Table 1.
Clinical Study of PPARγ Agonists
| Drug Name | Category | Activation Effect136 | Conclusion | Article Type |
|---|---|---|---|---|
| Pioglitazone | PPARγ Mono-Agonist | α25.2%, δ0.518%, γ104% PCG-1α>70%, SRC1>20% |
Oral Glucose Tolerance Test (OGTT) showed a reduction in blood glucose levels; ALT levels decreased; Improvements in steatosis, ballooning degeneration, and lobular inflammation were observed137 | RCT |
| The levels of fasting blood glucose, ALT, AST, γ-glutamyltransferase, and triglycerides were reduced, and insulin resistance was improved138 | META | |||
| PPARγ activation-mediated improvements in tissue pathology, liver enzymes, HOMA-IR, and reductions in blood lipids were consistent in both non-diabetic NAFLD patients and diabetic NAFLD patients. The incidence of edema was higher in the pioglitazone group139 | META | |||
| Improvement in left ventricular mechanics in undiagnosed ASCVD patients140 | PCS | |||
| Fatty degeneration, inflammation, ballooning, and improvement in liver function; reduction in blood glucose; no significant improvement in fibrosis markers141 | META | |||
| One year of low-dose pioglitazone treatment significantly improved hepatic fat degeneration and inflammation, as well as systemic and adipose tissue insulin resistance. The beneficial effects of pioglitazone on NAFLD were independent of blood glucose control142 | RCT | |||
| Compared to the tofogliflozin group, pioglitazone treatment showed no significant difference in improving hepatic fat degeneration and blood glucose levels, but it significantly increased adiponectin and HDL levels, and notably reduced triglyceride levels, although it caused weight gain143 | PCS | |||
| Pioglitazone shows better efficacy in women144 | RCT | |||
| Pioglitazone is the optimal therapy for treating steatosis and alleviating lobular inflammation145 | META | |||
| Decreased Bone Mineral Density (BMD) in the lumbar spine146 | PCS | |||
| Serum ALT levels, HbA1c, and fasting blood glucose were reduced; there was no significant reduction in visceral fat area147 | PCS | |||
| The prevalence of bladder cancer was very low in diabetic patients exposed to (or not exposed to) pioglitazone (<0.3%), and the beneficial effects of the drug on CVD and NASH were much greater. Therefore, the use of pioglitazone should be resumed148 | META | |||
| Rosiglitazone | PPARγ Mono-Agonist | Overall improvement in fatty degeneration, hepatocyte inflammation, ballooning degeneration, and fibrosis; serum transaminases were reduced149 | PCS | |
| Saroglitazar | PPARα/γ Dual-Agonist | α/δ13.3%, γ为24.9%PCG-1α <50%, SRC1<50% | Improvement in liver enzymes, serum glucose, and lipid profile, along with reduced liver stiffness, with no significant adverse effects150 | META |
| ALT, liver fat content, insulin resistance, and atherogenic dyslipidemia were improved151 | RCT | |||
| Regardless of weight loss, significant reductions were observed in CAP value, ALT, AST, HbA1c, LDL, total cholesterol, and triglyceride levels152 | PCS | |||
| lanifibranor | PPAR Pan-Agonist | α56.4%, γ89.4%, δ6.0%PCG-1α >100%,SRC1<50% | Liver enzyme levels were reduced, with improvements in lipids, inflammation, and fibrosis153 | RCT |
| Aleglitazar | PPARα/γ Dual-Agonist | Improvements in hepatic steatosis and fibrosis154 | RCT | |
| Fenofibrate | PPARα(/γ Dual) Agonist | Serum triglyceride levels were reduced, but the overall liver volume and total liver fat volume increased.155 | RCT | |
| Inflammatory factors (TNF-α), liver function (ALT, AST, GGT), markers related to matrix deposition (HA), liver fibrosis-associated cytokine (TGF-β1), lipid profile (total cholesterol, TG, LDL-C), blood glucose levels (FPI, FBG, HOMA-IR), and liver stiffness were significantly reduced; HDL-C was significantly increased.156 | PCS |
Abbreviations: RCT, randomized controlled trial; META, Meta-analysis; PCS, Prospective Clinical Study.