Glucose utilisation

From the above biomass production, calculate the yield coefficients. Based on definition, the yield of biomass on glucose means how much biomass is produced per gram of glucose utilised in a cell. The yield of biomass on glucose is calculated as follows ... 

The increase in insulin concentrations produced by sulphonylureas lowers blood glucose concentrations through decreased hepatic glucose output and increased glucose utilisation, mostly by muscle ( insulin, insulin receptor). 

For calculation of rate of ATP generation from glucose, assuming complete oxidation of glucose, multiply rate of glucose utilisation by 30. 

On the basis of the data in this table, the calculated rate of glucose utilisation by the brain of an adult is about 3 g/hr. This is consistent with a rate of about 80 g in 24 hours (Chapter 14). 

In skeletal muscle, glucose transport is non-equilibrium, so that an increase in activity of the transporter increases glucose utilisation. Factors that increase the activity of the transporter (e.g. the number of transporter molecules) in the membrane are insulin and sustained physical activity. In contrast, the hormone cortisol decreases the number of transporters in the membrane. This decreases glucose uptake and is one of the effects of cortisol that helps to maintain the normal blood glucose level (Chapter 12). 

The concentration of glucose in the blood is maintained as a balance between rates of glucose utilisation and glucose supply and changes in one or both of these can lead to hypoglycaemia. Three situations are considered. 

Hypoglycaemia caused by stimulation of the rate of glucose utilisation and inhibition of the rate of release of glucose by the liver... 

To provide an alternative fuel to glucose during starvation. Indeed, fatty acid oxidation restricts the rate of glucose utilisation, which maintains the blood glucose level, via a regulatory mechanism known as the glucose/ fatty acid cycle (Chapter 16). 

There are two tissues that cannot use long-chain fatty acids, the small intestine and the brain. Both can, however, oxidise ketone bodies and therefore can restrict glucose utilisation. It is not known why these tissues do not oxidise fatty acids possibly the activity of the enzymes in oxidation is very low. 

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... 

Figure 13.27 A possible mechanism by which a low blood glucose level could give rise to central fatigue. A low blood glucose level reduces the rate of glucose utilisation in the brain which decreases the ATP/ADP concentration ratio in the presunaptic neurone. This reduces the energy available for synthesis of neurotransmitters, packaging of neurotransmitter molecules into vesicles and exocytosis of neurotransmitter into synaptic cleft. This decreases electrical activity in postsynaptic neurones and hence in the motor pathway.

Figure 16.2 Redprocal relationship between the changes in the concentrations of glucose and fatty adds in blood during starvation in adult humans. As the glucose concentration decreases, fatty acids are released from adipose tissue (for mechanisms see Figure 16.4). The dotted line is an estimate of what would occur if fatty acid oxidation did not inhibit glucose utilisation. Such a decrease occurs if fatty acid oxidation in muscle is decreased by specific inhibitors.

Figure 16.5 Effect of malonyl-CoA on the glucose/fatty acid cycle. Malonyl-CoA is an inhibitor of fatty acid oxidation, so that it decreases fatty acid oxidation in muscle and thus facilitates glucose utilisation (See Figure 7.14). Malonyl-CoA is formed from acetyl-CoA via the enzyme acetyl-CoA carboxylase, which is activated by insulin. Insulin therefore has three separate effects to stimulate glucose utilisation in muscle.

The rise in the plasma level of hydroxybutyrate leads to an increase in its rate of oxidation by the brain which reduces the rate of glucose utilisation by this organ from about 100 g to about 40 g per day (see below). Of this 40 g, about half is produced from glycerol. 

The increased oxidation of fatty acids decreases the rate of glucose utilisation and oxidation by muscle, via the glucose/fatty acid cycle, which accounts for some of the insulin resistance in trauma. An additional factor may be the effect of cytokines on the insulin-signalling pathway in muscle. An increased rate of fatty acid oxidation in the liver increases the rate of ketone body production the ketones will be oxidised by the heart and skeletal muscle, which will further reduce glucose utilisation. This helps to conserve glucose for the immune and other cells. 

Cirrhosis Hyperglycaem i a Portosystemic shunting of insulin and decreased hepatic insulin breakdown leads to inhibition of muscle glucose utilisation and peripheral insulin resistance, leading to elevated glucose levels Hyperglycaemia, acidosis, osmotic diuresis... 

Carbohydrate metabolism gluconeogenesis is increased and peripheral glucose utilisation (transport across cell membranes) may be decreased (insulin antagonism) so that h5q>erglycaemia and sometimes glycosuria result. Latent diabetes becomes overt. 

Product quality of PHAs is very much dependent on the polyester composition (see 3.2.2.1). In 1987, Byrom found that poly-(3HB-co-3HV) can be produced in large-scale fed-batch culture by supplementing the nutritional medium of a glucose-utilising mutant of Alcaligenes eutrophus (today known as Cupriavidus necator) with propionic acid (precursor for 3HV formation) [50]. Later it was shown that the utilisation of valeric acid instead of propionic acid results in a higher proportion of 3HV units [51]. The improvements in product quality of co- and terpolyesters, however, results in an increase of the production costs of the polymer because of the high price of the precursors. 

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