p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?

Bengal, Eyal; Aviram, Sharon; Hayek, Tony

doi:10.3390/ijms21186480

Cited by 58 publications

(48 citation statements)

References 119 publications

(149 reference statements)

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“…Mitogen-activated protein kinase (MAPK), mainly consisting of three distinctive cascades, the JNK, p38 and ERK pathways, is a well-known and crucial signaling pathway in multiple diseases (58)(59)(60)(61). In the past decades, the role of MAPK cascade in the TGF-β1-relevant IPF has been gradually elucidated.…”

Section: Mapk-relevant Signaling Pathwaymentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

122

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Idiopathic pulmonary fibrosis (IPF) is a worldwide disease characterized by the chronic and irreversible decline of lung function. Currently, there is no drug to successfully treat the disease except for lung transplantation. Numerous studies have been devoted to the study of the fibrotic process of IPF and findings showed that transforming growth factor-β1 (TGF-β1) plays a central role in the development of IPF. TGF-β1 promotes the fibrotic process of IPF through various signaling pathways, including the Smad, MAPK, and ERK signaling pathways. There are intersections between these signaling pathways, which provide new targets for researchers to study new drugs. In addition, TGF-β1 can affect the fibrosis process of IPF by affecting oxidative stress, epigenetics and other aspects. Most of the processes involved in TGF-β1 promote IPF, but TGF-β1 can also inhibit it. This review discusses the role of TGF-β1 in IPF. Contents1. Introduction 2. TGF-β1-involved pathway in IPF 3. Discussion 4. Conclusion

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Section: Mapk-relevant Signaling Pathwaymentioning

confidence: 99%

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

2021

Int J Mol Med

122

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“…Among them we found MAPK1, which is an activated regulator found in FHL2−/− heart, also a known as an interactor of FHL2. It was previously shown that FHL2 represses MAPK1 activity in cardiomyocytes and this was related to the cardiac hypertrophy response, but MAPK1 is also involved in glucose diffusion and development of insulin resistance in obesity [46,47]. Energy expenditure can be increased by the process of adaptive thermogenesis of BAT, but we found no structural differences, with a trend towards higher expression of the key thermogenic protein UCP1 in FHL2−/− mice and a significant preference for the uptake from the circulation of fatty acids over glucose.…”

Section: Discussionmentioning

confidence: 99%

Four-and-a-half LIM domain protein 2 (FHL2) deficiency protects mice from diet-induced obesity and high FHL2 expression marks human obesity

et al. 2021

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Four-and-a-half LIM domain protein 2 (FHL2) Energy metabolism Energy expenditure Glucose uptake Lipid uptake White adipose tissue (WAT) Browning of WAT Objective: Four-and-a-Half-LIM-domain-protein 2 (FHL2) modulates multiple signal transduction pathways but has not been implicated in obesity or energy metabolism. In humans, methylation and expression of the FHL2 gene increases with age, and high FHL2 expression is associated with increased body weight in humans and mice. This led us to hypothesize that FHL2 is a determinant of diet-induced obesity. Methods: FHL2-deficient (FHL2−/−) and wild type male mice were fed a high-fat diet. Metabolic phenotyping of these mice, as well as transcriptional analysis of key metabolic tissues was performed. Correlation of the expression of FHL2 and relevant genes was assessed in datasets from white adipose tissue of individuals with and without obesity. Results: FHL2 Deficiency protects mice from high-fat diet-induced weight gain, whereas glucose handling is normal. We observed enhanced energy expenditure, which may be explained by a combination of changes in multiple tissues; mild activation of brown adipose tissue with increased fatty acid uptake, increased cardiac glucose uptake and browning of white adipose tissue. Corroborating our findings in mice, expression of FHL2 in human white adipose tissue positively correlates with obesity and negatively with expression of browning-associated genes. Conclusion: Our results position FHL2 as a novel regulator of obesity and energy expenditure in mice and human. Given that FHL2 expression increases during aging, we now show that low FHL2 expression associates with a healthy metabolic state.

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“…After this activation cascade occurred, increased levels of GLUT4 were produced in the cytosol and then moved to the cell membrane for glucose uptake ( Figure 7 ). Simultaneously, S. pastorianus extract elicited the activation of p38 MAPK, which plays an important role in GLUT4 activation ( Figure 7 ) [ 27 ]. Notably, the expression of PKC was raised in 3T3-L1 cells treated with S. pastorianus extract ( Figure 3 B).…”

Section: Discussionmentioning

confidence: 99%

Exploration of Hypoglycemic Activity of Saccharomyces pastorianus Extract and Evaluation of the Molecular Mechanisms

Huang

Chung

et al. 2021

Molecules

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Although the hypoglycemic potential of brewer’s yeast extract has been reported, there is limited information pertaining to the hypoglycemic ingredients of Saccharomyces pastorianus extract and their mechanisms of action available. This study aimed to investigate the in vivo and in vitro hypoglycemic effect of S. pastorianus extract and to elucidate its molecular mechanisms. S. pastorianus extract was mainly composed of proteins followed by carbohydrates. In diabetic rats, oral administration of S. pastorianus extract significantly reduced the levels of plasma glucose and enhanced the activity of hepatic glucose-6-phosphatase dehydrogenase. Treatment with S. pastorianus extract increased the localization of type 4 glucose transporter (GLUT4), PTP, and insulin receptor at 3T3-L1 cell membranes and raised the levels of P38 MAPK, PI3K, and AKT in the cytosol. In agreement with these results, pretreatment of 3T3-L1 cells with inhibitors of PTP, PI3K, Akt/PKB, and p38 MAPK inhibited glucose uptake induced by application of S. pastorianus extract. Most importantly, a 54 kDa protein with hypoglycemic activity was identified and suggested as the major ingredient contributing to the hypoglycemic activity of S. pastorianus extract. In summary, these results clearly confirm the hypoglycemic activity of S. pastorianus extract and provide critical insights into the underlying molecular mechanisms.

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p38 MAPK in Glucose Metabolism of Skeletal Muscle: Beneficial or Harmful?

Cited by 58 publications

References 119 publications

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

TGF‑β1: Gentlemanly orchestrator in idiopathic pulmonary fibrosis (Review)

Four-and-a-half LIM domain protein 2 (FHL2) deficiency protects mice from diet-induced obesity and high FHL2 expression marks human obesity

Exploration of Hypoglycemic Activity of Saccharomyces pastorianus Extract and Evaluation of the Molecular Mechanisms

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