scholarly journals Urine Tricarboxylic Acid Cycle Metabolites Predict Progressive Chronic Kidney Disease in Type 2 Diabetes

2018 ◽  
Vol 103 (12) ◽  
pp. 4357-4364 ◽  
Author(s):  
Jian-Jun Liu ◽  
Sylvia Liu ◽  
Resham L Gurung ◽  
Jianhong Ching ◽  
Jean-Paul Kovalik ◽  
...  
2020 ◽  
Vol 319 (6) ◽  
pp. C1011-C1019
Author(s):  
Kai Zou ◽  
Kristen Turner ◽  
Donghai Zheng ◽  
J. Matthew Hinkley ◽  
Benjamin A. Kugler ◽  
...  

The purpose of this study was to determine whether intramyocellular glucose partitioning was altered in primary human myotubes derived from severely obese women with type 2 diabetes. Human skeletal muscle cells were obtained from lean nondiabetic and severely obese Caucasian females with type 2 diabetes [body mass index (BMI): 23.6 ± 2.6 vs. 48.8 ± 1.9 kg/m2, fasting glucose: 86.9 ± 1.6 vs. 135.6 ± 12.0 mg/dL, n = 9/group]. 1-[14C]-Glucose metabolism (glycogen synthesis, glucose oxidation, and nonoxidized glycolysis) and 1- and 2-[14C]-pyruvate oxidation were examined in fully differentiated myotubes under basal and insulin-stimulated conditions. Tricarboxylic acid cycle intermediates were determined via targeted metabolomics. Myotubes derived from severely obese individuals with type 2 diabetes exhibited impaired insulin-mediated glucose partitioning with reduced rates of glycogen synthesis and glucose oxidation and increased rates of nonoxidized glycolytic products, when compared with myotubes derived from the nondiabetic individuals ( P < 0.05). Both 1- and 2-[14C]-pyruvate oxidation rates were significantly blunted in myotubes from severely obese women with type 2 diabetes compared with myotubes from the nondiabetic controls. Lastly, concentrations of tricarboxylic acid cycle intermediates, namely, citrate ( P < 0.05), cis-aconitic acid ( P = 0.07), and α-ketoglutarate ( P < 0.05), were lower in myotubes from severely obese women with type 2 diabetes. These data suggest that intramyocellular insulin-mediated glucose partitioning is intrinsically altered in the skeletal muscle of severely obese women with type 2 diabetes in a manner that favors the production of glycolytic end products. Defects in pyruvate dehydrogenase and tricarboxylic acid cycle may be responsible for this metabolic derangement associated with type 2 diabetes.


Author(s):  
Jiwoon Kim ◽  
Ji Sun Nam ◽  
Heejung Kim ◽  
Hye Sun Lee ◽  
Jung Eun Lee

Abstract. Background/Aims: Trials on the effects of cholecalciferol supplementation in type 2 diabetes with chronic kidney disease patients were underexplored. Therefore, the aim of this study was to investigate the effects of two different doses of vitamin D supplementation on serum 25-hydroxyvitamin D [25(OH)D] concentrations and metabolic parameters in vitamin D-deficient Korean diabetes patients with chronic kidney disease. Methods: 92 patients completed this study: the placebo group (A, n = 33), the oral cholecalciferol 1,000 IU/day group (B, n = 34), or the single 200,000 IU injection group (C, n = 25, equivalent to 2,000 IU/day). 52% of the patients had less than 60 mL/min/1.73m2 of glomerular filtration rates. Laboratory test and pulse wave velocity were performed before and after supplementation. Results: After 12 weeks, serum 25(OH)D concentrations of the patients who received vitamin D supplementation were significantly increased (A, -2.4 ± 1.2 ng/mL vs. B, 10.7 ± 1.2 ng/mL vs. C, 14.6 ± 1.7 ng/mL; p < 0.001). In addition, the lipid profiles in the vitamin D injection group (C) showed a significant decrease in triglyceride and a rise in HDL cholesterol. However, the other parameters showed no differences. Conclusions: Our data indicated that two different doses and routes of vitamin D administration significantly and safely increased serum 25(OH)D concentrations in vitamin D-deficient diabetes patients with comorbid chronic kidney disease. In the group that received the higher vitamin D dose, the lipid profiles showed significant improvement, but there were no beneficial effects on other metabolic parameters.


Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 1066-P ◽  
Author(s):  
KATHERINE R. TUTTLE ◽  
MARK LAKSHMANAN ◽  
BRIAN L. RAYNER ◽  
ROBERT S. BUSCH ◽  
ALAN G. ZIMMERMANN ◽  
...  

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 536-P
Author(s):  
MICHAEL BLANKENBURG ◽  
CSABA P. KOVESDY ◽  
SELINE EISENRING ◽  
ANNE FETT ◽  
EMILE W. SCHOKKER ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 233-OR
Author(s):  
KATHERINE R. TUTTLE ◽  
BRIAN L. RAYNER ◽  
MARK LAKSHMANAN ◽  
BRAD WOODWARD ◽  
ANITA KWAN ◽  
...  

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 532-P
Author(s):  
ZHANG CHENGHUI ◽  
WU YUNHONG ◽  
WANG SUYUAN ◽  
LI MINGXIA

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