Research Article Details
Article ID: | A04199 |
PMID: | 33719959 |
Source: | Curr Pharm Des |
Title: | The Effect of Metformin on Aminotransferase Levels, Metabolic Parameters and Body Mass Index in Nonalcoholic Fatty Liver Disease Patients: A Metaanalysis. |
Abstract: | BACKGROUND: Nonalcoholic fatty liver disease (NAFLD) is one of the most common reasons for the increase in serum alanine aminotransferase (ALT) and aspartate aminotransferase (AST) levels. Moreover, liver- associated death is approximately 10 times higher in patients with NAFLD than in common individuals. In theory, NAFLD is a kind of metabolic syndrome that manifests in the liver, and insulin resistance plays an important role in it. Therefore, drugs that improve insulin sensitivity may be effective for NAFLD. OBJECTIVE: The aim of this study was to evaluate the effect of metformin treatment on aminotransferase levels, metabolic parameters and body mass index in NAFLD patients via a meta-analysis of clinical trials. METHODS: A comprehensive search on PubMed, EMBASE, the Web of Science and the Cochrane Central Register of Controlled Trials was performed for randomized controlled trials (RCTs) on the effect of metformin treatment on aminotransferase levels, metabolic parameters and body mass index in NAFLD patients. Serum hepatic enzyme, lipid, glucose and insulin levels, homeostasis model assessment-insulin resistance (HOMA-IR) index and body mass index (BMI) at different follow-up points exhibited desirable outcomes. The final search was performed in January, 2021. RESULTS: In total, 10 RCTs with 459 patients were included. Compared with controls, metformin could effectively reduce serum fasting glucose and insulin levels and the HOMA-IR index in NAFLD patients at the 6-month follow-up. In addition, metformin could clearly reduce the serum ALT and HOMA-IR index at the 12-month follow-up. Although metformin was found to be effective in managing lipid metabolism and controlling BMI in NAFLD patients compared with that at baseline, the effect was similar to that in controls. In addition, the speed of metformin treatment seemed to be slower than that of controls. CONCLUSION: Compared to the controls, metformin could effectively reduce the serum fasting glucose and insulin levels and the HOMA-IR index in NAFLD patients at the 6-month follow-up and ALT and the HOMA-IR index at the 12-month follow-up. |
DOI: | 10.2174/1381612827666210315144821 |

Strategy ID | Therapy Strategy | Synonyms | Therapy Targets | Therapy Drugs | |
---|---|---|---|---|---|
S01 | Improve insulin resistance | insulin sensitizer; insulin resistance; glucose tolerance | Biguanide: increases 5-AMP activated protein kinase signaling; SGLT-2 inhibitor; Thiazalidinedione: selective PPAR-γ agonists; GLP-1 agonist | Metformin; Empagliflozin; Canagliflozin; Rosiglitazone; Pioglitazone; Liraglutide | Details |
S02 | Enhance lipid metabolism | triglyceride-lowering; lipid tolerance; lipid metabolism | 3-hydroxy-3-methylglutaryl coenzyme A (HMG-CoA) inhibitor; Decreases intestinal cholesterol absorption; FXR agonist; ACC inhibitor; FAS inhibitor; DGAT2 inhibitor; SCD-1 inhibitor | Atorvastatin; Ezetimibe; Obeticholic Acid; GS-9674; GS-0976; TVB-2640; IONIS-DGAT2rx; Aramchol; | Details |
Diseases ID | DO ID | Disease Name | Definition | Class | |
---|---|---|---|---|---|
I05 | 9352 | Type 2 diabetes mellitus | A diabetes that is characterized by chronic hyperglycaemia with disturbances of carbohydrate, fat and protein metabolism resulting from defects in insulin secretion, insulin action, or both. A diabetes mellitus that is characterized by high blood sugar, insulin resistance, and relative lack of insulin. http://en.wikipedia.org/wiki/Diabetes, http://en.wikipedia.org/wiki/Diabetes_mellitus_type_2 | disease of metabolism/inherited metabolic disorder/ carbohydrate metabolic disorder/glucose metabolism disease/diabetes/ diabetes mellitus | Details |
Drug ID | Drug Name | Type | DrugBank ID | Targets | Category | Latest Progress | |
---|---|---|---|---|---|---|---|
D225 | Metformin | Chemical drug | DB00331 | PRKAB1 inducer activator; ETEDH inhibitor; GPD1 inhibitor | Improve insulin resistance | Under clinical trials | Details |
D199 | L-alanine | Chemical drug | DB00160 | KYNU | -- | Failed in clinical trials | Details |
D328 | Serine | Chemical drug | DB00133 | SRR | Improve insulin resistance | Under clinical trials | Details |
D182 | Insulin | Biological drug | DB00030 | INSR agonist; CPE modulator&product of | -- | Under clinical trials | Details |
D316 | S-adenosyl-L-methionine | Chemical drug | DB00118 | GNMT cofactor | Antiviral | Under clinical trials | Details |
D157 | Glucophage | Chemical drug | DB00331 | -- | -- | Under clinical trials | Details |