Glucose uptake

The model description is a simplification of reality only two species are present in the liquid phase, that is, water and glucose. The biomass is taken at a constant uniform concentration in the fermenter. For the glucose uptake, simple Monod kinetics is used Glucose (s) -I- Biomass (X) Biomass (X) -I- Ethanol -i-. with the 

The figure shows that similar results can be obtained as found in the experiments. 

The fate of G6P is complex and differs from cell type to cell type. The following six routes represent the quantitatively most important fates of G6P (cf. Fig. 6.6a)  

It can enter glycolysis and the Krebs TCA cycle to be oxidized into CO2 and H2O. This is the ultimate fate for glucose. 

It can be stored as glycogen inside cells, mainly liver and muscle cells. The stores are limited to a total maximum near 1000 g glucose [63]. 

It can be converted to fat and stored inside cells. This is under normal conditions taking place in the adipocytes. The stores are practically unlimited. A year s glucose intake can be stored as 40 kg fat. 

It can be converted to lactate and leave the cell again. This can take place in almost all cells in the body. Similarly, almost all cells can take up lactate, convert it to pyruvate, and let it re-enter one of the other routes. 

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The modes of action for niclosamide are interference with respiration and blockade of glucose uptake. It uncouples oxidative phosphorylation in both mammalian and taenioid mitochondria (22,23), inhibiting the anaerobic incorporation of inorganic phosphate into adenosine triphosphate (ATP). Tapeworms are very sensitive to niclosamide because they depend on the anaerobic metaboHsm of carbohydrates as their major source of energy. Niclosamide has selective toxicity for the parasites as compared with the host because Httle niclosamide is absorbed from the gastrointestinal tract. Adverse effects are uncommon, except for occasional gastrointestinal upset. 

The complex thioamide lolrestat (8) is an inhibitor of aldose reductase. This enzyme catalyzes the reduction of glucose to sorbitol. The enzyme is not very active, but in diabetic individuals where blood glucose levels can. spike to quite high levels in tissues where insulin is not required for glucose uptake (nerve, kidney, retina and lens) sorbitol is formed by the action of aldose reductase and contributes to diabetic complications very prominent among which are eye problems (diabetic retinopathy). Tolrestat is intended for oral administration to prevent this. One of its syntheses proceeds by conversion of 6-methoxy-5-(trifluoroniethyl)naphthalene-l-carboxyl-ic acid (6) to its acid chloride followed by carboxamide formation (7) with methyl N-methyl sarcosinate. Reaction of amide 7 with phosphorous pentasulfide produces the methyl ester thioamide which, on treatment with KOH, hydrolyzes to tolrestat (8) 2[. 

Glucose uptake T AS160 f GLUT4 translocation Muscle... 

Glucose uptake T Myocyte enhancer factor-2 f GLUT4 expression Muscle... 

Glucose uptake T f GLUT 1 activity Many cells... 

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... 

Antidiabetic Drugs other than Insulin. Figure 3 The antihyperglycaemic effect of metformin involves enhanced insulin-mediated suppression of hepatic glucose production and muscle glucose uptake. Metformin also exerts non-insulin-dependent effects on these tissues, including reduced fatty acid oxidation and increased anaerobic glucose metabolism by the intestine. FA, fatty acid f, increase i decrease. 

There is weak expression of PPARy in muscle, liver and other tissues, enabling TZDs to support the effects of insulin in these tissues, notably increased glucose uptake in muscle and reduced glucose production in liver. TZDs may also affect nutrient metabolism by skeletal muscle through a direct mitochondrial action that is independent of PPARy. 

Biological actions Adipocyte differentiation fatty acid uptake lipogenesis glucose uptake other effects on nutrient metabolism which lower hepatic glucose production... 

GLUT4 is a glucose transporter exclusively expressed in tissues with insulin-sensitive glucose uptake (heart, muscle, fat). Under basal conditions, GLUT4 is predominantly located in intracellular vesicles, and is... 

Physiologically muscle-derived NO regulates skeletal muscle contractility and exercise-induced glucose uptake. nNOS is located at the plasma membrane of skeletal muscle and facilitates diffusion of NO to the vasculature to regulate muscle perfusion. 

The exact mechanism by which PPARy ligands affect insulin resistance (improved glucose uptake by peripheral tissues, most notably skeletal muscle) remains unclear. 

Katz, A., Broberg, S., Sahlin, K., Wahren, J. (1986a). Leg glucose uptake during maximal dynamic exercise in humans. Am. J. Physiol. 251, E65-E70. 

In starvation, glucose must be ptovided for the brain and erythrocytes initially, this is supphed from hver glycogen reserves. To spare glucose, muscle and other tissues reduce glucose uptake in response to lowered insuhn secretion they also oxidize fatty acids and ketone bodies preferentially to glucose. 

Shikonm stimulates glucose uptake in 3T3-L1 adipocytes via an insulin-independent tyrosine kinase pathway. Biochem. Biophys Res Commun. 292 (3) 642-51. 

Thiazolidinediones are known to increase insulin sensitivity by stimulating peroxisome proliferator-activated receptor gamma (PPAR-y). Stimulation of PPAR-y results in a number of intracellular and extracellular changes, including an increased number of insulin receptors, increased insulin receptor sensitivity, decreased plasma fatty acid levels, and an increase in a host of intracellular signaling proteins that enhance glucose uptake. 

Newport Glucose uptake. How many glucose transporters can the cell put in the membrane ... 

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