Gluconeogenesis hormonal

By 4 hours after a meal, the liver is supplying glucose to the blood not only by the process of glycogenolysis but also by the process of gluconeogenesis. Hormonal changes canse peripheral tissues to release precursors that provide carbon for gluconeogenesis, specifically lactate, amino acids, and glycerol. 

Pilkis, S. J., El-Maghrabi, M. R., and Claus, T. H., 1988. Hormonal regulation of hepatic gluconeogenesis and glycolysis. Annual Review of Biochemistry 57 755-783. 

U (No CaM) < O Q. CL Heart, kidney, Brain, liver, widespread Cardiac function, Ca2+-dependent regulation, hormonal regulation of gluconeogenesis, cell proliferation, coincidence detector for NO... 

Vitamin B6-coenzyme is involved in a variety of reactions, e.g., in the immune system, gluconeogenesis, erythrocyte fimction, niacin formation, nervous system, lipid metabolism, and in hormone modulation/gene expression [1, 2]. 

In adipose tissue, the effect of the decrease in insulin and increase in glucagon results in inhibition of lipo-genesis, inactivation of lipoprotein lipase, and activation of hormone-sensitive lipase (Chapter 25). This leads to release of increased amounts of glycerol (a substrate for gluconeogenesis in the liver) and free fatty acids, which are used by skeletal muscle and liver as their preferred metabolic fuels, so sparing glucose. 

These two kinase enzymes are involved in regulation of gluconeogenesis by hormones. 

Hormones can modify the concentration of precursors, particularly the lipolytic hormones (growth hormone, glucagon, adrenaline) and cortisol. The lipolytic hormones stimulate lipolysis in adipose tissue so that they increase glycerol release and the glycerol is then available for gluconeogenesis. Cortisol increases protein degradation in muscle, which increases the release of amino acids (especially glutamine and alanine) from muscle (Chapter 18). 

Initially the level of insulin decreases, favouring increased rates of lipolysis, fatty acid oxidation, muscle protein degradation, glycogenolysis and gluconeogenesis. It soon increases, however, as a result of insulin resistance, when the stimulation of the above processes will depend on the cytokine levels. For details of endocrine hormone effects, see Chapter 12. For details of cytokines see Chapter 17. 

In relatively recent years, it has become clear that under-nntrition of mother leads to low birth weight of the baby and this can increase the risk of development of degenerative disease in later life, e.g. hypertension, obesity, type 2 diabetes. One hypothesis is that the foetus adapts meta-bolically to deficiencies by increasing the number of cells in organs that perform specific functions that can overcome the deficiency, e.g. an increase in the number of liver cells that carry out gluconeogenesis, an increase in cells in the adrenal cortex to produce more of the chronic stress hormone, cortisol. These changes are carried over into adnlthood which can lead to an inadequate response of the liver to insulin so that insulin resistance develops. So far, however, it is unclear whether deficiencies in specific nntrients or undemutrition per se are responsible for snch changes (Chapter 15). 

Phosphoenolpyruvate carboxykinase (PEP-CK), a key enzyme in gluconeogenesis, is regulated by several hormones, all of which affect the transcription of the PEP-CK gene. Cortisol, glucagon, and thyroxin induce PEP-CK, while insulin inhibits its induction (see p. 158). 

Mechanism of Action A natural hormone derived from animal sources, usually beef or pork, fhat is involved in normal mefabolism, growfh, and development, especially the central nervous system (CNS) of infanfs. Possesses cafabolic and anabolic effecfs. Provides both levothyroxine and liothyronine hormones. Therapeutic Effect Increases basal metabolic rate, enhances gluconeogenesis, stimulates protein synthesis. 

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