Metabolism schematic

Type of metabolism Schematic reaction (not balanced) Energy yield ... 

FIGURE 18.5 Schematic representation of types of multienzyme systems carrying out a metabolic pathway (a) Physically separate, soluble enzymes with diffusing intermediates, (b) A multienzyme complex. Substrate enters the complex, becomes covalently bound and then sequentially modified by enzymes Ei to E5 before product is released. No intermediates are free to diffuse away, (c) A membrane-bound multienzyme system. 

Figure 18.1 Schematic representation for the prediction of the complete metabolic profile of a molecule using databases and a machine learning approach. In this example various metabolite rules are used to illustrate how this method will be implemented. Molecule B could also represent metabolites derived from Molecule A.

Figure 13.4 Histamine synthesis, metabolism and receptors. Current knowledge does not justify presentation of a schematic histaminergic synapse. (1) Histidine decarboxylase (2) histamine-A-methyltransferase (3) mono amine oxidase (MAOb)...

A schematic representation of the metabolism of lipoproteins is shown in Fig. 12 [170]. Chylomicrons are synthesized and secreted by the small intestine. They are hydrolyzed in blood by the enzyme lipoprotein lipase... 

FIGURE 20.1 Schematic illustration of lycopene metabolic pathway by CM02. (a) 5-cis Lycopene and 13-cis lycopene are preferentially cleaved by CM02 at 9, 10 -double bond. The cleavage product, apo-lO -lycopenal, can be further oxidized to apo-lO -lycopenol or reduced to apo-lO -lycopenoic acid, depending on the presence of NAD+ or NADH. (b) Chemical structures of apo-lO -lycopenoic acid, acyclo-retinoic acid, and all-frans retinoic acid. (Adapted from Hu, K.Q. et al., J. Biol. Chem., 281, 19327, 2006. With permission.)... 

Figure 7.1 Schematic of the prototypical dopaminergic synapse. Pre- and post-synaptic components of a dopaminergic synapse summarizing molecular pathways for dopamine synthesis, metabolism, and second messenger effects following Dl-like or D2-like receptor activation. (See also Plate 6.)...

Fig. 7.9. Schematic illustration of P-glycoprotein (P-gp) transport and CYP 3A4 metabolism of R/S-verapamil in the human jejunum. It is assumed that the drug must be absorbed before being metabolized by CYP...

Fig. 18.3. ACAT model schematic. The diagram includes the consideration of six states (unreleased, undissolved, dissolved, degraded, metabolized, and absorbed), 18 compartments [nine gastrointestinal (stomach, seven small intestine, and colon) and nine...

Figure 14.4 Schematic diagram comparing the bulk and molecular schemes for the metabolic fate of macronutrient components between diet and consumer tissues...

FIGURE 28-5 Schematic illustration of the movement of cytoskeletal elements in slow axonal transport. Slow axonal transport represents the movement of cytoplasmic constituents including cytoskeletal elements and soluble enzymes of intermediary metabolism at rates of 0.2-2 mm/day which are at least two orders of magnitude slower than those observed in fast axonal transport. As proposed in the structural hypothesis and supported by experimental evidence, cytoskeletal components are believed to be transported down the axon in their polymeric forms, not as individual subunit polypeptides. Cytoskeletal polypeptides are translated on cytoplasmic polysomes and then are assembled into polymers prior to transport down the axon in the anterograde direction. In contrast to fast axonal transport, no constituents of slow transport appear to be transported in the retrograde direction. Although the polypeptide composition of slow axonal transport has been extensively characterized, the motor molecule(s) responsible for the movement of these cytoplasmic constituents has not yet been identified. 

Aiming to construct explicit dynamic models, Eqs. (5) and (6) provide the basic relationships of all metabolic modeling. All current efforts to construct large-scale kinetic models are based on an specification of the elements of Eq (5), usually involving several rounds of iterative refinement For a schematic workflow, see again Fig. 4. In the following sections, we provide a brief summary of the properties of the stoichiometric matrix (Section III.B) and discuss the most common functional form of enzyme-kinetic rate equations (Section III.C). A selection of explicit kinetic models is provided in Table I. TABLE I Selected Examples of Explicit Kinetic Models of Metabolisin 1 ... 

Specifically, SKM seeks to overcome several known deficiencies of stoichiometric analysis While stoichiometric analysis has proven immensely effective to address the functional capabilities of large metabolic networks, it fails for the most part to incorporate dynamic aspects into the description of the system. As one of its most profound shortcomings, the steady-state balance equation allows no conclusions about the stability or possible instability of a metabolic state, see also the brief discussion in Section V.C. The objectives and main requirements in devising an intermediate approach to metabolic modeling are as follows, a schematic summary is depicted in Fig. 25 ... 

Figure 5.5 Schematic representation of drug absorption, distribution, metabolism, and excretion.

Drugs absorbed through the gastrointestinal tract pass into the hepatic portal vein, which drains into the liver. The liver metabolizes the drug, which leads to reduction in the availability of the drug for interaction with receptors. This is called first pass metabolism. A schematic representation of the process of drug in the body is given in Fig. 5.7. 

From a DMPK perspective, a common goal is to be able to compare multiple compounds based on their absorption, distribution, metabolism and excretion (ADME) properties as well their preclinical PK properties [8, 12-22]. Therefore, lead optimization typically is performed as an iterative process that uses the DMPK data to select structural modifications that are then tested to see whether the DMPK properties of the series have been improved. This iterative process is shown schematically in Fig. 13.2. Clearly an important element for the successful lead optimization of a series of NCEs is the ability to perform the DMPK assays in a higher throughput manner. The focus of this chapter will be to discuss ways that mass spectrometry (MS), particularly HPLC-MS/MS can be used to support the early PK studies for NCEs in a higher throughput manner. 

Fig. 2.1 Schematic illustrating hepatic extraction with Q, blood flow and Cf intrinsic clearance (metabolism).

Specific damage to bacteria is particularly practicable when a substance interferes with a metabolic process that occurs in bacterial but not in host cells. Clearly this applies to inhibitors of cell wall synthesis, because human and animal cells lack a cell wall. The points of attack of antibacterial agents are schematically illustrated in a grossly simplified bacterial cell, as depicted in (2). 

The paperback atlas concludes with a series of schematic metabolic charts (pp. 407-419). These plates, which are not accompanied by explanatory text apart from a brief introduction on p.406, show simplified versions of the most important synthetic and degradative pathways. The charts are mainly intended for reference, but they can also be used to review previously learned material. The enzymes catalyzing the various reactions are only indicated by their EC numbers. Their names can be found in the systematically arranged and annotated enzyme list (pp. 420-430). 

The following 13 plates (pp. 407-419) provide a concise schematic overview of the most important metabolic pathways. Explanatory text is deliberately omitted from them. 

Figure 5.7. Schematic representation of therapeutic protein (A) being filtered and (B) metabolized in the kidneys. Protein reabsorption in proximai tabie is iimited.

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