Acer tegmentosum Maxim  Inhibits Adipogenesis in  3t3-l1  Adipocytes and Attenuates Lipid Accumulation in Obese Rats Fed a High-Fat Diet

There is no author summary for this article yet. Authors can add summaries to their articles on ScienceOpen to make them more accessible to a non-specialist audience.

Abstract

We investigated the effect of Acer tegmentosum Maxim (ATM) on adipocyte differentiation in 3T3-L1 cells and anti-obesity properties in obese rats fed a high-fat diet (HFD). Cellular lipid content in DMI (dexamethasone, 3–isobutyl–1–methylxanthine, and insulin mixture)-treated cells increased, while ATM treatment caused a significant reduction in lipid accumulation in differentiated 3T3-L1 cells. ATM (60 ug/mL) caused inhibition of adipogenesis via down-regulation of the CCAAT/enhancer binding protein β ( C/EBPβ) (48%), C/EBPα (66%), and peroxisome proliferator-activated receptor γ ( PPARγ) (64%) expressions in 3T3-L1 cells. Moreover, ATM induced a decrease in the expressions of adipocyte-specific genes, such as adipocyte fatty acid-binding protein-2 ( aP2), fatty acid synthase ( FAS), and lipoprotein lipase ( LPL). Protein kinase B ( Akt) and glycogen synthase kinase 3β ( GSK3β) phosphorylation was also decreased by ATM treatment of 3T3-L1 adipocytes. We investigated the anti-obesity effects of ATM on HFD-induced obese rats. Rats fed with an HFD demonstrated elevations in body weight gain, while the administration of ATM reversed body weight (BW) gains and adipose tissue weights in rats fed an HFD. ATM supplementation caused a decrease in the circulating triglyceride and total cholesterol levels and led to inhibition of lipid accumulation in the adipose tissues in HFD-induced obese rats. Epididymal fat exhibited significantly larger adipocytes in the HFD group than it did in the ATM-treated group. These results demonstrate that ATM administration caused a reduction in adiposity via attenuation in adipose tissue mass and adipocyte size.

Related collections

Most cited references 40

Record: found
Abstract: not found
Article: not found

Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement.

Scott M. Grundy, James I Cleeman, Stephen R Daniels … (2005)

0 comments Cited 1061 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

Association between insulin resistance and the development of cardiovascular disease

Valeska Ormazabal, Soumyalekshmi Nair, Omar Elfeky … (2018)

For many years, cardiovascular disease (CVD) has been the leading cause of death around the world. Often associated with CVD are comorbidities such as obesity, abnormal lipid profiles and insulin resistance. Insulin is a key hormone that functions as a regulator of cellular metabolism in many tissues in the human body. Insulin resistance is defined as a decrease in tissue response to insulin stimulation thus insulin resistance is characterized by defects in uptake and oxidation of glucose, a decrease in glycogen synthesis, and, to a lesser extent, the ability to suppress lipid oxidation. Literature widely suggests that free fatty acids are the predominant substrate used in the adult myocardium for ATP production, however, the cardiac metabolic network is highly flexible and can use other substrates, such as glucose, lactate or amino acids. During insulin resistance, several metabolic alterations induce the development of cardiovascular disease. For instance, insulin resistance can induce an imbalance in glucose metabolism that generates chronic hyperglycemia, which in turn triggers oxidative stress and causes an inflammatory response that leads to cell damage. Insulin resistance can also alter systemic lipid metabolism which then leads to the development of dyslipidemia and the well-known lipid triad: (1) high levels of plasma triglycerides, (2) low levels of high-density lipoprotein, and (3) the appearance of small dense low-density lipoproteins. This triad, along with endothelial dysfunction, which can also be induced by aberrant insulin signaling, contribute to atherosclerotic plaque formation. Regarding the systemic consequences associated with insulin resistance and the metabolic cardiac alterations, it can be concluded that insulin resistance in the myocardium generates damage by at least three different mechanisms: (1) signal transduction alteration, (2) impaired regulation of substrate metabolism, and (3) altered delivery of substrates to the myocardium. The aim of this review is to discuss the mechanisms associated with insulin resistance and the development of CVD. New therapies focused on decreasing insulin resistance may contribute to a decrease in both CVD and atherosclerotic plaque generation.

0 comments Cited 480 times – based on 0 reviews      Review now

Bookmark

Record: found
Abstract: found
Article: found

Is Open Access

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

David Ipsen, Jens Lykkesfeldt, Pernille Tveden-Nyborg (2018)

Non-alcoholic fatty liver disease (NAFLD) is currently the world’s most common liver disease, estimated to affect up to one-fourth of the population. Hallmarked by hepatic steatosis, NAFLD is associated with a multitude of detrimental effects and increased mortality. This narrative review investigates the molecular mechanisms of hepatic steatosis in NAFLD, focusing on the four major pathways contributing to lipid homeostasis in the liver. Hepatic steatosis is a consequence of lipid acquisition exceeding lipid disposal, i.e., the uptake of fatty acids and de novo lipogenesis surpassing fatty acid oxidation and export. In NAFLD, hepatic uptake and de novo lipogenesis are increased, while a compensatory enhancement of fatty acid oxidation is insufficient in normalizing lipid levels and may even promote cellular damage and disease progression by inducing oxidative stress, especially with compromised mitochondrial function and increased oxidation in peroxisomes and cytochromes. While lipid export initially increases, it plateaus and may even decrease with disease progression, sustaining the accumulation of lipids. Fueled by lipo-apoptosis, hepatic steatosis leads to systemic metabolic disarray that adversely affects multiple organs, placing abnormal lipid metabolism associated with NAFLD in close relation to many of the current life-style-related diseases.

0 comments Cited 348 times – based on 0 reviews      Review now

Bookmark

All references

Author and article information

Journal

Journal ID (nlm-ta): Nutrients

Journal ID (iso-abbrev): Nutrients

Journal ID (publisher-id): nutrients

Title: Nutrients

Publisher: MDPI

ISSN (Electronic): 2072-6643

Publication date (Electronic): 07 December 2020

Publication date Collection: December 2020

Volume: 12

Issue: 12

Electronic Location Identifier: 3753

Affiliations

[1 ]Institute of Animal Medicine, College of Veterinary Medicine, Gyeongsang National University, Jinju 660-701, Korea; greatcho2000@ 123456nate.com (H.-H.C.); insectraon@ 123456naver.com (S.-H.K.); sunhee5321@ 123456naver.com (S.-H.J.); wonck@ 123456gnu.ac.kr (C.W.)

[2 ]Department of Foods and Nutrition, Gyeongsang National University, Jinju 660-701, Korea; bodry96@ 123456hanmail.net

[3 ]Department of Public Health, Division of Environmental Health Science, New York Medical College, Valhalla, NY 10595, USA; HongDuck_Kim@ 123456nymc.edu

[4 ]Department of Food Science and Biotechnology, Daegu University, Gyungsan 712-714, Korea

Author notes

[* ]Correspondence: skyey7@ 123456daegu.ac.kr (T.H.K.); jaehcho@ 123456gnu.ac.kr (J.-H.C.); Tel.: +82-53-850-6533 (T.H.K.); +82-55-772-2358 (J.-H.C.)

Author information

Chungkil Won https://orcid.org/0000-0002-3105-1869

Article

Publisher ID: nutrients-12-03753

DOI: 10.3390/nu12123753

PMC ID: 7762257

PubMed ID: 33297378

SO-VID: f5b19558-43ee-4f96-87e7-d2da5267a437

License:

Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license ( http://creativecommons.org/licenses/by/4.0/).

Acer tegmentosum Maxim Inhibits Adipogenesis in 3t3-l1 Adipocytes and Attenuates Lipid Accumulation in Obese Rats Fed a High-Fat Diet

Read this article at

Abstract

Related collections

Karger: Nutrition and Dietetics

Most cited references 40

Diagnosis and management of the metabolic syndrome: an American Heart Association/National Heart, Lung, and Blood Institute Scientific Statement.

Association between insulin resistance and the development of cardiovascular disease

Molecular mechanisms of hepatic lipid accumulation in non-alcoholic fatty liver disease

Author and article information

Journal

Affiliations

Author notes

Author information

Article

History

Categories

Comments

Comment on this article

Similar content 169

Most referenced authors 872