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Research Paper Volume 12, Issue 3 pp 2584-2594
LDL-C plays a causal role on T2DM: a Mendelian randomization analysis
Relevance score: 8.753647Wenbin Pan, Weiju Sun, Shuo Yang, He Zhuang, Huijie Jiang, Hong Ju, Donghua Wang, Ying Han
Keywords: low-density lipoprotein cholesterol, type 2 diabetes mellitus, casual effect, Mendelian randomization, type 1 diabetes mellitus
Published in Aging on February 10, 2020
Principles of using genetic variants as instrumental variable to estimate the causal influence of exposure factors on disease. There is a strong correlation between genetic variation and exposure factors (γ≠0), and the genetic variation is independent of the confounding factors affecting the relationship between “exposure factors -outcomes” (φ1=0). Furthermore, genetic variation can only affect the outcomes through exposure factors but not other paths (φ2 = 0).
Forest plot of the ORs and 95%CIs of the instrumental variables.
The processes of SNPs selection.
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Research Paper Volume 11, Issue 14 pp 4943-4969
D-ribose is elevated in T1DM patients and can be involved in the onset of encephalopathy
Relevance score: 8.463278Lexiang Yu, Yao Chen, Yong Xu, Tao He, Yan Wei, Rongqiao He
Keywords: D-ribose, benfotiamine (BTMP), cognitive impairment, type 1 diabetic encephalopathy, type 1 diabetes mellitus (T1DM), diabetic encephalopathy
Published in Aging on July 15, 2019
Increase in the levels of D-ribose and related enzymes in type 1 diabetic rats. Male SD rats (6–8 weeks) were intraperitoneally injected with STZ (70 mg/kg bw, n=30) and maintained for 10 weeks. Rats injected with saline were used as controls (n=10). Levels of D-ribose in urine were measured at different time intervals (panel A). D-ribose levels in serum (panel B) and the brain (panel C) were determined within 3 days after dissection. The expression and activity levels of ribokinase, transketolase (TKT), 5-phosphoribosyl 1-pyrophosphate (PRPP) and glucose-6 phosphate dehydrogenase (G6PD) in the brain were measured with ELISA kits (panel D and E). All values are expressed as the mean ± S.E.M. *, P < 0.05; **, P < 0.01; ***, P < 0.001.
Effect of benfotiamine (BTMP) on the levels of D-ribose, D-glucose and TKT in T1DM rats. Conditions for the preparation of T1DM rats are shown in Figure 1. Male rats (6-8 weeks) were divided into four groups as follows: T1DM rats were gavaged with benfotiamine (BTMP, 300 mg/kg bw, once daily) dissolved in carboxymethylcellulose (CMC) (90) (T1DM+BTMP, n=20); T1DM rats were gavaged with CMC (T1DM, n=20); normal SD rats were gavaged with CMC (Control, n=10) and BTMP (n=10) as negative and positive controls, respectively. The expression levels of transketolase (TKT) in the brain (panel A) and liver (panel B) were measured with ELISA kits. After 10 weeks of domestication, D-ribose levels in the serum (panel C) and brain (panel D) of rats were measured, and D-glucose levels were measured in the brain (panel F). Fasting blood glucose (FBG) was measured every other week (panel E). “*” compared to the control group. “#” represents the difference between the T1DM and T1DM+BTMP groups. All values are expressed as the mean ± S.E.M. *, P < 0.05; ***, P < 0.001; #, P < 0.05; ##, P < 0.01; ###, P < 0.001.
Rescue of spatial learning and memory abilities in T1DM rats with BTMP. Animal groups and treatments were as described in Figure 2 except that rats were subjected to Y maze and Morris water maze tests. The accuracy of Y maze alternation was detected (panel A). The escape latency (panel B), percentage of time spent in the target quadrant (panel C) and number of platform crossings (panel D) were recorded. Representative images of the performance path are shown (panel E). “*” represents the difference between the Control and T1DM groups. “#” represents the difference between the T1DM and T1DM+benfotiamine (BTMP) groups. The number of those groups are control (n=10), BTMP (n=9), T1DM (n=15) and T1DM+BTMP (n=15). All values are expressed as the mean ± S.E.M. *, P < 0.05; #, P < 0.05; ##, P < 0.01.
Nissl staining of hippocampal neurons of rats treated with BTMP. Animal groups and treatment were as described in Figure 2 except that hippocampal slices were prepared and stained with cresyl violet (panel A). Numbers of necrotic neurons were counted under a microscope as described in the Materials and Methods (panel B). The number of those groups are control (n=10), BTMP (n=9), T1DM (n=10) and T1DM+BTMP (n=10). All values are expressed as the mean ± S.E.M. “*” compared to the control group. “#” represents the difference between the T1DM and T1DM+BTMP groups. All values are expressed as the mean ± S.E.M. **, P < 0.01; #, P < 0.05; ##, P < 0.01.
Comparison of D-ribose levels between T1DM patients and normal participants. Patients with T1DM (T1DM group) and age-matched normal participants (control group, n=16) were enrolled for determination of their D-ribose concentrations. D-ribose levels in serum (panel A) and urine (panel B) were measured by HPLC as previously described [17]. All values are shown as the mean ± S.E.M. *, P < 0.05; ***, P < 0.001.
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Research Paper Volume 3, Issue 4 pp 368-373
Association of PTPN22 1858T/T genotype with type 1 diabetes, Graves' disease but not with rheumatoid arthritis in Russian population
Relevance score: 9.064649Daria Zhebrun, Yulia Kudryashova, Alina Babenko, Alexei Maslyansky, Natalya Kunitskaya, Daria Popcova, Alexandra Klushina, Elena Grineva, Anna Kostareva, Evgeny Shlyakhto
Keywords: type 1 diabetes, Graves' disease, rheumatoid arthritis, protein tyrosine phosphatase nonreceptor 22, single-nucleotide polymorphism
Published in Aging on April 6, 2011