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Arachidonic acid supplementation attenuates adipocyte inflammation but not adiposity in high fat diet induced obese mice.
Roy, Sourav; Ripon, Md Abdur Rahman; Begum, Rahima; Bhowmik, Dipty Rani; Amin, Mohammad Tohidul; Islam, Md Aminul; Ahmed, Firoz; Hossain, Mohammad Salim.
Afiliação
  • Roy S; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Ripon MAR; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Begum R; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Bhowmik DR; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Amin MT; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Islam MA; Department of Microbiology, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Ahmed F; Department of Microbiology, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh.
  • Hossain MS; Department of Pharmacy, Noakhali Science and Technology University, Noakhali, 3814, Bangladesh. Electronic address: pharmasalim@yahoo.com.
Biochem Biophys Res Commun ; 608: 90-95, 2022 06 11.
Article em En | MEDLINE | ID: mdl-35397428
ABSTRACT
Obesity is associated with low-grade chronic inflammation and has a remarkable role in the pathophysiology of metabolic complications. In triggering these inflammatory responses, the arachidonic acid (AA) cascade plays a key role. However, there is a lack of data on how supplementary AA would affect obesity, adipose tissue inflammation, and the AA cascade in obesity. This study aims to investigate how AA supplementation affects obesity, adipocyte morphology, inflammation, and AA cascade signaling. Male Swiss Albino mice were used in our experiment. The mice were fed high-fat diets to induce obesity, and these obese mice were treated with two different doses of AA for 3 weeks. A normal diet non-obese group and an untreated obese group were kept as controls. Bodyweight and daily food intake data were recorded during that period. After the treatment period, blood serum and white adipose tissue of the experimental mice were collected for colorimetric lipid profile tests, histology, and mRNA extraction. The ΔΔCT method was employed for calculating the relative mRNA expression of target genes. The findings of our study suggest that AA has no significant effects on body weight, visceral adiposity, adipose tissue morphology, and serum lipid profile. However, AA treatment has resulted in a significant down-regulation of pro-inflammatory markers as well as the COX pathway. Besides, up-regulation of 12/15-LOX has been observed, indicating the metabolism pathway of supplementary AA through the LOX pathway. Our findings indicate that AA treatment may not provide significant benefits in terms of body weight, visceral fat mass, or serum lipid profile. However, it has effectively alleviated obesity-induced adipocyte inflammation in high-fat diet-induced obese mice.
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Texto completo: 1 Base de dados: MEDLINE Assunto principal: Adiposidade / Dieta Hiperlipídica Tipo de estudo: Etiology_studies Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Bangladesh

Texto completo: 1 Base de dados: MEDLINE Assunto principal: Adiposidade / Dieta Hiperlipídica Tipo de estudo: Etiology_studies Idioma: En Revista: Biochem Biophys Res Commun Ano de publicação: 2022 Tipo de documento: Article País de afiliação: Bangladesh