Evidence map›Paper›PMID 38854471›Full record

ArticleNutrition research and practice2024

Kaempferol ameliorates metabolic syndrome by inhibiting inflammation and oxidative stress in high-fat diet-induced obese mice.

Su-Kyung Shin, Eun-Young Kwon

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Article in Nutrition research and practice, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.

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0cells of the map it votes in
4citing papers in PubMed
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1 · What the graph read from it

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3 · Its place in the literature

Who cites it

4 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

2 authors.

Su-Kyung ShinDepartment of Food Science and Nutrition, Kyungpook National University, Daegu 41566, Korea.ORCID https://orcid.org/0000-0002-8918-3995
Eun-Young KwonDepartment of Food Science and Nutrition, Kyungpook National University, Daegu 41566, Korea.ORCID https://orcid.org/0000-0001-8357-9158

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

BACKGROUND/

objectivesKaempferol (Ka) is one of the most widely occurring flavonoids found in large amounts in various plants. Ka has anti-obesity, antioxidant, and anti-inflammatory effects. Despite the numerous papers documenting the efficacy of Ka, some controversy remains. Therefore, this study examined the impact of Ka using 3T3-L1 and high-fat diet-induced obese mice. MATERIALS/

methods3T3-L1 cells were treated with 50 μM Ka from the initiation of 3T3-L1 differentiation at D0 until the completion of differentiation on D8. Thirty male mice (C57BL/6J, 4 weeks old) were divided into 3 groups: normal diet (ND), high-fat diet (HFD), and HFD + 0.02% (w/w) Ka (Ka) group. All mice were fed their respective diets

resultsKa suppressed the hypertrophy of 3T3-L1 cells, and the Ka-supplemented mice showed a significant decrease in perirenal, retroperitoneal, mesenteric, and subcutaneous fat compared to the HFD group. Ka supplementation in high-fat diet-induced obese mice also improved the overall blood lipid concentration (total cholesterol, non-high-density lipoprotein-cholesterol, phospholipids, and apolipoprotein B). Ka supplementation in high-fat-induced obesity mice reduced hepatic steatosis and insulin resistance by modulating the hepatic lipid (glucose-6-phosphate dehydrogenase, fatty acid synthase, malic enzyme, phosphatidate phosphohydrolase, and β-oxidation) activities and glucose (glucokinase, phosphoenolpyruvate carboxykinase, and G6pase)-regulating enzymes. Ka supplementation ameliorated the erythrocyte and hepatic mitochondrial H

conclusionKa may be beneficial for preventing diet-induced obesity, inflammation, oxidative stress, and diabetes.

Indexed as

fatty liverinflammationmetabolic syndromeObesityoxidative stress

Identifiers

PMID38854471
PMCPMC11156765

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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 OpenQuestion graph.