Glucose deprivation attenuates sortilin levels in skeletal muscle cells

Ariga, Miyako; Yoneyama, Yoshimasa; Fukushima, Toshiaki; Ishiuchi, Yuri; Ishii, Takayuki; Sato, Hitoshi; Hakuno, Fumihiko; Nedachi, Taku; Takahashi, Shin‐Ichiro

doi:10.1507/endocrj.ej16-0319

Cited by 14 publications

(12 citation statements)

References 44 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Fine-tuning of the expression level of both proteins is crucial in order to maintain insulin mediated glucose transport inside the cells (Figure 2). For example, formation of Glut4 storage vesicles in adipocytes and skeletal muscle cells correlates with the expression of sortilin (Ariga et al, 2008; Shi et al, 2008; Ariga et al, 2017). In addition, insulin dependent translocation of Glut4 is clearly correlated with the presence of sortilin in adipocytes (Huang et al, 2013).…”

Section: Sortilin a Sorting Protein For Glucose Transporter Glut4 Imentioning

confidence: 99%

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

et al. 2019

View full text Add to dashboard Cite

The pharmacological properties and physiological roles of the type I receptor sortilin, also called neurotensin receptor-3, are various and complex. Sortilin is involved in important biological functions from neurotensin and pro-Nerve Growth Factor signaling in the central nervous system to regulation of glucose and lipid homeostasis in the periphery. The peripheral functions of sortilin being less extensively addressed, the focus of the current review is to discuss recent works describing sortilin-induced molecular mechanisms regulating blood glucose homeostasis and insulin signaling. Thus, an overview of several roles ascribed to sortilin in diabetes and other metabolic diseases are presented. Investigations on crucial cellular pathways involved in the protective effect of sortilin receptor on beta cells, including recent discoveries about regulation of cell fate, are also detailed. In addition, we provide a special focus on insulin secretion regulation involving complexes between sortilin and neurotensin receptors. The last section comments on the future research areas which should be developed to address the function of new effectors of the sortilin system in the endocrine apparatus.

show abstract

Section: Sortilin a Sorting Protein For Glucose Transporter Glut4 Imentioning

confidence: 99%

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

et al. 2019

View full text Add to dashboard Cite

show abstract

“…The present study found that expression of sortilin, one of the PGRN receptors, was significantly reduced by glucose deprivation. We recently discovered similar glucose‐dependent control of sortilin expression in skeletal muscle cells . Moreover, sortilin expression in liver was repressed in both genetic (ob/ob) mice and high‐fat diet models , and control of sortilin expression may thus vary between tissues and organs.…”

Section: Discussionmentioning

confidence: 99%

Glucose deprivation regulates the progranulin–sortilin axis in PC12 cells

et al. 2016

Self Cite

View full text Add to dashboard Cite

Progranulin ( PGRN ) is a growth factor implicated in several neurodegenerative diseases, such as frontotemporal lobar degeneration. Despite its important role in the central nervous system ( CNS ), the mechanisms controlling PGRN expression in the CNS are largely unknown. Recent evidence, however, suggested that several stressors, such as hypoxia, acidosis, or oxidative stress, induce PGRN expression. The present study was mainly aimed at determining whether and, if so, how glucose deprivation affects PGRN expression in PC 12 cells. Initially, it was found that glucose deprivation gradually induced PGRN gene expression in PC 12 cells. To elucidate the underlying molecular mechanisms, several intracellular signalings that were modified in response to glucose deprivation were examined. Both adenosine monophosphate kinase ( AMPK ) activation and changes in osmotic pressure, which are modified by extracellular glucose concentration, had no effect on PGRN gene expression; on the other hand, p38 activation in response to glucose deprivation played an important role in inducing PGRN gene expression. It was also found that expression of sortilin, a PGRN receptor implicated in PGRN endocytosis, was dramatically reduced by glucose deprivation. In contrast to glucose‐dependent regulation of PGRN gene expression, AMPK activation played a central role in reducing sortilin expression. Overall, the present study suggests that the PGRN –sortilin axis is modulated by glucose deprivation via two distinct mechanisms. As PGRN is neuroprotective, this system may represent a new neuroprotective mechanism activated by glucose deprivation in the CNS .

show abstract

“…Concerning this notion, fine-tuning of the expression contents of sortilin and myotubes are considered to be essential to maintain the insulin-induced intracellular transport of glucose. For instance, several research studies have shown that the formation of GLUT4-accumulated vesicles within the adipocyte and skeletal muscle cells was closely associated with the gene expression content of SORT1 (83,96). Moreover, the insulin-mediated translocation of GLUT4 has also been shown to be strongly correlated with the gene expression contents of SORT1 within the adipocyte (82).…”

Section: Role Of Sortilin In Modulating Serum Glucose Metabolismmentioning

confidence: 99%

“…Currently, obesity and diabetes mellitus has been shown to be synergistically correlated with impaired glucose metabolism within adipocytes, which is induced by the decreased intracellular expression levels of glucose transporter 4 (GLUT4) (81)(82)(83). Indeed, within the 3T3-L1 preadipocyte, SORT1 gene is a component of GLUT4 vesicles (84,85).…”

Section: Adipocytementioning

confidence: 99%

Emerging roles of sortilin in affecting the metabolism of glucose and lipid profiles

Chen

et al. 2021

Bosn J of Basic Med Sci

View full text Add to dashboard Cite

Dyslipidemia has recently been identified as an important factor in modulating the progression of several health conditions, grouped as cardio-metabolic syndrome and including obesity,insulin resistance, and atherosclerosis. Among multiple factors which regulate the development of cardio-metabolic syndrome, sortilin has been found in multiple cell types, such as adipocyte, hepatocyte, and macrophage, suggesting that sortilin is correlated to the development and the severity of cardio-metabolic syndrome. Consistently, several genome-wide association (GWAS) and basic experimental research studies are being conducted to find novel gene loci involved in regulating the pathological progression of cardio-metabolic syndrome. According to these data, both SORT1 gene and sortilin protein have an important function in regulating the circulating lipid and glucose metabolism resulting in modulation of disease progression. In this comprehensive review, we summarize the recent research results in regards to sortilin function in modulating the circulating lipid and glucose metabolism. Moreover, we also discuss and analyze the emerging evidence elucidating the potential mechanisms by which sortilin affects synthesis and secretion of lipid and glucose.

show abstract

Glucose deprivation attenuates sortilin levels in skeletal muscle cells

Cited by 14 publications

References 44 publications

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

Sortilin in Glucose Homeostasis: From Accessory Protein to Key Player?

Glucose deprivation regulates the progranulin–sortilin axis in PC12 cells

Emerging roles of sortilin in affecting the metabolism of glucose and lipid profiles

Contact Info

Product

Resources

About