Evidence map›Paper›PMID 34825068›Full record

ArticleBiochemistry and biophysics reports2021

Metformin treatment reverses high fat diet- induced non-alcoholic fatty liver diseases and dyslipidemia by stimulating multiple antioxidant and anti-inflammatory pathways.

Tahmina Yasmin, Md Mizanur Rahman, Ferdous Khan, Fariha Kabir, Kamrun Nahar, Shoumen Lasker, Md Didarul Islam, Mohammad Maqsud Hossain, Raquibul Hasan, Sohel Rana and 1 more

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Biochemistry and biophysics reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.

0numbers the graph read from it
0cells of the map it votes in
27citing papers in PubMed
3.5field-weighted citation impact, top 6% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

27 citing papers in PubMed, 39 citations in OpenAlex.

  1. Trial
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  5. Metformin Alone and in Combinations Alter the Methylation Patterns ofEndocrine, metabolic & immune disorders drug targets · 2026
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

11 authors at 3 institutions in 2 countries.

Tahmina YasminDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Md Mizanur RahmanDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Ferdous KhanDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Fariha KabirDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Kamrun NaharDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Shoumen LaskerDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Md Didarul IslamDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
Mohammad Maqsud HossainDepartment of Biochemistry and Microbiology and NSU Genome Research Institute (NGRI), North South University, Dhaka, 1229, Bangladesh.
Raquibul HasanDepartment of Pharmaceutical Sciences, College of Pharmacy, Mercer University, 3001 Mercer University Drive, Atlanta, GA, 30341, United States.
Sohel RanaDepartment of Pharmacy, Jahangir Nagar University, Savar, Dhaka, 1342, Bangladesh.
Md Ashraful AlamDepartment of Pharmaceutical Sciences, North South University, Dhaka, 1229, Bangladesh.
North South University · BDJahangirnagar University · BDMercer University Health Sciences Center · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeThis current study investigated the effect of metformin treatment on hepatic oxidative stress and inflammation associated with nonalcoholic fatty liver disease (NADLD) in high fat diet (HFD) fed rats.

methodWistar rats were fed with a HFD or laboratory chow diet for 8 weeks. Metformin was administered orally at a dose of 200 mg/kg. Body weight, food and water intake were recorded on daily basis. Oral glucose tolerance test (OGTT), biochemical analysis and histological examinations were conducted on plasma and tissue samples. Antioxidant and anti-inflammatory mRNA expression was analyzed using reverse transcription polymeric chain reaction (RT-PCR).

resultsMetformin treatment for 8 weeks prevented HFD-induced weight gain and decreased fat deposition in HFD fed rats. Biochemical analysis revealed that metformin treatment significantly attenuated nitro-oxidative stress markers malondialdehyde (MDA), advanced protein oxidation product (APOP), and excessive nitric oxide (NO) levels in the liver of HFD fed rats. Gene expression analysis demonestrated that metformin treatment was associated with an enhanced expression of antioxidant genes such as Nrf-2, HO-1, SOD and catalase in liver of HFD fed rats. Metformin treatment also found to modulate the expression of fat metabolizing and anti-inflammatory genes including PPAR--γ, C/EBP-α, SREBP1c, FAS, AMPK and GLUT-4. Consistent with the biochemical and gene expression data, the histopathological examination unveiled that metformin treatment attenuated inflammatory cells infiltration, steatosis, hepatocyte necrosis, collagen deposition, and fibrosis in the liver of HFD fed rats.

conclusionIn conclusion, this study suggests that metformin might be effective in the prevention and treatment of HFD-induced steatosis by reducing hepatic oxidative stress and inflammation in the liver.

Indexed as

ALP, alkaline phosphataseALT, alanine aminotransferaseAMPK, AMP-activated protein kinaseAPOP, advanced protein oxidation productAST, aspartate aminotransferaseATP, Adinosine triphosphateAUC, area under the curveCAT, catalaseFAS, Fatty acid synthaseHDL, high density lipoproteinHF, High fatHSCs, Hepatic stellate cellsIACUC, Institutional Animal Care and Use CommitteeIL-6, interleukin-6InflammationLDL, low density lipoproteinLipid peroxidationMDA, MalondialdehydeMetforminMet, MetforminMPO, MyeloperoxidaseNAFLD, nonalcoholic fatty liver diseaseNon-alcoholic fatty liver diseaseNO, nitric oxideObesityOGTT, Oral glucose tolerance testPBS, Phosphate buffer salinePGC-1α, peroxisome proliferator-activated receptor γ coactivator 1PPAR-γ, peroxisome proliferator-activated receptor γROS, reactive oxygen speciesSOD, Superoxide dismutaseSREBP1c, sterol regulatory element-binding protein 1cTBARS, Thiobarbituric acid reactive substancesTBA, Thiobarbituric acid

Identifiers

PMID34825068
PMCPMC8605070
OpenAlexW3213841030

What Socratic holds

Textmetadata
LicenceCC BY-NC-ND
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the Socratic graph.