What is insulin-independent transport system of glucose?
Thus, insulin-independent glucose transport through GLUT1 can meet the basal needs of the muscle cell. If glucose entrance through GLUT1 and the activation of the hexosamine pathway is abundant, it can decrease the insulin-mediated glucose transport through GLUT4 leading to insulin resistance.
What is translocation of insulin?
Insulin stimulates glucose uptake by altering the subcellular distribution of glucose transporter 4 (Glut4) from intracellular stores to the plasma membrane, a process known as Glut4 translocation (1, 2). Defects in this process are observed in insulin resistance, type II diabetes mellitus, and metabolic syndrome.
How does insulin cause GLUT4 translocation?
Insulin stimulates glucose uptake into the skeletal muscle cells, which requires GLUT4 translocation to the plasma membrane. Upon insulin stimulation, GLUT4 undergoes exocytosis and is targeted to the plasma membrane.
What is the insulin-dependent transporter?
Among the known GLUTs, GLUT4 is the main insulin-dependent transporter, which makes it a suitable candidate for developing a potential medical intervention. Nonetheless, our results indicated that GLUT2 had the most reduced levels in both cellular models and the brain VSMCs of the patients.
What is the role of GLUT4 transporter?
GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells.
How does insulin work GLUT4?
GLUT4 functions for the insulin-dependent translocation of glucose. Thus, insulin stimulates the uptake of glucose by GLUT4 in the muscle cell where hexokinase converts it to glucose-6-phosphate so that the cell may utilize it for either glycolysis for energy or for the formation of glycogen when glucose is abundant.
How is GLUT4 activated?
The mechanism for GLUT4 is an example of a cascade effect, where binding of a ligand to a membrane receptor amplifies the signal and causes a cellular response. In this case, insulin binds to the insulin receptor in its dimeric form and activates the receptor’s tyrosine-kinase domain.
What is simple translocation?
A genetic change in which a piece of one chromosome breaks off and attaches to another chromosome. Sometimes pieces from two different chromosomes will trade places with each other. Translocations may lead to medical problems such as leukemia, breast cancer, schizophrenia, muscular dystrophy, and Down syndrome.
What is the relationship between GLUT4 insulin and glucose quizlet?
What is the relationship between insulin and glucose? Insulin is released from the pancreas to the receptors in the cell, which sends signals to the GLUT4 protein to allow the glucose into the cell.
Is GLUT4 insulin-dependent?
GLUT4 is an insulin-regulated glucose transporter that is responsible for insulin-regulated glucose uptake into fat and muscle cells. In the absence of insulin, GLUT4 is mainly found in intracellular vesicles referred to as GLUT4 storage vesicles (GSVs).
Is GLUT2 insulin-dependent?
GLUT4 is an insulin-dependent GLUT (Brosius et al., 1992; Cooper et al., 1993; Standley and Rose, 1994; Kahn et al., 1995; Banz et al., 1996) whereas GLUT2 is, in contrast, an insulin-independent transporter (Pyla et al., 2013).
What is GLUT4 how is it regulated by insulin?
Insulin stimulates glucose transport by promoting translocation of the insulin-sensitive glucose transporter isoform 4 (GLUT4) from an intracellular compartment to the cell surface. This movement is accomplished by stimulation of GLUT4 exocytosis as well as inhibition of endocytosis.
Is GLUT4 a protein carrier?
Glucose transporter type 4 (GLUT4), also known as solute carrier family 2, facilitated glucose transporter member 4, is a protein encoded, in humans, by the SLC2A4 gene. GLUT4 is the insulin-regulated glucose transporter found primarily in adipose tissues and striated muscle (skeletal and cardiac).
Why does GLUT4 need insulin?
What is the role of GLUT4 transporters?
Why is GLUT4 important?
GLUT4 is one of the most important downstream sites of the insulin receptor because it sits at the rate-limiting step in the insulin transduction signal pathway. It has been reported that GLUT4 protein and mRNA are reduced in type 2 diabetes (Chen et al., 2003).
What are the two types of translocation?
There are two main types of translocations: reciprocal and Robertsonian.
What are the three types of translocation?
1. simple translocations (one break involved) 2. reciprocal translocations (two breaks involved) 3. shift type translocations (three breaks involved) 4.
How do insulin and GLUT4 transport proteins work to increase glucose uptake by the muscle cells quizlet?
In skeletal muscle and fat cells, insulin binds to the insulin receptor which causes the active recruitment of the glucose transporter, GLUT 4, to the cell surface. Once located at the cell surface, GLUT 4 increases the amount of glucose that enters fat and skeletal muscle cells.
What process happens when GLUT4 permits transport of glucose into the cell?
The gene that encodes GLUT4 was cloned and mapped in 1989. At the cell surface, GLUT4 permits the facilitated diffusion of circulating glucose down its concentration gradient into muscle and fat cells.
Is GLUT2 insulin dependent?
What is GLUT2 and GLUT4?
GLUT1 is the major glucose transporter in brain, placenta and erythrocytes, GLUT2 is found in the pancreas, liver and kidneys, GLUT3 is neuronal and placental, while GLUT4 is the insulin-responsive transporter found in skeletal muscle, heart and adipose tissue.
Why is regulation of GLUT4 needed?
GLUT4 plays an important role in the adaptation of skeletal muscle to increased metabolic demand during periods of prolonged muscle contraction. It is this latter function that may explain the mechanism by which exercise promotes insulin sensitivity in healthy, insulin-resistant people.
What is the function of GLUT4?
What activates GLUT4?
a | Insulin stimulates glucose transporter type 4 (GLUT4) storage vesicle (GSV) translocation by inhibiting the interaction between TUG (tether containing UBX domain for GLUT4) and GLUT4 and by stimulating AKT-catalysed phosphorylation of AS160, which inhibits the GTPase-activating protein (GAP) activity of AS160 …