File Name: glucose transporters and insulin action .zip
- Glucose transporters and insulin action: Some insights into diabetes management
- Signaling pathways in insulin action: molecular targets of insulin resistance
- Regulatory Mechanism of Skeletal Muscle Glucose Transport by Phenolic Acids
- Insulin Signaling and the Regulation of Glucose Transport
Type 2 diabetes mellitus T2DM is one of the most severe public health problems in the world. In recent years, evidences show a commonness of utilization of alternative medicines such as phytomedicine for the treatment of T2DM. Phenolic acids are the most common compounds in non-flavonoid group of phenolic compounds and have been suggested to have a potential to lower the risk of T2DM. Skeletal muscle is the major organ that contributes to the pathophysiology of T2DM. Studies have shown that several phenolic acids caffeic acid, chlorogenic acid, gallic acid, salicylic acid, p-coumaric acid, ferulic acid, sinapic acid have antidiabetic effects, and these compounds have been implicated in the regulation of skeletal muscle glucose metabolism, especially glucose transport.
Glucose transporters and insulin action: Some insights into diabetes management
Randhawa, Amira Klip; Insulin action on glucose transporters through molecular switches, tracks and tethers. Biochem J 15 July ; 2 : — Glucose entry into muscle cells is precisely regulated by insulin, through recruitment of GLUT4 glucose transporter-4 to the membrane of muscle and fat cells. Work done over more than two decades has contributed to mapping the insulin signalling and GLUT4 vesicle trafficking events underpinning this response. In spite of this intensive scientific research, there are outstanding questions that continue to challenge us today. Sign In or Create an Account.
Metrics details. Gaps remain in our understanding of the precise molecular mechanisms by which insulin regulates glucose uptake in fat and muscle cells. Recent evidence suggests that insulin action involves multiple pathways, each compartmentalized in discrete domains. Upon activation, the receptor catalyzes the tyrosine phosphorylation of a number of substrates. One family of these, the insulin receptor substrate IRS proteins, initiates activation of the phosphatidylinositol 3-kinase pathway, resulting in stimulation of protein kinases such as Akt and atypical protein kinase C. The receptor also phosphorylates the adapter protein APS, resulting in the activation of the G protein TC10, which resides in lipid rafts. TC10 can influence a number of cellular processes, including changes in the actin cytoskeleton, recruitment of effectors such as the adapter protein CIP4, and assembly of the exocyst complex.
Signaling pathways in insulin action: molecular targets of insulin resistance
Insulin stimulates glucose uptake in muscle and adipose cells primarily by recruiting GLUT4 from an intracellular storage pool to the plasma membrane. Dysfunction of this process known as insulin resistance causes hyperglycemia, a hallmark of diabetes and obesity. Thus the understanding of the mechanisms underlying this process at the molecular level may give, an insight into the prevention and treatment of these health problems. GLUT4 in rat adipocytes, for example, constantly recycles between the cell surface and an intracellular pool by endocytosis and exocytosis, each of which is regulated by an insulin-sensitive and GLUT4-selective sorting mechanism. Our working hypothesis has been that this sorting mechanism includes a specific interaction of a cytosolic protein with the GLUT4 cytoplasmic domain.
Although diabetes has been identified as a major risk factor for atrial fibrillation, little is known about glucose metabolism in the healthy and diabetic atria. Glucose transport into the cell, the rate-limiting step of glucose utilization, is regulated by the Glucose Transporters GLUTs. We hypothesized that GLUT-4 and -8 translocation to the atrial cell surface will be regulated by insulin and impaired during insulin-dependent diabetes. GLUT protein content was measured by Western blotting in healthy cardiac myocytes and type 1 streptozotocin-induced, T1Dx diabetic rodents. Active cell surface GLUT content was measured using a biotinylated photolabeled assay in the perfused heart. Akt and AS phosphorylation was not impaired in the diabetic atria, suggesting the presence of an intact insulin signaling pathway. This was confirmed by the rescued translocation of GLUT-4 and -8 to the atrial cell surface upon insulin stimulation in the atria of type 1 diabetic subjects.
Regulatory Mechanism of Skeletal Muscle Glucose Transport by Phenolic Acids
Perspective Free access Address correspondence to: Jeffrey E. Phone: ; Fax: ; E-mail: jeffrey-pessin uiowa. Find articles by Pessin, J.
The ability of insulin to stimulate glucose uptake into muscle and adipose tissue is central to the maintenance of whole-body glucose homeostasis. Deregulation of insulin action manifests itself as insulin resistance, a key component of type II diabetes mellitus T2DM.
Insulin Signaling and the Regulation of Glucose Transport
Obesity associated with systemic inflammation induces insulin resistance IR , with consequent chronic hyperglycemia. These pathways promote greater translocation of GLUT4 and consequent glucose uptake by the skeletal muscle. In this sense, the association between autophagy and exercise has also demonstrated a relevant role in the uptake of muscle glucose. Insulin, in turn, uses a phosphoinositide 3-kinase PI3K -dependent mechanism, while exercise signal may be triggered by the release of calcium from the sarcoplasmic reticulum. The objective of this review is to describe the main molecular mechanisms of IR and the relationship between PE and glucose uptake.
GLUT4, the major isoform in insulin-responsive tissue, translocates from an intracellular pool to the cell surface and as such determines insulin-stimulated glucose uptake. However, despite intensive research over 50 years, the insulin-dependent and -independent pathways that mediate GLUT4 translocation are not fully elucidated in any species. Insulin resistance IR is one of the hallmarks of equine metabolic syndrome and is the most common metabolic predisposition for laminitis in horses. IR is characterized by the impaired ability of insulin to stimulate glucose disposal into insulin-sensitive tissues.
Whether any of these interactions is actually responsible for the insulin-induced GLUT regulation is yet to be determined. Introduction. Glucose transport in animal.
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The effect of insulin on glucose transport and glucose transporters was studied in perfused rat heart. Glucose transport was measured by the efflux of labelled 3-O-methylglucose from hearts preloaded with this hexose. Insulin stimulated 3-O-methylglucose transport by: a doubling the maximal velocity Vmax ; b decreasing the Kd from 6. Glucose transporters in enriched plasma and microsomal membranes from heart were quantified by the [3H]cytochalasin-B-binding assay. When added to normal hearts, insulin produced the following changes in the glucose transporters: a it increased the translocation of transporters from an intracellular pool to the plasma membranes; b it increased from 1. The data provide evidence that the stimulatory effect of insulin on glucose transport may be due not to the sole translocation of intracellular glucose transporters to the plasma membrane, but to changes in the functional properties thereof. Full text is available as a scanned copy of the original print version.
Тот, что был пониже ростом, смерил его холодным взглядом. - Сюда, мистер Беккер. Быстрее. Беккер повернулся и побежал, но успел сделать только один шаг. Мужчина выхватил оружие и выстрелил.
- Может быть, вы могли бы подойти. - Понимаете, я не могу отойти от телефона, - уклончиво отозвался Ролдан. - Но если вы в центре, то это совсем недалеко от. - Извините, но для прогулок час слишком поздний. Тут рядом полицейский участок. Я занесу им, а вы, когда увидите мистера Густафсона, скажете ему, где его паспорт.
Стратмор сощурил .
Какие же страшные были у него руки. - Вот тут-то вы и рассмотрели его кольцо. Глаза Клушара расширились. - Так полицейский сказал вам, что это я взял кольцо.
Несколько операторов очумело перебегали от одного терминала к другому, волоча за собой распечатки и отдавая какие-то распоряжения. В помещении царила атмосфера полного хаоса. Сьюзан завороженно смотрела на захватывающую дух технику.
Кольцо, которое отдает умирающий, - дурная примета. - Вы знаете эту девушку? - Беккер приступил к допросу. Брови Росио выгнулись.
ГЛАВА 27 Тени в зале шифровалки начали удлиняться и терять четкость. Автоматическое освещение постепенно становилось ярче. Сьюзан по-прежнему молча сидела за компьютером, ожидая вестей от Следопыта.
- Взмахом руки Клушар величественно отверг вопрос Беккера. - Они не преступницы - глупо было бы искать их, как обычных жуликов.