Regulation of Gluconeogenesis

Tissues involved in glucose conservation are liver, skeletal muscle, and adipose. Signals that attune the body 

Effects of glucagon, glucocorticoids, and insulin on the pathways of carbohydrate and lipid metabolism. G-6-P, Glucose-6-phosphate PEP, phosphoenolpyruvate OA, oxaloacetate FA, fatty acid  

The sources of carbon for hepatic glucose formation are hepatic glycogen, lactate from red blood cells or skeletal 

Glucose homeostasis in the fasting state. TG, Triacylglycerol RBC, red blood cells FA, fatty acid AA, amino acid. 

Triacylglycerol storage in high-fat and high-carbohydrate diets. FA, Fatty acid TG, triacylglycerol. 

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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... 

There are two unusual aspects to the regulation of gluconeogenesis. The first step in the reaction, the formation of oxaloacetate from pyruvate, requires the presence of acetyl-CoA. This is a check to make sure that the TCA cycle is adequately fueled. If there s not enough acetyl-CoA around, the pyruvate is needed for energy and gluconeogenesis won t happen. However, if there s sufficient acetyl-CoA, the pyruvate is shifted toward the synthesis of glucose. 

The cycle plays a role in the regnlation of gluconeogenesis bnt this is achieved via another enzyme, which is involved only in regulation of gluconeogenesis, phosphofrncto-2-kinase. 

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

Uptake of Ca2+ into cells, or release of this ion from intracellular stores, is a major regulatory mechanism in many if not all cells (see Section E). Mn2+ activates phosphoenolpyruvate carboxykinase (Eq. 13-46) and maybe a regulator of gluconeogenesis.142 Iron controls the synthesis of ferritin and of transferrin receptors137 (Chapter 16). The specific metal ions present in many biological macromolecules are likely to participate in additional regulatory processes. 

The enzyme responsible for this step is fructose 1,6-bisphosphatase. Like its glycolytic counterpart, it is an allosteric enzyme that participates in the regulation of gluconeogenesis. We will return to its regulatory properties later in the chapter. 

Figure 16.30. Reciprocal Regulation of Gluconeogenesis and Glycolysis in the Liver. The level of fructose 2,6-bisphosphate is high in the fed state and low in starvation. Another important control is the inhibition of pyruvate kinase by phosphorylation during starvation.

Figure 30.6. Regulation of Gluconeogenesis. Fructose 1,6-bisphosphatase is the principal enzyme controlling the rate of gluconeogenesis.

This chapter discusses the pathways by which L-tryptophan is metabolized into a variety of metabolites, many of which have important physiological functions. A few metabolites are cited here briefly. Quinolinic acid is involved in the regulation of gluconeogenesis. Picolinic acid is involved in normal intestinal absorption of zinc. The body s pool of nicotinamide adenine dinucleotide (NAD) is influenced by L-tryptophan s metabolic conversion to niacin. Finally, L-tryptophan is the precursor of several neuroactive compounds, the most important of which is serotonin (5-HT), which participates as a neurochemical substrate for a variety of normal behavioral and neuroendocrine functions. Serotonin derived from L-tryptophan allows it to become involved in behavioral effects, reflecting altered central nervous system function under conditions that alter tryptophan nutrition and metabolism. 

See also Gluconeogenesis Enzymatic Reactions, Gluconeogenesis Molecular Intermediates, Regulation of Gluconeogenesis and Glycogen, Glycolysis,... 

See also Regulation of Gluconeogenesis, Fructose-2,6-Bisphosphate in Gluconeogenesis Regulation, Gluconeogenesis Enzymes, Glycolysis Enzymes, AMP... 

See also Gluconeogenesis Precursors, Gluconeogenesis Substrates, Gluconeogenesis Enzymes, Regulation of Gluconeogenesis... 

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