pirinixic acid has been researched along with Diabetes Mellitus, Type 2 in 14 studies
pirinixic acid: structure
Diabetes Mellitus, Type 2: A subclass of DIABETES MELLITUS that is not INSULIN-responsive or dependent (NIDDM). It is characterized initially by INSULIN RESISTANCE and HYPERINSULINEMIA; and eventually by GLUCOSE INTOLERANCE; HYPERGLYCEMIA; and overt diabetes. Type II diabetes mellitus is no longer considered a disease exclusively found in adults. Patients seldom develop KETOSIS but often exhibit OBESITY.
| Excerpt | Relevance | Reference |
|---|---|---|
| " c-5-[6-(4-Methanesulfonyloxyphenyl)hexyl]-2-methyl-1,3-dioxane-r-2-carboxylic acid 13c exhibited potent hypoglycemic and lipid lowering activity with high oral bioavailability in animal models." | 1.35 | Discovery of a highly orally bioavailable c-5-[6-(4-Methanesulfonyloxyphenyl)hexyl]-2-methyl-1,3-dioxane-r-2-carboxylic acid as a potent hypoglycemic and hypolipidemic agent. ( Basu, S; Giri, S; Godha, A; Goel, A; Goswami, A; Jain, M; Makadia, P; Patel, H; Patel, M; Patel, P; Patil, P; Pingali, H; Shah, S; Zaware, P, 2008) |
| "Rosiglitazone treatment decreased adiponectin and resistin mRNA levels by 57 and 72%, respectively (P < 0." | 1.31 | Differential regulation of adipocytokine mRNAs by rosiglitazone in db/db mice. ( Chapman, H; Clapham, JC; Holder, JC; Lister, CA; Moore, GB; Piercy, V; Smith, SA, 2001) |
| Timeframe | Studies, this research(%) | All Research% |
|---|---|---|
| pre-1990 | 0 (0.00) | 18.7374 |
| 1990's | 0 (0.00) | 18.2507 |
| 2000's | 9 (64.29) | 29.6817 |
| 2010's | 4 (28.57) | 24.3611 |
| 2020's | 1 (7.14) | 2.80 |
| Authors | Studies |
|---|---|
| Li, Z | 2 |
| Liao, C | 1 |
| Ko, BC | 1 |
| Shan, S | 1 |
| Tong, EH | 1 |
| Yin, Z | 1 |
| Pan, D | 1 |
| Wong, VK | 1 |
| Shi, L | 1 |
| Ning, ZQ | 1 |
| Hu, W | 1 |
| Zhou, J | 1 |
| Chung, SS | 1 |
| Lu, XP | 1 |
| Pingali, H | 1 |
| Jain, M | 1 |
| Shah, S | 1 |
| Basu, S | 1 |
| Makadia, P | 1 |
| Goswami, A | 1 |
| Zaware, P | 1 |
| Patil, P | 1 |
| Godha, A | 1 |
| Giri, S | 1 |
| Goel, A | 1 |
| Patel, M | 1 |
| Patel, H | 1 |
| Patel, P | 1 |
| Gao, Q | 1 |
| Hanh, J | 1 |
| Váradi, L | 1 |
| Cairns, R | 1 |
| Sjöström, H | 1 |
| Liao, VW | 1 |
| Wood, P | 1 |
| Balaban, S | 1 |
| Ong, JA | 1 |
| Lin, HY | 1 |
| Lai, F | 1 |
| Hoy, AJ | 1 |
| Grewal, T | 1 |
| Groundwater, PW | 1 |
| Hibbs, DE | 1 |
| Sæther, T | 1 |
| Paulsen, SM | 1 |
| Tungen, JE | 1 |
| Vik, A | 1 |
| Aursnes, M | 1 |
| Holen, T | 1 |
| Hansen, TV | 1 |
| Nebb, HI | 1 |
| Sblano, S | 1 |
| Cerchia, C | 1 |
| Laghezza, A | 1 |
| Piemontese, L | 1 |
| Brunetti, L | 1 |
| Leuci, R | 1 |
| Gilardi, F | 1 |
| Thomas, A | 1 |
| Genovese, M | 1 |
| Santi, A | 1 |
| Tortorella, P | 1 |
| Paoli, P | 1 |
| Lavecchia, A | 1 |
| Loiodice, F | 1 |
| Bulhak, AA | 1 |
| Jung, C | 1 |
| Ostenson, CG | 1 |
| Lundberg, JO | 1 |
| Sjöquist, PO | 1 |
| Pernow, J | 1 |
| Chen, R | 1 |
| Liang, F | 1 |
| Morimoto, S | 1 |
| Li, Q | 1 |
| Moriya, J | 1 |
| Yamakawa, J | 1 |
| Takahashi, T | 1 |
| Iwai, K | 1 |
| Kanda, T | 1 |
| Zheng, Z | 1 |
| Yang, Y | 1 |
| Shao, H | 1 |
| Liu, Z | 1 |
| Lu, X | 1 |
| Xu, Y | 1 |
| He, X | 1 |
| Jiang, W | 1 |
| Jiang, Q | 1 |
| Zhao, B | 1 |
| Zhang, H | 1 |
| Si, S | 1 |
| Kim, H | 1 |
| Haluzik, M | 1 |
| Asghar, Z | 1 |
| Yau, D | 1 |
| Joseph, JW | 1 |
| Fernandez, AM | 1 |
| Reitman, ML | 1 |
| Yakar, S | 1 |
| Stannard, B | 1 |
| Heron-Milhavet, L | 1 |
| Wheeler, MB | 1 |
| LeRoith, D | 1 |
| Srinivasan, S | 1 |
| Hatley, ME | 1 |
| Reilly, KB | 1 |
| Danziger, EC | 1 |
| Hedrick, CC | 1 |
| Bouzakri, K | 1 |
| Roques, M | 1 |
| Debard, C | 1 |
| Berbe, V | 1 |
| Rieusset, J | 1 |
| Laville, M | 1 |
| Vidal, H | 1 |
| Nakamachi, T | 1 |
| Nomiyama, T | 1 |
| Gizard, F | 1 |
| Heywood, EB | 1 |
| Jones, KL | 1 |
| Zhao, Y | 1 |
| Fuentes, L | 1 |
| Takebayashi, K | 1 |
| Aso, Y | 1 |
| Staels, B | 1 |
| Inukai, T | 1 |
| Bruemmer, D | 1 |
| Satapati, S | 1 |
| He, T | 1 |
| Inagaki, T | 1 |
| Potthoff, M | 1 |
| Merritt, ME | 1 |
| Esser, V | 1 |
| Mangelsdorf, DJ | 1 |
| Kliewer, SA | 1 |
| Browning, JD | 1 |
| Burgess, SC | 1 |
| Moore, GB | 1 |
| Chapman, H | 1 |
| Holder, JC | 1 |
| Lister, CA | 1 |
| Piercy, V | 1 |
| Smith, SA | 1 |
| Clapham, JC | 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 |
14 other studies available for pirinixic acid and Diabetes Mellitus, Type 2
| Article | Year |
|---|---|
Design, synthesis, and evaluation of a new class of noncyclic 1,3-dicarbonyl compounds as PPARalpha selective activators.
Topics: Adipose Tissue; Administration, Oral; Aldehydes; Animals; Blood Glucose; Diabetes Mellitus, Type 2; | 2004 |
Discovery of a highly orally bioavailable c-5-[6-(4-Methanesulfonyloxyphenyl)hexyl]-2-methyl-1,3-dioxane-r-2-carboxylic acid as a potent hypoglycemic and hypolipidemic agent.
Topics: Animals; Carboxylic Acids; Diabetes Mellitus, Type 2; Dioxanes; Humans; Hypoglycemic Agents; Hypolip | 2008 |
Identification of dual PPARα/γ agonists and their effects on lipid metabolism.
Topics: 3T3-L1 Cells; Animals; Cell Line; Diabetes Mellitus, Type 2; Drug Design; HEK293 Cells; Humans; Liga | 2015 |
Synthesis and biological evaluations of marine oxohexadecenoic acids: PPARα/γ dual agonism and anti-diabetic target gene effects.
Topics: Animals; Cells, Cultured; Chlorocebus aethiops; COS Cells; Diabetes Mellitus, Type 2; Dose-Response | 2018 |
A chemoinformatics search for peroxisome proliferator-activated receptors ligands revealed a new pan-agonist able to reduce lipid accumulation and improve insulin sensitivity.
Topics: Cheminformatics; Diabetes Mellitus, Type 2; Humans; Hypoglycemic Agents; Insulin Resistance; Ligands | 2022 |
PPAR-alpha activation protects the type 2 diabetic myocardium against ischemia-reperfusion injury: involvement of the PI3-Kinase/Akt and NO pathway.
Topics: Androstadienes; Animals; Blood Glucose; Body Weight; Cardiotonic Agents; Diabetes Mellitus, Type 2; | 2009 |
The effects of a PPARalpha agonist on myocardial damage in obese diabetic mice with heart failure.
Topics: Adiponectin; Animals; Diabetes Mellitus, Type 2; Disease Models, Animal; Female; Heart Failure; Mice | 2010 |
Two thiophenes compounds are partial peroxisome proliferator-activated receptor α/γ dual agonists.
Topics: Animals; Cell Culture Techniques; Diabetes Mellitus, Type 2; Drug Evaluation, Preclinical; Genes, Re | 2011 |
Peroxisome proliferator-activated receptor-alpha agonist treatment in a transgenic model of type 2 diabetes reverses the lipotoxic state and improves glucose homeostasis.
Topics: Animals; Diabetes Mellitus, Type 2; Gluconeogenesis; Glucose; Glucose Clamp Technique; Homeostasis; | 2003 |
Modulation of PPARalpha expression and inflammatory interleukin-6 production by chronic glucose increases monocyte/endothelial adhesion.
Topics: Animals; Aorta; Cell Adhesion; Diabetes Mellitus, Type 2; Endothelial Cells; Endothelium, Vascular; | 2004 |
WY-14643 and 9- cis-retinoic acid induce IRS-2/PI 3-kinase signalling pathway and increase glucose transport in human skeletal muscle cells: differential effect in myotubes from healthy subjects and Type 2 diabetic patients.
Topics: Adult; Diabetes Mellitus, Type 2; Glucose; Humans; Insulin; Insulin Receptor Substrate Proteins; Int | 2004 |
PPARalpha agonists suppress osteopontin expression in macrophages and decrease plasma levels in patients with type 2 diabetes.
Topics: Animals; Bezafibrate; Cell Line; Diabetes Mellitus, Type 2; Gene Expression Regulation; Humans; Hypo | 2007 |
Partial resistance to peroxisome proliferator-activated receptor-alpha agonists in ZDF rats is associated with defective hepatic mitochondrial metabolism.
Topics: Animals; Blood Glucose; Diabetes Mellitus, Type 2; Fatty Acids, Nonesterified; Gluconeogenesis; Gluc | 2008 |
Differential regulation of adipocytokine mRNAs by rosiglitazone in db/db mice.
Topics: Adiponectin; Adrenergic beta-Agonists; Animals; Blood Glucose; Diabetes Mellitus, Type 2; Female; Ge | 2001 |