Green tea (–)‐epigallocatechin gallate inhibits <scp>IGF</scp>‐<scp>I</scp> and <scp>IGF</scp>‐<scp>II</scp>stimulation of 3T3‐<scp>L</scp>1 preadipocyte mitogenesis via the 67‐k<scp>D</scp>a laminin receptor, but not <scp>AMP</scp>‐activated protein kinase pathway

Ku, Hui Chen; Liu, Hang Seng; Hung, Pei Fang; Chen, Chialin; Liu, Hsien Chun; Chang, Hsin Huei; Tsuei, Yi Wei; Shih, Li Jane; Lin, Ching Ling; Lin, Chih Ming; Kao, Ying-Jer

doi:10.1002/mnfr.201100438

Cited by 39 publications

(33 citation statements)

References 54 publications

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“…Ku et al . () reported that tea polyphenol EGCG inhibited adipocyte differentiation of 3T3‐L1 cells through inhibiting ERK phosphorylation up to 50 μ m , although there was no effect on JNK activation. The EGCG effects appeared to be selective for ERK pathway.…”

Section: Discussionmentioning

confidence: 97%

Impacts of Camellia kucha and its main chemical components on the lipid accumulation in 3T3‐L1 adipocytes

Wong

et al. 2016

Int J of Food Sci Tech

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Summary Camellia kucha, a wild tea plant with potent antioxidant potential, has been consumed as local beverage for a long history. It is featured for the presence of theacrine and low content of caffeine. Interestingly, compared with caffeine showed strong stimulant effect, theacrine showed sedation, hypnoses and promoting memory function. In this study, the anti‐adipogenic ability of Kucha tea (KT) and its main components were evaluated in mouse 3T3‐L1 cells. The results indicated that KT acted significantly to decrease lipid droplet accumulation. Moreover, KT decreased the expression of major transcription factors of adipogenesis pathway, such as PPAR γ and C/EBP α. KT also decreased the mRNA and protein levels of fatty acid synthase, fatty acid translocase, steroylcoenzyme A desaturase‐1, lipoprotein lipase and acetyl‐CoA carboxylase‐1. Furthermore, KT suppressed the activation of ERK, p38 and JNK.

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Section: Discussionmentioning

confidence: 97%

Impacts of Camellia kucha and its main chemical components on the lipid accumulation in 3T3‐L1 adipocytes

Wong

et al. 2016

Int J of Food Sci Tech

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“…In more specialized conditions, LAMR has also been shown to interact with the GM‐CSF receptor (Chen et al, ; Ando et al, ), insulin‐like growth factor receptors I and II (Ku et al, ), insulin receptor and insulin receptor substrates (IRS‐1/2/4) (Ku et al, ), the T‐cell specific adaptor protein TSAd (Park et al, ). LAMR also potentially serves as a receptor for both the anti‐angiogenic agent pigment epithelium‐derived factor (PEDF) (Bernard et al, ) and the pro‐survival pro‐angiogenic midkine protein, which may induce nuclear localization of LAMR (Salama et al, ).…”

Section: /67‐kda Laminin Receptor Functionmentioning

confidence: 99%

Looking into laminin receptor: critical discussion regarding the non‐integrin 37/67‐kDalaminin receptor/RPSAprotein

2015

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The 37/67-kDa laminin receptor (LAMR/RPSA) was originally identified as a 67-kDa binding protein for laminin, an extracellular matrix glycoprotein that provides cellular adhesion to the basement membrane. LAMR has evolutionary origins, however, as a 37-kDa RPS2 family ribosomal component. Expressed in all domains of life, RPS2 proteins have been shown to have remarkably diverse physiological roles that vary across species. Contributing to laminin binding, ribosome biogenesis, cytoskeletal organization, and nuclear functions, this protein governs critical cellular processes including growth, survival, migration, protein synthesis, development, and differentiation. Unsurprisingly given its purview, LAMR has been associated with metastatic cancer, neurodegenerative disease and developmental abnormalities. Functioning in a receptor capacity, this protein also confers susceptibility to bacterial and viral infection. LAMR is clearly a molecule of consequence in human disease, directly mediating pathological events that make it a prime target for therapeutic interventions. Despite decades of research, there are still a large number of open questions regarding the cellular biology of LAMR, the nature of its ability to bind laminin, the function of its intrinsically disordered C-terminal region and its conversion from 37 to 67 kDa. This review attempts to convey an in-depth description of the complexity surrounding this multifaceted protein across functional, structural and pathological aspects.

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“…For example, plant extracts including polyphenols, resveratrol, curcumin, and proanthocyanidins, have become increasingly popular in the past decades for their anti-adipogenic properties [1,13,14]. It was also reported that herbal medicine was effective as potential therapy for fatty liver disease, diabetes, and metabolic syndrome [15].…”

Section: Introductionmentioning

confidence: 99%

Tenebrio molitor Larvae Inhibit Adipogenesis through AMPK and MAPKs Signaling in 3T3-L1 Adipocytes and Obesity in High-Fat Diet-Induced Obese Mice

Seo

Goo

Chung

et al. 2017

IJMS

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Despite the increasing interest in insect-based bioactive products, the biological activities of these products are rarely studied adequately. Larvae of Tenebrio molitor, the yellow mealworm, have been eaten as a traditional food and provide many health benefits. Therefore, we hypothesized that T. molitor larvae might influence adipogenesis and obesity-related disorders. In the present study, we investigated the anti-adipogenic and antiobesity effects of T. molitor larvae in vitro and in vivo. The lipid accumulation and triglyceride content in mature adipocytes was reduced significantly (up to 90%) upon exposure to an ethanol extract of T. molitor larvae, without a reduction in cell viability. Exposure also resulted in key adipogenic and lipogenic transcription factors. Additionally, in adipogenic differentiation medium the extract induced phosphorylation of adenosine monophosphate (AMP)-activated protein kinase and mitogen-activated protein kinases. Daily oral administration of T. molitor larvae powder to obese mice fed high-fat diet attenuated body weight gain. We also found that the powder efficiently reduced hepatic steatosis as well as aspartate and alanine transaminase enzyme levels in mice fed a high-fat diet. Our results suggest that T. molitor larvae extract has an antiobesity effect when administered as a food supplement and has potential as a therapeutic agent for obesity.

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Green tea (–)‐epigallocatechin gallate inhibits IGF‐I and IGF‐IIstimulation of 3T3‐L1 preadipocyte mitogenesis via the 67‐kDa laminin receptor, but not AMP‐activated protein kinase pathway

Abstract: The results of this study suggest that EGCG mediates anti-IGF-I and anti-IGF-II signals in preadipocyte mitogenesis via the 67LR but not the AMPK pathway.

Cited by 39 publications

References 54 publications

Impacts of Camellia kucha and its main chemical components on the lipid accumulation in 3T3‐L1 adipocytes

Impacts of Camellia kucha and its main chemical components on the lipid accumulation in 3T3‐L1 adipocytes

Looking into laminin receptor: critical discussion regarding the non‐integrin 37/67‐kDalaminin receptor/RPSAprotein

Tenebrio molitor Larvae Inhibit Adipogenesis through AMPK and MAPKs Signaling in 3T3-L1 Adipocytes and Obesity in High-Fat Diet-Induced Obese Mice

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