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Cited by 34

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Protective effect of D-(-)-quinic acid as food supplement in modulating AMP-activated protein kinase signalling pathway activation in HFD induced obesity

Dong, Jie, Zheng, HaiLong, Zeng, Qiuyao, Zhang, Xian, Du, Liang, Bais, Souravh·2022·Human & Experimental Toxicology
DOI 10.1177/09603271221119804
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Abstract

Background: Dietary quinic acid given as the nutritional supplement, which may leads to tryptophan and nicotinamide production in the intestinal tract and NAD + precursor which can prevent from the negative consequences of high fat diet (HFD) consumption. Objective: The present study was designed to assess in vivo and in vitro effect of D-(−)-Quinic acid in high-fat diet induced hyperlipidemia in mice. Material and methods: Thirty six albino mice were randomly divided in six groups and each group had six mice. Group I, controlled mice given normal pellet diet, Group-II mice, administered with high fat diet (HFD), Group-III mice given standard drug, Atorvastatin (20 mg/kg, p.o.) along with HFD to mice and Group IV, V and VI mice received D-(−)-Quinic acid at a dose of 75, 150 and 300 mg/kg, respectively in separate group along with HFD to mice. After completion of trial (49 days) the animals were sacrificed and evaluated for body weight, organ fat pad weight, and changes in weight of liver, heart and kidney and also for biochemical parameters, expression of adipogenic and inflammation markers in adipose tissues, and histology examination of liver tissue. Results: In vitro testing results showed, D-(−)-Quinic acid potentially inhibit α-glucosidase enzyme activity as compared to acarbose. The D-(−)-Quinic acid showed significant hypolipidemic activity by decreasing the increased level of cholesterol, triglyceride level, LDL, VLDL and other hepatic parameters like SGOT and SGPT in serum. D-(−)-Quinic acid reduces the mRNA expression level of PPAR-γ2, TNF-α, IL-1β and IL-6 in adipose tissue in hyperlipidemic mice.

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Cited by

Metadata

Authors
Dong, J., Zheng, H., Zeng, Q., Zhang, X., Du, L., & Bais, S.
Affiliations
  • Department of Clinical Laboratory, Guangzhou Twelfth People’s Hospital, Guangzhou, P.R. China
  • Department of Endocrinology, The First Affiliated Hospital of Hainan Medical University, Haikou, P.R. China
  • Department of Clinical Laboratory Medi-cine, Sun Yat-sen University Cancer Center, State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangzhou, P.R. China
  • Department of Endocrinology and Metabolism, Sinopharm Dongfeng General Hospital, Hubei University of Medicine, Shiyan 442008, Hubei, PR China.
  • Institute of Pharmaceutical Science, Sage University, Indore, India
ORCID
Venue
Human & Experimental Toxicology
Publisher
SAGE Publications
Published
2022-01
Volume
41
ISSN
  • 0960-3271
  • 1477-0903
DOI
10.1177/09603271221119804
Cited by
34
References
1
Language
en
Licence
creativecommons.org/licenses/by-nc/4.0/ (unspecified)
Funders
Institutional funding

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Bibliographic data: Semantic Scholar, OpenAlex, Crossref.

Contains information from the Semantic Scholar Academic Graph Datasets, made available under the ODC Attribution License (ODC-BY 1.0).

Semantic Scholar’s data is described in: Kinney, R., et al. (2023). The Semantic Scholar Open Data Platform. arXiv:2301.10140.