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Glycogenolysis - Pathway, Steps, Animation, …
Presentation Summary : Carbohydrates metabolism. ... By promoting liver glycogenesis and thus converting glucose to glycogen. ... Promoting gluconeogenesis from the breakdown of protein.
Glucose is one of the most important energy sourcesfor the human organism. It is usually stored in the liver andmuscle cells in the form of glycogen (). After eating, elevated bloodglucose is converted into glycogen (). During the conversion, bloodglucose is firstly transported into cells by the plasma membraneprotein glucose transporter (GLUT), and its four isoforms, GLUT1,GLUT2, GLUT3 and GLUT4, have been well-characterized (). GLUT4 is primarily expressed inmuscle and fat cells. The insulin signaling pathway plays animportant role in regulating its translocation (). Insulin binds to the IR andinduces the autophosphorylation of the receptor at tyrosineresidues (). Followingautophosphorylation, the receptor further recruits the IRS andpromotes its phosphorylation at tyrosine residues (). Phosphorylated IRS subsequentlybinds to the regulatory subunit, p85, of the phosphoinositide-3kinase (PI3K) and activates its catalytic subunit p110, which isresponsible for stimulating the phosphoinositide-dependent kinase(PDK) (). As the upstreamkinase of Akt, activated PDK promotes the phosphorylation of Akt atThr308 and Ser473 (), andphosphorylated Akt mediates the translocation of GLUT from thecytoplasm to the membrane ()(). Apart from its role inGLUT translocation, Akt has also been implicated in regulatingglycogen synthesis. Glycogen synthase (GS) is a key enzyme involvedin converting glucose into glycogen, and there are two isoforms inmammals, the muscle isoform ()and the liver isoform (). Bothisoforms are inactivated due to phosphorylation at the NH2- orCOOH-terminal residues mediated by glycogen synthesis kinase 3(GSK3) (). Insulindephosphorylates and restores the function of GS through Akt- orprotein kinase A-mediated phoshorylation and the inactivation ofGSK3 (,). In skeletal muscle, insulinenhances glycogen synthesis in the absence of GSK3 phosphorylation(). Glucose-6 phosphateinduces glycogen synthesis through the activation of GS in a cyclicAMP-stimulated protein kinase-dependent manner ().
glucose as glycogen and oxidizesit to ..
Presentation Summary : • Gluconeogenesis: ... Glycogen is broken down by a separatepathway known as glycogenolysis.• ... Carbohydrate Metabolism
Presentation Summary : Glucose and Glycogen ... Difference Between Liver and Muscle Things to Know and Do Before Class How Insulin works to affect genes for gluconeogenesis. How glycogen ...
2020 Other Images: Glycogen Synthesis Pathway
As small non-coding RNAs, miRNAs play a pivotal rolein post-transcriptional regulation. miRNAs can bind to and promotethe deadenylation and degradation of target mRNAs (,). Translational repression is anotherimportant function of miRNAs. It can directly bind to the 3′-UTR oftarget mRNAs and inhibit the translational initiation (). Studies have demonstrated thatmiRNAs are involved in the regulation of multiple insulinresistance-induced diseases (). In T2D, miR-144 has been shown to promote insulinresistance by directly targeting mRNA (). The suppression of IRS1 mediated bymiR-126 has also been shown to result in mitochondrial dysfunctionand insulin resistance (). Thesitmulation of Akt activation by insulin is critical forglycometabolism, and the obesity-induced miR-143 overexpression hasbeen shown to lead to hyperglycemia by inactivating the Aktsignaling pathway (). A studyusing let-7 family transgenic mice demonstrated that let-7overexpression may contribute to the development of T2D (). Protein tyrosine phosphatase 1B(PTP1B) impairs the insulin signaling pathway through thedephosphorylation of IR at tyrosine residues. The 3′-UTR of mRNA is the target of miR-122, and decreased miR-122expression has been shown to result in hepatic insulin resistance(). In mouse models ofobesity, miR-103/107 is upregulated. The blockage of miR-103/107has been shown to promote insulin sensitivity by elevatingcaveolin-1-mediated IR activation (). Phosphatase and tensin homologdeleted on chromosome 10 (PTEN), the direct target of miR-21(), is the key phosphotase ofAkt which can negatively regulate the Akt signaling pathway. Ininsulin-resistant adipocytes, the suppressed expression of miR-21and impaired Akt signaling pathway has been observed (). The transport of glucose is alsoregulated by miRNAs, and the transmembrane protein GLUTs play anessential role in glucose transport. Elevated miR-133 levels havebeen shown to reduce the insulin-stimulated glucose uptake bydownregulating GLUT4 expression (). In cardiomyocytes, miR-223 has beenshown to promote GLUT4 expression and increase glucose uptake(). Insulin resistance is theintrinsic complication of polycystic ovary syndrome (PCOS), andoverexpressed miR-93 in patients with PCOS binds to the 3′-UTR of mRNA and reduces its protein translation (). Microarray analysis has furtherindicated that the expression of several miRNAs is alteredfollowing burn injury. In comparison with normal skin tissue, atotal of 32 upregluated and 34 downregulated miRNAs were identifiedin the skin tissue of patients who sustained burn injuries(). The expression levels ofmiR-144 in the skin tissue of the burned patients, which candirectly target the 3′-UTR of mRNA (), were 16-fold higher than those innormal skin tissue (). Thissuggests that miRNAs, such as miR-144, play an essential role inpromoting burn-induced insulin resistance by suppressing theactivation of the IR/IRS signaling pathway.
Schematic diagram of burn-inducedinsulin resistance through the suppression of thephosphoinositide-3 kinase (PI3K)/Akt signaling pathway mediated byinsulin receptor substrate 1 (IRS1) degradation. After burn injury,the blood concentration of tumor necrosis factor (TNF)-α,interleukin (IL) and lipopolysacchride (LPS) is significantlyincreased. TNF-α binds to its receptor and induces inducible nitricoxide synthase (iNOS) production. ILs, IL-6 in particular, bind tocorresponding receptors and promote the expression of suppressor ofcytokine signaling-3 (SOCS3). LPS binds to CD14 with the help ofthe LPS binding protein (LBP) and activates the intracellularsignaling pathway. All the cytokines induce IRS1 proteindegradation, which suppresses the PI3K/Akt signaling pathway, andsubsequently suppresses glucose transporter (GLUT) translocationand glycogen synthesis, which results in burn-induced insulinresistance and hyperglycemia.
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Glycogen Synthesis and Degradation - YouTube
Presentation Summary : Inborn Errors of Metabolism. Acute Presentation. ... (part of gluconeogenesis) ... Liver glycogen releases glucose into the circulation.
19-3-2012 · Glycogen Synthesis and Degradation ..
Newly synthesized and glycosylated enters a continuously recycling pathway that concentrates most of the in intracellular membrane systems in unstimulated muscle cells.
Glycogenesis and Glycogenolysis Animation ..
Presentation Summary : From here, we see gluconeogenesis. 3. ... Similar to glycogen synthesis, ... Carbohydrate Metabolism in Plants Last modified by:
Glycogen Synthesis and Metabolism
Elevated glucose levels are rapidly returned to normal (5–6 mM) even after huge caloric ingestions, and they are maintained at only slightly lower levels during longterm starvation. Such control prevents severe dysfunctions such as loss of consciousness due to hypoglycemia and toxicity to peripheral tissues in response to the chronic hyperglycemia of diabetes. The major cellular mechanism for disposal of an exogenous glucose load is insulin-stimulated glucose transport into skeletal muscle. Skeletal muscle both stores glucose as glycogen and oxidizesit to produce energy following the transport step. The principal glucose transporter protein that mediates this uptake is one isoform (Gene name, ; protein name: ) of a family of sugar transporter proteins. The glucose transporter is thus a major mediator of glucose removal from the circulation and a key regulator of whole-body glucose homeostasis.
Under normal conditions, this carrier is located in the cytoplasmic vesicles and its translocation to the cell membrane is stimulated by the binding of insulin receptor membrane. This process facilitates the movement of glucose from the interstitial fluid within the cell. When the blood glucose concentration returns to normal and the insulin is removed, the molecules of are slowly removed from the plasma membrane by endocytosis and sequestered in intracellular vesicles.
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is strongly associated with type II diabetes. “Diabetogenic” factors including alpha and cellular stress induce insulin resistance through inhibition of functions. Serine/threonine phosphorylation, interaction with regulation of the expression, modification of the cellular localization, and degradation represent the molecular mechanisms stimulated by them. Various kinases (ERK, beta, zeta, theta and mTOR) are involved in this process. The development of type II diabetes requires impaired beta-cell function. Chronic hyperglycemia has been shown to induce multiple defects in beta-cells. Hyperglycemia has been proposed to lead to large amounts of reactive oxygen species (ROS) in beta-cells, with subsequent damage to cellular components including -1. Loss of -1, a critical regulator of insulin promoter activity, has also been proposed as an important mechanism leading to beta-cell dysfunction. Although there is little doubt as to the importance of genetic factors in type II diabetes, genetic analysis is difficult due to complex interaction among multiple susceptibility genes and between genetic and environmental factors. Genetic studies have therefore given very diverse results. Kir6.2 and are two of the candidate genes. It is known that Kir6.2 and play central roles in insulin secretion and insulin signal transmission, respectively.
In the insulin resistance the exocytose of insulin-stimulated, in skeletal muscle, is impaired because the inhibition of functions blocks the insulin’s pathways.
Other reasons for the failure of exocytosis may be the presence of conditions impairing cytoplasmic vesicles movement (lack of calcium or iron overload eg).
This causes a constant hyperglycemia that lead to a worse diabetes, because the skeletal muscle is the most tissue that regulates the glucose homeostasis and its impairement is very dangerous for the patient health.
Moreover insulin-stimulated phosphorylation is impaired in skeletal muscle of type II diabetic patients ().
Therefore this pathways are important in type II diabetes and the study of them would be important and useful for type II diabetes therapy.
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