Gluconeogenesis in liver

Fructose 2,6-Bisphosphate Plays a Unique Role in the Regulation of Glycolysis Gluconeogenesis in Liver... 

Major amino acids emanating from muscle are alanine (destined mainly for gluconeogenesis in liver and forming part of the glucose-alanine cycle) and glutamine (destined mainly for the gut and kidneys). 

In liver, cAMP activates gluconeogenesis, but in muscle, it activates glycolysis. Let s do liver first, and the muscle answer will just be the opposite. So, we want to activate gluconeogenesis in liver in response to increased phosphorylation (increased levels of cAMP). Phosphorylation of our enzyme (PFK-2) must have an effect that is consistent with the activation of gluconeogenesis. If gluconeogenesis is on and glycolysis is off, the level of fructose 2,6-bisphosphate (an activator of glycolysis) must fall. If fructose 2,6-bisphosphate is to fall, the PFK-2 that synthesizes it must be made inactive. So, in liver, phosphorylation of PFK-2 must inactivate the enzyme. 

Activation of cAMP phosphodiesterase, which decreases levels of cAMP and thus the activity of protein kinase A. This results in decreased rates of lipolysis in adipose tissue and glycogenolysis and gluconeogenesis in liver. 

Failure of Insulin to suppress gluconeogenesis in liver leads to overproduction of new glucose, which exacerbates the elevation of blood glucose due to decreased uptake of dietary glucose by muscle and adipose. 

The answer is D. Only the liver and kidneys can synthesize glucose by gluconeogenesis. All the other organs listed are dependent on provision of glucose from blood, either supplied by the diet or by gluconeogenesis in liver and the kidneys. 

Maintenance of adrenal cortex Promotes secretion of steroids, oxidative phosphorylation in adrenal cortex Mobilizes and increases oxidation of free fatty acid in adipose tissue Increases gluconeogenesis in liver increases cyclic adenosine monophosphate (AMP) in adrenal cortex Decreases urea formation in liver... 

Fig.1 Flowchart of gluconeogenesis in liver cells, which explains the role of GP and GS in the interconversion between glucose and glycogen (modified from Somsak et al. 2003) [7]...

Gluconeogenesis in liver is strongly promoted by glucagon and adrenaline. The effects, mediated by cAMP, include stimulation of fructose 1,6-bisphospha-tase and inhibition of phosphofructo-l-kinase, both caused by the drop in the level of fructose The conversion of pyruvate to PEP via oxaloacetate is also promoted by glucagon. This occurs primarily by stimulation of pyruvate carboxylase (Eq. 

Fig. 43.6. Effects of epinephrine on fuel metabolism and pancreatic endocrine function. Epinephrine (Epi) stimulates glycogen breakdown in muscle and liver, gluconeogenesis in liver, and lipolysis in adipose tissue. Epinephrine further reinforces these effects because it increases the secretion of glucagon, a hormone that shares many of the same effects as epinephrine. Epi also inhibits insulin release but stimulates glucagon release from the pancreas.

The Cori cycle is a pathway in which there is cycling of glucose due to glycolysis in muscle and gluconeogenesis in liver. The blood transports lactate from muscle to liver and glucose from liver to muscle. 

Gluconeogenesis is a process which occurs mainly in the liver and serves to maintain the glucose levels in blood, brain and muscle. The relationship of glycolysis in muscle to gluconeogenesis in liver is indicated in Figure 11.23. 

Exton, J. H., and Park, C. R., 1967, Control of gluconeogenesis in liver. I. General features of gluconeogenesis in the perfused liver of rats, J. Biol. Chem. 242 2622. 

Newsholme, E. A., and Gevers, W., 1967, Control of glycolysis and gluconeogenesis in liver and kidney cortex, Vitam. Horm. 25 1. 

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