Milk thistle seed cold press oil attenuates markers of the metabolic syndrome in a mouse model of dietary-induced obesity.


Journal

Journal of food biochemistry
ISSN: 1745-4514
Titre abrégé: J Food Biochem
Pays: United States
ID NLM: 7706045

Informations de publication

Date de publication:
12 2020
Historique:
received: 08 07 2020
revised: 23 09 2020
accepted: 24 09 2020
pubmed: 14 10 2020
medline: 22 6 2021
entrez: 13 10 2020
Statut: ppublish

Résumé

Milk thistle cold press oil (MTO) is an herbal remedy derived from Silybum marianum which contains a low level of silymarin and mixture of polyphenols and flavonoids. The effect of MTO on the cardiovascular and metabolic complications of obesity was studied in mice that were fed a high-fat diet (HFD) for 20 weeks and treated with MTO for the final 8 weeks of the diet. MTO treatment attenuated HFD-induced obesity, fasting hyperglycemia, hypertension, and induced markers of mitochondrial fusion and browning of white adipose. Markers of inflammation were also attenuated in both adipose and the liver of MTO-treated mice. In addition, MTO resulted in the improvement of liver fibrosis. These results demonstrate that MTO has beneficial actions to attenuate dietary obesity-induced weight gain, hyperglycemia, hypertension, inflammation, and suggest that MTO supplementation may prove beneficial to patients exhibiting symptoms of metabolic syndrome. PRACTICAL APPLICATIONS: Natural supplements are increasingly being considered as potential therapies for many chronic cardiovascular and metabolic diseases. Milk thistle cold press oil (MTO) is derived from Silybum marianum which is used as a dietary supplement in different parts of the world. The results of the present study demonstrate that MTO supplementation normalizes several metabolic and cardiovascular complications arising from dietary-induced obesity. MTO supplementation also had anti-inflammatory actions in the adipose as well as the liver. These results suggest that supplementation of MTO into the diet of obese individuals may afford protection against the worsening of cardiovascular and metabolic disease and improve inflammation and liver fibrosis.

Identifiants

pubmed: 33047319
doi: 10.1111/jfbc.13522
pmc: PMC7770619
mid: NIHMS1654084
doi:

Types de publication

Journal Article Research Support, N.I.H., Extramural

Langues

eng

Sous-ensembles de citation

IM

Pagination

e13522

Subventions

Organisme : NHLBI NIH HHS
ID : P01 HL051971
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM104357
Pays : United States
Organisme : NIGMS NIH HHS
ID : P20 GM121334
Pays : United States
Organisme : NIDDK NIH HHS
ID : R01 DK121748
Pays : United States
Organisme : NHLBI NIH HHS
ID : R56 HL139561
Pays : United States

Informations de copyright

© 2020 Wiley Periodicals LLC.

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Auteurs

Hsin-Hsueh Shen (HH)

Department of Medicine, New York Medical College, Valhalla, NY, USA.
Department and Institute of Pharmacology, National Defense Medical Center, Taipei, Taiwan.

Ragin Alex (R)

Department of Pharmacology, New York Medical College, Valhalla, NY, USA.

Lars Bellner (L)

Department of Pharmacology, New York Medical College, Valhalla, NY, USA.

Marco Raffaele (M)

Department of Medicine, New York Medical College, Valhalla, NY, USA.
Department of Drug Sciences, University of Catania, Catania, Italy.

Maria Licari (M)

Department of Medicine, New York Medical College, Valhalla, NY, USA.
Department of Drug Sciences, University of Catania, Catania, Italy.

Luca Vanella (L)

Department of Drug Sciences, University of Catania, Catania, Italy.

David E Stec (DE)

Department of Physiology and Biophysics, Cardiorenal and Metabolic Diseases Research Center, University of Mississippi Medical Center, Jackson, MS, USA.

Nader G Abraham (NG)

Department of Medicine, New York Medical College, Valhalla, NY, USA.
Department of Pharmacology, New York Medical College, Valhalla, NY, USA.

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Classifications MeSH