scholarly journals Effects of type 2 diabetes mellitus on gene expression profile of meibomian glands in mice

2019 ◽  
Vol 97 (S263) ◽  
Author(s):  
Erdost Yildiz ◽  
Noushin Zibandeh ◽  
Berna Özer ◽  
Afsun Sahin
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Gene Expression Profile ◽  
Expression Profile ◽  
Meibomian Glands

scholarly journals Transcriptional Profiling and Biological Pathway(s) Analysis of Type 2 Diabetes Mellitus in a Pakistani Population

2020 ◽  
Vol 17 (16) ◽  
pp. 5866
Author(s):  
Zarish Noreen ◽  
Christopher A. Loffredo ◽  
Attya Bhatti ◽  
Jyothirmai J. Simhadri ◽  
Gail Nunlee-Bland ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mitochondrial Dysfunction ◽  
Signaling Pathway ◽  
Health Concern ◽  
Receptor Signaling ◽  
Small Pilot Study

The epidemic of type 2 diabetes mellitus (T2DM) is an important global health concern. Our earlier epidemiological investigation in Pakistan prompted us to conduct a molecular investigation to decipher the differential genetic pathways of this health condition in relation to non-diabetic controls. Our microarray studies of global gene expression were conducted on the Affymetrix platform using Human Genome U133 Plus 2.0 Array along with Ingenuity Pathway Analysis (IPA) to associate the affected genes with their canonical pathways. High-throughput qRT-PCR TaqMan Low Density Array (TLDA) was performed to validate the selected differentially expressed genes of our interest, viz., ARNT, LEPR, MYC, RRAD, CYP2D6, TP53, APOC1, APOC2, CYP1B1, SLC2A13, and SLC33A1 using a small population validation sample (n = 15 cases and their corresponding matched controls). Overall, our small pilot study revealed a discrete gene expression profile in cases compared to controls. The disease pathways included: Insulin Receptor Signaling, Type II Diabetes Mellitus Signaling, Apoptosis Signaling, Aryl Hydrocarbon Receptor Signaling, p53 Signaling, Mitochondrial Dysfunction, Chronic Myeloid Leukemia Signaling, Parkinson’s Signaling, Molecular Mechanism of Cancer, and Cell Cycle G1/S Checkpoint Regulation, GABA Receptor Signaling, Neuroinflammation Signaling Pathway, Dopamine Receptor Signaling, Sirtuin Signaling Pathway, Oxidative Phosphorylation, LXR/RXR Activation, and Mitochondrial Dysfunction, strongly consistent with the evidence from epidemiological studies. These gene fingerprints could lead to the development of biomarkers for the identification of subgroups at high risk for future disease well ahead of time, before the actual disease becomes visible.

scholarly journals Effects of Casein Kinase 2 Alpha 1 Gene Expression on Mice Liver Susceptible to Type 2 Diabetes Mellitus and Obesity

2020 ◽  
Vol 17 (1) ◽  
pp. 13-20 ◽  
Author(s):  
Yu-Ching Lan ◽  
Yeh-Han Wang ◽  
Hsin-Han Chen ◽  
Sui-Foon Lo ◽  
Shih-Yin Chen ◽  
...  
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Casein Kinase ◽  
Casein Kinase 2 ◽  
Mice Liver

scholarly journals The Pattern of Peroxisome Proliferator-activated Receptor Gamma Coactivator 1-alpha Gene Expression in Type-2 Diabetes Mellitus Rat Model Liver: Focus on Exercise

2021 ◽  
Vol 9 (T3) ◽  
pp. 124-128
Author(s):  
Yetty Machrina ◽  
Dharma Lindarto ◽  
Yunita Sari Pane ◽  
Novita Sari Harahap
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Rat Model ◽  
Moderate Intensity ◽  
Peroxisome Proliferator ◽  
Peroxisome Proliferator Activated Receptor ◽  
Treatment Groups

BACKGROUND: Peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC-1α) has an important role in mitochondria biogenesis which generated cellular metabolism. Carbohydrate metabolism in the liver is crucial to maintain plasma blood glucose. AIM: This research aimed to determine the expression of PGC-1α gene in the liver type-2 diabetes mellitus (T2DM) rat model, after treatment with a focus on exercise. METHODS: We used 25 healthy male Wistar rats as subjects. Rats were modified to T2DM models by feeding a high-fat diet and low-dose streptozotocin injection. We divided the rats into five groups, that is, sedentary group as a control and four others as treatment groups. The exercise was assigned for treatment groups by a run on the treadmill as moderate intensity continuous (MIC), highintensity continuous (HIC), slow interval (SI), and fast interval (FI). The treatment groups were exercise throughout 8 weeks with a frequency of 3 times a week. RESULTS: The results showed that expression of PGC-1α gene was lower in all treatment groups compared to controls (p < 0.05). Expression in HIC was higher than MIC (p < 0.05), so was the expression in FI more than SI (p < 0.05). CONCLUSIONS: Exercise affected PGC-1α gene expression in the liver of the T2DM rat model. The expression of PGC-1α was linear with exercise intensity.

scholarly journals Identification of Perturbed Pathways Rendering Susceptibility to Tuberculosis in Type 2 Diabetes Mellitus Patients Using BioNSi Simulation of Integrated Network of Implicated Human Genes

2021 ◽  
Author(s):  
Jyoti Rani ◽  
Anasuya Bhargav ◽  
Malabika Datta ◽  
Urmi Bajpai ◽  
Srinivasan Ramachandran
Keyword(s):  
Gene Expression ◽  
Diabetes Mellitus ◽  
Type 2 Diabetes ◽  
Type 2 Diabetes Mellitus ◽  
Mapk Signaling ◽  
Differentially Expressed ◽  
P Value ◽  
Receptor Signaling ◽  
Chronic Hyperglycemia

Abstract Adaptive immune response of the Th1 arm is the main defense against tuberculosis (TB). However, in Type 2 Diabetes Mellitus (T2DM) patients, chronic hyperglycemia and inflammation underlie susceptibility to TB and results in poor TB control. The molecular pathways causing susceptibility of diabetics to tuberculosis is not fully understood. Here, an integrative pathway-based approach is used to investigate the perturbed pathways in T2DM patients rendering susceptibility to TB. We obtained 36 genes implicated in the Type 2 diabetes associated tuberculosis (T2DMTB) from literature. Gene expression analysis on T2DM patients’ data (GSE28168) showed that DEFA1 is differentially expressed at Padj < 0.05. The genes CAMP, CD14, CORO1A, LAMP1, TLR4, IL17F and SOCS3 were differentially expressed in T2DM patients at P value < 0.05. 7 microRNAs associated with these T2DMTB genes were obtained from NetworkAnalyst and verified for their literature evidences. The hsa-miR-146a microRNA was differentially expressed at Padj < 0.05. The human host TB susceptibility genes TNFRSF10A, MSRA, GPR148, SLC37A3, PXK, PROK2, REV3L, PGM1, HIST3H2A, PLAC4, LETM2, EMP2 and were also differentially expressed at Padj < 0.05. We included all these genes and added the remaining 28 genes from the T2DMTB set and the rest of differentially expressed genes at Padj < 0.05 in STRING and obtained a well-connected network with high confidence score greater than 0.7. From this network we extracted the KEGG pathways at FDR < 0.05 and retained only Diabetes and TB pathways among the disease pathways. The network was simulated with BioNSi using gene expression data from GSE26168. The Necroptosis pathway showed the maximum perturbations in T2DM patients, followed by NOD-like receptor signaling, Toll-like receptor signaling, NF-kappa-B signaling and MAPK signaling. These pathways likely underlie susceptibility to TB in T2DM patients.

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