clofibric acid has been researched along with Inflammation in 12 studies
Clofibric Acid: An antilipemic agent that is the biologically active metabolite of CLOFIBRATE.
clofibric acid : A monocarboxylic acid that is isobutyric acid substituted at position 2 by a p-chlorophenoxy group. It is a metabolite of the drug clofibrate.
Inflammation: A pathological process characterized by injury or destruction of tissues caused by a variety of cytologic and chemical reactions. It is usually manifested by typical signs of pain, heat, redness, swelling, and loss of function.
| Excerpt | Relevance | Reference |
|---|---|---|
| "Oxidative stress and inflammation have been considered the main factors in the liver injury of clofibrate (CF)." | 4.02 | The combination of sesamol and clofibric acid moieties leads to a novel potent hypolipidemic agent with antioxidant, anti-inflammatory and hepatoprotective activity. ( Cheng, L; Guo, M; He, Y; Jiang, H; Liu, J; Ren, C; Shi, Y; Sun, M; Wang, B; Wang, W; Wang, X; Xie, Y; Xu, X, 2021) |
| "The metabolic syndrome is defined as the clustering of cardiovascular risk factors, such as glucose intolerance, hyperinsulinemia, dyslipidemia, coagulation disturbances and hypertension." | 2.43 | Therapeutical effects of PPAR agonists assessed by biomarker modulation. ( Chinetti-Gbaguidi, G; Fruchart, JC; Staels, B, 2005) |
| "Since atherosclerosis is now regarded as an inflammatory disease and those inflammatory cells play critical important roles in the initiation and development of atherosclerosis, we hypothesize that anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects." | 1.33 | Anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects. ( Ye, HJ; Zhao, SP, 2006) |
| "Fenofibrate treatment decreased hepatic macrophage accumulation and abolished steatosis." | 1.33 | Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates. ( Buffat, L; Gijbels, MJ; Hofker, MH; Maeda, N; Noel, B; Shiri-Sverdlov, R; Staels, B; van Bilsen, M; van Gorp, PJ; Wouters, K, 2006) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 10 (83.33) | 29.6817 |
| 2010's | 1 (8.33) | 24.3611 |
| 2020's | 1 (8.33) | 2.80 |
| Authors | Studies |
|---|---|
| Saunders, MJ | 1 |
| Edwards, BS | 1 |
| Zhu, J | 1 |
| Sklar, LA | 1 |
| Graves, SW | 1 |
| Xie, Y | 1 |
| Liu, J | 1 |
| Shi, Y | 1 |
| Wang, B | 1 |
| Wang, X | 1 |
| Wang, W | 1 |
| Sun, M | 1 |
| Xu, X | 1 |
| Jiang, H | 1 |
| Guo, M | 1 |
| He, Y | 1 |
| Ren, C | 1 |
| Cheng, L | 1 |
| Panadero, MI | 1 |
| González, MC | 1 |
| Herrera, E | 1 |
| Bocos, C | 1 |
| Benani, A | 1 |
| Heurtaux, T | 1 |
| Netter, P | 1 |
| Minn, A | 1 |
| Lee, JH | 1 |
| Joe, EH | 1 |
| Jou, I | 1 |
| Staels, B | 3 |
| Fruchart, JC | 2 |
| Okopień, B | 1 |
| Krysiak, R | 1 |
| Kowalski, J | 1 |
| Madej, A | 1 |
| Belowski, D | 1 |
| Zieliński, M | 1 |
| Herman, ZS | 1 |
| Ye, HJ | 1 |
| Zhao, SP | 1 |
| Chinetti-Gbaguidi, G | 1 |
| Shiri-Sverdlov, R | 1 |
| Wouters, K | 1 |
| van Gorp, PJ | 1 |
| Gijbels, MJ | 1 |
| Noel, B | 1 |
| Buffat, L | 1 |
| Maeda, N | 1 |
| van Bilsen, M | 1 |
| Hofker, MH | 1 |
| Broncel, M | 1 |
| Wójcicka, G | 1 |
| Jamroz-Wiśniewska, A | 1 |
| Horoszewicz, K | 1 |
| Bełtowski, J | 1 |
| Trial | Phase | Enrollment | Study Type | Start Date | Status | ||
|---|---|---|---|---|---|---|---|
| Modulation of Insulin Secretion and Insulin Sensitivity in Bangladeshi Type 2 Diabetic Subjects by an Insulin Sensitizer Pioglitazone and T2DM Association With PPARG Gene Polymorphism.[NCT01589445] | Phase 4 | 77 participants (Actual) | Interventional | 2008-11-30 | Completed | ||
| [information is prepared from clinicaltrials.gov, extracted Sep-2024] | |||||||
Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | mmol/l (Mean) | |
|---|---|---|
| Baseline FSG | 3rd Month FSG | |
| Metformin ( 002 Group) | 6.2 | 6.5 |
| Pioglitazone (001 Group) | 6.9 | 5.4 |
Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | μU/ml (Mean) | |
|---|---|---|
| Baseline FSI | 3rd month FSI | |
| Metformin ( 002 Group) | 13.0 | 13.9 |
| Pioglitazone (001 Group) | 16.2 | 12.3 |
Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin. (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | percentage (Mean) | |
|---|---|---|
| Baseline HbA1c | 3rd month HbA1c | |
| Metformin ( 002 Group) | 7.8 | 7.0 |
| Pioglitazone (001 Group) | 7.3 | 6.7 |
"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1: Homeostatic Model Assessment of Beta cell function(HOMA percent B) Analysis 2: Homeostatic Model Assessment of Insulin Sensitivity (Homa percent S)" (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | percentage (Mean) | |||
|---|---|---|---|---|
| Baseline HOMA percent beta cells function | 3rd month HOMA percent beta cells function | Baseline HOMA percent sensitivity | 3rd month HOMA percent sensitivity | |
| Metformin ( 002 Group) | 109.3 | 116.0 | 76.2 | 67.2 |
| Pioglitazone (001 Group) | 118.9 | 132.3 | 51.1 | 69.3 |
"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1: Homeostasis Model Assessment Insulin Resistance(HOMA IR) Analysis 2: Quantitative Insulin sensitivity Check Index(QUICKI)" (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | Score on a scale ( SI unit) (Mean) | |||
|---|---|---|---|---|
| Baseline QUICKI | 3rd month QUICKI | Baseline HOMA IR | 3rd month HOMA IR | |
| Metformin ( 002 Group) | 0.57 | 0.54 | 3.7 | 4.3 |
| Pioglitazone (001 Group) | 0.52 | 0.59 | 5.1 | 2.9 |
"Response rate was defined by ≥10% decrease of FSG or/and ≥1% decrease of HbA1c from the baseline values after 3 months treatment.48 responded to pioglitazone and 32 responded to metformin.~Analysis 1:Total Cholesterol(TC) Analysis 2:Triglyceride(TG) Analysis 3:High Density Lipoprotein(HDL) Analysis 4:Low Density Lipoprotein(LDL)" (NCT01589445)
Timeframe: 3 months for each drug
| Intervention | mg/dl (Mean) | |||||||
|---|---|---|---|---|---|---|---|---|
| Baseline TC | 3rd month TC | Baseline TG | 3rd month TG | Baseline HDL | 3rd month HDL | Baseline LDL | 3rd month LDL | |
| Metformin (002 Group) | 193.0 | 177.0 | 166.0 | 175.0 | 34.4 | 34.7 | 125.6 | 112.0 |
| Pioglitazone (001 Group) | 182.0 | 178 | 183 | 195 | 33 | 33.2 | 112.8 | 105.5 |
5 reviews available for clofibric acid and Inflammation
| Article | Year |
|---|---|
Factors modulating fibrates response: therapeutic implications and alternative strategies.
Topics: Animals; Clofibric Acid; Gene Expression Regulation; Glucose; Humans; Inflammation; Lipid Metabolism | 2009 |
Therapeutic roles of peroxisome proliferator-activated receptor agonists.
Topics: Cardiovascular Diseases; Clofibric Acid; Diabetes Mellitus, Type 2; Humans; Hyperlipidemias; Inflamm | 2005 |
Therapeutical effects of PPAR agonists assessed by biomarker modulation.
Topics: Animals; Atherosclerosis; Biomarkers; Cardiovascular Diseases; Clofibric Acid; Humans; Inflammation; | 2005 |
[Fibrates and markers of inflammation].
Topics: Atherosclerosis; Biomarkers; C-Reactive Protein; Cholesterol, HDL; Cholesterol, LDL; Clofibric Acid; | 2007 |
Liver X receptors (LXRs). Part I: structure, function, regulation of activity, and role in lipid metabolism.
Topics: Alzheimer Disease; Atherosclerosis; Cholesterol; Clofibric Acid; Diabetes Mellitus; DNA-Binding Prot | 2007 |
1 trial available for clofibric acid and Inflammation
| Article | Year |
|---|---|
Monocyte release of tumor necrosis factor-alpha and interleukin-1beta in primary type IIa and IIb dyslipidemic patients treated with statins or fibrates.
Topics: Adult; Anticholesteremic Agents; C-Reactive Protein; Clofibric Acid; Cytokines; Diabetes Mellitus, T | 2005 |
6 other studies available for clofibric acid and Inflammation
| Article | Year |
|---|---|
Microsphere-based flow cytometry protease assays for use in protease activity detection and high-throughput screening.
Topics: Animals; Biotinylation; Flow Cytometry; Fluorescence Resonance Energy Transfer; Green Fluorescent Pr | 2010 |
The combination of sesamol and clofibric acid moieties leads to a novel potent hypolipidemic agent with antioxidant, anti-inflammatory and hepatoprotective activity.
Topics: Animals; Anti-Inflammatory Agents, Non-Steroidal; Antioxidants; Benzodioxoles; Clofibric Acid; Dose- | 2021 |
Activation of peroxisome proliferator-activated receptor alpha in rat spinal cord after peripheral noxious stimulation.
Topics: Acyl-CoA Oxidase; Animals; Clofibric Acid; DNA-Binding Proteins; Electrophoretic Mobility Shift Assa | 2004 |
PPAR-alpha activators suppress STAT1 inflammatory signaling in lipopolysaccharide-activated rat glia.
Topics: Animals; Animals, Newborn; Arachidonic Acids; Blotting, Western; Cells, Cultured; Chemokine CCL2; Cl | 2005 |
Anti-atherogenic properties of fibrates may be largely due to their anti-inflammatory effects.
Topics: Adipocytes; Anti-Inflammatory Agents; Atherosclerosis; Clofibric Acid; Endothelial Cells; Humans; In | 2006 |
Early diet-induced non-alcoholic steatohepatitis in APOE2 knock-in mice and its prevention by fibrates.
Topics: Animals; Apolipoprotein E2; Apolipoproteins E; ATP-Binding Cassette Transporters; Clofibric Acid; Di | 2006 |