Glucose, insulin stimulated uptake

GLUT 4 Heart and skeletal muscle, adipose tissue Insulin-stimulated uptake of glucose... 

Insulin stimulates uptake of glucose and amino acids by cells, glycogen and protein synthesis, and storage of lipids. It inhibits glycogenolysis, gluconeogenesis, breakdovm of stored triglycerides, and ketogenesis. 

Metformin restrains hepatic glucose production principally by suppression of gluconeogenesis. The mechanisms involve potentiation of insulin action and decreased hepatic extraction of certain gluconeogenic substrates such as lactate. In addition, metformin reduces the rate of hepatic glycogenolysis and decreases the activity of hepatic glucose-6-phosphatase. Insulin-stimulated glucose uptake and glycogenesis by skeletal muscle is increased by metformin mainly by increased... 

Carayannopoulos, M. O., et al. GLUT8 is a glucose transporter responsible for insulin-stimulated glucose uptake in the blastocyst. Proc. Natl. Acad. Sci. U. S. A. 2000, 97, 7313-7318. 

It was discovered nearly 20 years ago that V(V) as vanadate and V(IV) as vanadyl can mimic some of the effects of insulin (stimulate glucose uptake and oxidation and glycogen synthesis) (512, 513). Vanadate is an effective insulin mimetic in the diabetic rat (514), but has proved to be too toxic for human use. Vanadyl, as VOS04, is also unsuitable because high doses are needed on account of its poor oral absorption. Vanadium complexes with organic ligands have proved to be less toxic and can have improved aqueous solubility and lipophil-icity. 

GLUT 4 Skeletal muscle Adipose tissue 5 mM Insulin-stimulated glucose uptake... 

To gain further insight into the mechanisms involved in defective insulin-stimulated glucose uptake in skeletal muscle of insulin-resistant subjects, the possible role of IMCL in the pathogenesis of skeletal muscle insulin resistance and type 2 diabetes mellitus was explored by comparing insulin sensitivity (GIR) and IMCL content of insulin-resistant and insulin-sensitive offsprings of patients with type 2 diabetes. Twenty-six healthy subjects were included in the first study, 13 of them classified as insulin-sensitive and further 13 as insulin-resistant. Metabolic and anthropometric data are given in Table 4. 

Changes in the blood levels of these hormones all contribute to regulation of blood glncose level in several conditions. After a meal glucose utilisation is increased, since insulin stimulates glucose uptake by muscle and inhibits release of fatty acids from adipose tissue. Physical activity... 

Insulin stimulates glucose uptake by muscle and adipose tissue (Table 23-3), where the glucose is converted to glucose 6-phosphate. In the liver, insulin also activates... 

The uptake of glucose by brain, liver, kidneys, erythrocytes, and the islets of Langerhans is unaffected by insulin. However, in muscle and adipose tissues insulin stimulates glucose uptake. Part of this effect results from insulin-induced translocation of molecules of the 509-residue glucose transport protein GLUT4 (Chapter 8) from the cytosol into the plasma membrane where it can function.354-3563 Insulin apparently also increases the rate of synthesis of the transporters. 

In a placebo-controlled study in six patients with type 2 diabetes mellitus thalidomide 150 mg/day for 3 weeks reduced insulin-stimulated glucose uptake by 31% and glycogen synthesis by 48% (1115). However, it had no effect on rates of glycolysis, carbohydrate oxidation, non-oxidative glycolysis, lipolysis, free fatty acid oxidation, or re-esterification. The authors concluded that thalidomide increases insulin resistance in obese patients with type 2 diabetes. 

Tlpl T Insulin stimulated glycogen T Glucose uptake, i FFA... 

Szalkowski, D., White-Carrington, S., Berger, J., and Zhang, B. (1995). Antidiabetic Thiazolidinediones Block the Inhibitory Effect of Tumor Necrosis Factor-a on Differentiation, Insulin-Stimulated Glucose Uptake, and Gene Expression in 3T3-L1 Cells. Endocrinology 136, 1474—1481. 

Sweeney, G., Keen, J., Somwar, R., Konrad, D., Garg, R., and Klip, A. 2001. High leptin levels acutely inhibit insulin-stimulated glucose uptake without affecting glucose transporter 4 translocation in 16 rat skeletal muscle cells. Endocrinology 142 4806-4812. 

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