Snow crab proteins hydrolysate increases in vitro insulin-stimulated glucose uptake in L6 muscle cells

Glucose uptake patterns of guavanoic acid and guavanoic acid functionalized gold nanoparticles in the presence of genistein (IRTK inhibitor) and wortmannin (PI3K inhibitor).

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Formulation and characterisation of insulin-loaded chitosan nanoparticles capable of inducing glucose uptake in skeletal muscle cells in vitro

Journal of Drug Delivery Science and Technology ◽

10.1016/j.jddst.2020.101738 ◽

2020 ◽

Vol 57 ◽

pp. 101738 ◽

Cited By ~ 6

Author(s):

Chun Y. Wong ◽

Hani Al-Salami ◽

Crispin R. Dass

Keyword(s):

Skeletal Muscle ◽

Glucose Uptake ◽

Chitosan Nanoparticles ◽

Muscle Cells ◽

Skeletal Muscle Cells

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Unique mechanism of GLUT3 glucose transporter regulation by prolonged energy demand: increased protein half-life

Biochemical Journal ◽

10.1042/bj3330713 ◽

1998 ◽

Vol 333 (3) ◽

pp. 713-718 ◽

Cited By ~ 42

Author(s):

Zayna A. KHAYAT ◽

Anthony L. McCALL ◽

Amira KLIP

Keyword(s):

Glucose Uptake ◽

Protein Content ◽

Glucose Transport ◽

Half Life ◽

Glucose Transporter ◽

Muscle Cells ◽

Mrna Levels ◽

Glut1 Protein ◽

L6 Muscle Cells

L6 muscle cells survive long-term (18 h) disruption of oxidative phosphorylation by the mitochondrial uncoupler 2,4-dinitrophenol (DNP) because, in response to this metabolic stress, they increase their rate of glucose transport. This response is associated with an elevation of the protein content of glucose transporter isoforms GLUT3 and GLUT1, but not GLUT4. Previously we have reported that the rise in GLUT1 expression is likely to be a result of de novo biosynthesis of the transporter, since the uncoupler increases GLUT1 mRNA levels. Unlike GLUT1, very little is known about how interfering with mitochondrial ATP production regulates GLUT3 protein expression. Here we examine the mechanisms employed by DNP to increase GLUT3 protein content and glucose uptake in L6 muscle cells. We report that, in contrast with GLUT1, continuous exposure to DNP had no effect on GLUT3 mRNA levels. DNP-stimulated glucose transport was unaffected by the protein-synthesis inhibitor cycloheximide. The increase in GLUT3 protein mediated by DNP was also insensitive to cycloheximide, paralleling the response of glucose uptake, whereas the rise in GLUT1 protein levels was blocked by the inhibitor. The GLUT3 glucose transporter may therefore provide the majority of the glucose transport stimulation by DNP, despite elevated levels of GLUT1 protein. The half-lives of GLUT3 and GLUT1 proteins in L6 myotubes were determined to be about 15 h and 6 h respectively. DNP prolonged the half-life of both proteins. After 24 h of DNP treatment, 88% of GLUT3 protein and 57% of GLUT1 protein had not turned over, compared with 25% in untreated cells. We conclude that the long-term stimulation of glucose transport by DNP arises from an elevation of GLUT3 protein content associated with an increase in GLUT3 protein half-life. These findings suggest that disruption of the oxidative chain of L6 muscle cells leads to an adaptive response of glucose transport that is distinct from the insulin response, involving specific glucose transporter isoforms that are regulated by different mechanisms.

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AN IN VITRO STUDY OF SYZYGIUM CUMINI SEED EXTRACT ON GLUCOSE UPTAKE ACTIVITY IN L-6 CELL LINES

Journal of Drug Delivery and Therapeutics ◽

10.22270/jddt.v9i4-a.3419 ◽

2019 ◽

Vol 9 (4-A) ◽

pp. 256-259

Author(s):

Maneemegalai Sivaprakasam ◽

Narmatha M

Keyword(s):

Diabetes Mellitus ◽

Skeletal Muscle ◽

Glucose Uptake ◽

Ethanol Extract ◽

Muscle Cells ◽

Skeletal Muscle Cells ◽

Syzygium Cumini ◽

Rat Skeletal Muscle ◽

Uptake Activity

Diabetes mellitus is the most common endocrine disorder. The plant Syzygium cumini has been used in traditional medicine for the treatment of diabetes. The present study investigated the effect of ethanol extract of S. cumini seeds on uptake of glucose by L-6 rat skeletal muscle cells. S. cumini seeds were extracted with varying solvents and quantitative phytochemical analysis was carried out, ethanol extract of seeds exhibited higher content of tested phytochemicals. The effect of different concentrations (300µg/ml – 1000µg/ml) of ethanol extract of seeds were studied on glucose uptake activity of L-6 rat skeletal muscle cells. It was observed that with the increase in concentration, the glucose uptake activity was also increased. The results of the study supports and demonstrates the antidiabetic potential of ethanol seed extracts of Syzygium cumini utilizing in vitro model. KEY WORDS: Diabetes mellitus, Syzygium cumini, phytochemicals, glucose uptake, L-6 cells

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1-Deoxysphingolipids, Early Predictors of Type 2 Diabetes, Compromise the Functionality of Skeletal Myoblasts

Frontiers in Endocrinology ◽

10.3389/fendo.2021.772925 ◽

2021 ◽

Vol 12 ◽

Author(s):

Duyen Tran ◽

Stephen Myers ◽

Courtney McGowan ◽

Darren Henstridge ◽

Rajaraman Eri ◽

...

Keyword(s):

Type 2 Diabetes ◽

Skeletal Muscle ◽

Glucose Uptake ◽

Muscle Cells ◽

Skeletal Muscle Cells ◽

Muscle Dysfunction ◽

Dependent Manner

Metabolic dysfunction, dysregulated differentiation, and atrophy of skeletal muscle occur as part of a cluster of abnormalities associated with the development of Type 2 diabetes mellitus (T2DM). Recent interest has turned to the attention of the role of 1-deoxysphingolipids (1-DSL), atypical class of sphingolipids which are found significantly elevated in patients diagnosed with T2DM but also in the asymptomatic population who later develop T2DM. In vitro studies demonstrated that 1-DSL have cytotoxic properties and compromise the secretion of insulin from pancreatic beta cells. However, the role of 1-DSL on the functionality of skeletal muscle cells in the pathophysiology of T2DM still remains unclear. This study aimed to investigate whether 1-DSL are cytotoxic and disrupt the cellular processes of skeletal muscle precursors (myoblasts) and differentiated cells (myotubes) by performing a battery of in vitro assays including cell viability adenosine triphosphate assay, migration assay, myoblast fusion assay, glucose uptake assay, and immunocytochemistry. Our results demonstrated that 1-DSL significantly reduced the viability of myoblasts in a concentration and time-dependent manner, and induced apoptosis as well as cellular necrosis. Importantly, myoblasts were more sensitive to the cytotoxic effects induced by 1-DSL rather than by saturated fatty acids, such as palmitate, which are critical mediators of skeletal muscle dysfunction in T2DM. Additionally, 1-DSL significantly reduced the migration ability of myoblasts and the differentiation process of myoblasts into myotubes. 1-DSL also triggered autophagy in myoblasts and significantly reduced insulin-stimulated glucose uptake in myotubes. These findings demonstrate that 1-DSL directly compromise the functionality of skeletal muscle cells and suggest that increased levels of 1-DSL observed during the development of T2DM are likely to contribute to the pathophysiology of muscle dysfunction detected in this disease.

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