during the clamp. The correction of acidosis significantly increased the glucose infusion rate necessary to maintain euglycemia (acid 6.44 +/- 0.89 vs. bicarbonate 7.38 +/- 0.90 mg.kg-1.min-1, P < 0.01) and significantly decreased PD in the basal state (acid 126.4 +/- 8.1 vs. bicarbonate 100.1 +/- 6.9 mumol.kg-1.h-1, P < 0.001). Hyperinsulinemia decreased PD in both studies (acid basal 126.4 +/- 8.1 vs. clamp 96.5 +/- 7.7, P < 0.001; bicarbonate basal 100.1 +/- 6.9 vs. clamp 88.2 +/- 5.5 mumol.kg-1.h-1, P = 0.06), its effect being unaltered by acidosis, with a reduction of 24% before and 12% after the correction of acidosis. In conclusion, acidosis contributes to the insulin resistance of CRF but does not affect the action of insulin on PD.

Sign in / Sign up

Export Citation Format

Share Document