|
Impaired glucose tolerance
|
0.310 |
AlteredExpression
|
phenotype |
BEFREE |
In conclusion, our observations suggested that ginsenoside Rg1 inhibited dietary-induced obesity and improved obesity-related insulin resistance and glucose intolerance by activation of the AMPK pathway.
|
29513799 |
2018 |
|
Impaired glucose tolerance
|
0.310 |
Biomarker
|
phenotype |
CTD_human |
AMP-activated protein kinase-deficient mice are resistant to the metabolic effects of resveratrol.
|
19934007 |
2010 |
|
Insulin Resistance
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
AMP-activated protein kinase-deficient mice are resistant to the metabolic effects of resveratrol.
|
19934007 |
2010 |
|
Cardiomyopathies, Primary
|
0.300 |
Biomarker
|
group |
CTD_human |
Comparative phenotypic assessment of cardiac pathology, physiology, and gene expression in C3H/HeJ, C57BL/6J, and B6C3F1/J mice.
|
21037199 |
2010 |
|
Myocardial Diseases, Secondary
|
0.300 |
Biomarker
|
group |
CTD_human |
Comparative phenotypic assessment of cardiac pathology, physiology, and gene expression in C3H/HeJ, C57BL/6J, and B6C3F1/J mice.
|
21037199 |
2010 |
|
Cerebrovascular accident
|
0.300 |
Therapeutic
|
group |
CTD_human |
Effects of metformin in experimental stroke.
|
20847317 |
2010 |
|
Acute Cerebrovascular Accidents
|
0.300 |
Therapeutic
|
disease |
CTD_human |
Effects of metformin in experimental stroke.
|
20847317 |
2010 |
|
Insulin Sensitivity
|
0.300 |
Biomarker
|
phenotype |
CTD_human |
AMP-activated protein kinase-deficient mice are resistant to the metabolic effects of resveratrol.
|
19934007 |
2010 |
|
Cardiomegaly
|
0.300 |
Therapeutic
|
phenotype |
CTD_human |
AMPKalpha2 counteracts the development of cardiac hypertrophy induced by isoproterenol.
|
18812163 |
2008 |
|
Cardiac Hypertrophy
|
0.300 |
Therapeutic
|
phenotype |
CTD_human |
AMPKalpha2 counteracts the development of cardiac hypertrophy induced by isoproterenol.
|
18812163 |
2008 |
|
Gastric Adenocarcinoma
|
0.300 |
GeneticVariation
|
disease |
UNIPROT |
|
|
|
|
Alzheimer's Disease
|
0.100 |
Biomarker
|
disease |
BEFREE |
The circRNA-miRNA-mRNA network was most involved in the MAPK, mTOR, AMPK, and WNT signaling pathways in Alzheimer's disease.
|
31834549 |
2020 |
|
Alzheimer's Disease
|
0.100 |
PosttranslationalModification
|
disease |
BEFREE |
These results suggest that diet control to achieve euglycaemia in an insulin-deficient DM condition may be harmful because of the greater possibility of AD development through increased tau phosphorylation by AMPK activation in the hippocampus.
|
31799531 |
2020 |
|
Arteriosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We describe largely nonoverlapping genetic determinants in AMPK genes for diabetes-/atherosclerosis-related traits, which reflect the metabolic pathways controlled by the enzyme.
|
31512724 |
2020 |
|
Atherosclerosis
|
0.100 |
GeneticVariation
|
disease |
BEFREE |
We describe largely nonoverlapping genetic determinants in AMPK genes for diabetes-/atherosclerosis-related traits, which reflect the metabolic pathways controlled by the enzyme.
|
31512724 |
2020 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
AMPK is generally a tumor suppressor.However, once cancer arises, AMPK becomes a tumor promoter instead, driving cancer development.
|
31787232 |
2020 |
|
Malignant Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
Given the pivotal role of AMPK in metabolism, whether ouabain affects cancer cell metabolism remains elusive.
|
31515527 |
2020 |
|
Diabetes Mellitus
|
0.100 |
AlteredExpression
|
group |
BEFREE |
Since AMPK is a direct regulator of tau phosphorylation, we hypothesized that strict diet control to achieve euglycaemia affects tau protein phosphorylation through increased AMPK activity in the hippocampus of DM rats.
|
31799531 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.100 |
AlteredExpression
|
disease |
BEFREE |
Finally, possible mechanisms of antidiabetic activity of L-SGgly were identified as increasing GLP-1 levels and activating liver AMPK in T2DM rats.
|
31586692 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.100 |
Biomarker
|
disease |
BEFREE |
MLF significantly improved skeletal muscle insulin resistance and mitochondrial function in db/db mice and L6 myocytes through AMPK-PGC-1α signaling pathway, and our findings support the therapeutic effects of MLF on type 2 diabetes.
|
31639486 |
2020 |
|
Diabetes Mellitus, Non-Insulin-Dependent
|
0.100 |
Biomarker
|
disease |
BEFREE |
Cardiac function was examined with echocardiography before sacrifice at both 3 M and 6 M. SFN prevented T2D-induced progression of cardiac dysfunction, remodeling (hypertrophy and fibrosis), inflammation, and oxidative damage in wild-type diabetic mice, but not in AMPKα2-KO mice.
|
31706979 |
2020 |
|
Hyperglycemia
|
0.100 |
Biomarker
|
disease |
BEFREE |
T2D was established by feeding 3-month high-fat diet (HFD) to induce insulin resistance, followed by an intraperitoneal injection of streptozotocin (STZ) to induce mild hyperglycemia in both AMPKα2-KO and wild-type (WT) mice.
|
31706979 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
The signaling pathway activated by metformin (LKB1/AMPK/mTOR) is implicated in tumor suppression in ApcMin/+ mice via metformin-induced reduction in polyp burden, increased ratio of pAMPK/AMPK, decreased pmTOR/mTOR ratio, and decreased pS6Ser235/S6Ser235 ratio in polyps.
|
31818851 |
2020 |
|
Neoplasms
|
0.100 |
GeneticVariation
|
group |
BEFREE |
The expression levels of miR31, miR92a, KRAS oncogene, and the c-MYC transcription factor were subexpressed upon 72 h post-treatment with kaempferol-3-<i>O</i>-glycoside compared with the control without treatment (<i>P</i> < .05); in contrast, the tumor suppressor genes AMPK (∼4.85, <i>P</i> = .005) and APC (∼2.71, <i>P</i> = .066) tumor suppressors genes were overexpressed.
|
31441682 |
2020 |
|
Neoplasms
|
0.100 |
Biomarker
|
group |
BEFREE |
AMPK is generally a tumor suppressor.However, once cancer arises, AMPK becomes a tumor promoter instead, driving cancer development.
|
31787232 |
2020 |