Ch06

261 views

Published on

Published in: Health & Medicine, Business
0 Comments
0 Likes
Statistics
Notes
  • Be the first to comment

  • Be the first to like this

No Downloads
Views
Total views
261
On SlideShare
0
From Embeds
0
Number of Embeds
2
Actions
Shares
0
Downloads
9
Comments
0
Likes
0
Embeds 0
No embeds

No notes for slide
  • FIGURE 24.2 The Food Guide Pyramid (USDA). The recommended choices reflect a diet based primarily on carbohydrates. Smaller amounts of proteins and lipids are sufficient to meet the body’s needs.
  • FIGURE 24.4 Leptin has multiple effects on metabolism. It affects the brain, lowering appetite. It also inactivates acetyl-CoA carboxylase (ACC). Reduced activity of ACC leads to a reduction in malonyl- CoA, which stimulates fatty-acid oxidation and reduces fatty-acid synthesis. ( From Nature, Vol. 415 (January 17, 2002), Fig 1, p. 268. Copyright © 2002 Nature. Reprinted with permission. )
  • FIGURE 19.15 A summary of anabolism, showing the central role of the citric acid cycle. Note that there are pathways for the biosynthesis of carbohydrates, lipids, and amino acids. OAA is oxaloacetate, and ALA is  -aminolevulinic acid. Symbols are as in Figure 19.10.)
  • FIGURE 24.5 Endocrine cells secrete hormones into the bloodstream, which transports them to target cells.
  • FIGURE 24.6 A simple feedback control system involving an endocrine gland and a target organ.
  • FIGURE 24.7 Hormonal control system showing the role of the hypothalamus, pituitary, and target tissues. See Table 24.3 for the names of the hormones.
  • FIGURE 24.8 Nonsteroid hormones bind exclusively to plasmamembrane receptors, which mediate the cellular responses to the hormone. Steroid hormones exert their effects either by binding to plasma-membrane receptors or by diffusing to the nucleus, where they modulate transcriptional events.
  • FIGURE 24.9 Activation of adenylate cyclase by heterotrimeric G proteins. Binding of hormone to its receptor causes a conformational change that induces the receptor to catalyze a replacement of GDP by GTP on G  . The G  (GTP) complex dissociates from G  and binds to adenylate cyclase, stimulating synthesis of cAMP. Bound GTP is slowly hydrolyzed to GDP by the intrinsic GTPase activity of G  . G  (GDP) dissociates from adenylate cyclase and reassociates with G  . G  and G  are lipidanchored proteins. Adenylate cyclase is an integral membrane protein consisting of 12 transmembrane  -helical segments.
  • FIGURE 24.9 Activation of adenylate cyclase by heterotrimeric G proteins. Binding of hormone to its receptor causes a conformational change that induces the receptor to catalyze a replacement of GDP by GTP on G  . The G  (GTP) complex dissociates from G  and binds to adenylate cyclase, stimulating synthesis of cAMP. Bound GTP is slowly hydrolyzed to GDP by the intrinsic GTPase activity of G  . G  (GDP) dissociates from adenylate cyclase and reassociates with G  . G  and G  are lipidanchored proteins. Adenylate cyclase is an integral membrane protein consisting of 12 transmembrane  -helical segments.
  • Tyrosine and epinephrine. The hormone epinephrine is metabolically derived from the amino acid tyrosine.
  • FIGURE 24.14 When epinephrine binds to its receptor, the binding activates a stimulatory G protein, which in turn activates adenylate cyclase. The cAMP thus produced activates a cAMPdependent protein kinase. The phosphorylation reactions catalyzed by the cAMP-dependent kinase suppress the activity of glycogen synthase and enhance that of phosphorylase kinase. Glycogen phosphorylase is activated by phosphorylase kinase, leading to glycogen breakdown.
  • FIGURE 24.15 Binding of glucagon to its receptor sets off the chain of events that leads to the activation of a cAMP-dependent protein kinase. The enzymes phosphorylated in this case are phosphofructokinase-2, which is inactivated, and fructose- bis phosphatase-2, which is activated. The combined result of phosphorylating these two enzymes is to lower the concentration of fructose-2,6- bis phosphate (F2,6P). A lower concentration of F2,6P leads to allosteric activation of the enzyme fructose- bis phosphatase, thus enhancing gluconeogenesis. At the same time, the lower concentration of F2,6P implies that phosphofructokinase is lacking a potent allosteric activator, with the result that glycolysis is suppressed.
  • FIGURE 24.16 Proinsulin is an 86-residue precursor to insulin (the sequence shown here is human proinsulin). Proteolytic removal of residues 31 through 65 yields insulin. Residues 1 through 30 (the B chain) remain linked to residues 66 through 86 by a pair of interchain disulfide bridges.
  • Ch06

    1. 1. Basic Biochemistry II BCM301 Chapter 6:Integration, Specialization, and Regulation of Metabolism
    2. 2.  At this point, we’ll consider how organisms arrange/organize the metabolic symphony to meet their energy needs. Discussion will include how: Body maintains energy balance (homeostasis) It deals with starvation It responds to the loss of control from diabetes mellitus
    3. 3. Biochemistry & nutrition Table 24-2, p.666
    4. 4. Food pyramid Fig. 24-2, p.668
    5. 5. Obesity-Define as - Has beenweighing at least established in20% more than micetheir ideal weight - in mice, leptin is- several 16kDa proteininventions: that produced byartificial obesity (ob) genesweeteners, fat - mutation in thissubstitutes gene will lead to- protein leptin deficiency ofplays a role in the leptincontrol of obesity
    6. 6. Organ specialization
    7. 7. Brain
    8. 8. Muscle The Cori Cycle
    9. 9. Liver The Glucose Alanine Cycle
    10. 10.  The fate of G6P varies with metabolic requirements – depends on the glucose demand G6P can be converted to glucose by glucose-6- phosphatase (transport via bloodstream to the peripheral organs) G6P can be converted to glycogen – when body’s demand for glucose is low G6P can be converted to acetyl-CoA via glycolysis and action of pyruvate dehydrogenase (this glucose- derived acetyl-CoA used in the synthesis of f.acids) G6P can be degraded via pentose phosphate pathway (to generate NADPH required for f.acids biosynthesis and liver’s many other biosynthetic functions)
    11. 11.  The liver can synthesize or degrade TAGs When metabolic fuel is needed, f.acids are degraded to acetyl-CoA and then to ketone bodies (export via bloodstream to the peripheral tissues) When the demand is low, f.acids are used to synthesize TAGs (secreted into the bloodstream as VLDL for uptake by adipose tissue) Amino acids are important metabolic fuel The liver degrades amino acids to a variety of intermediates (begin with a.acid transamination to yield α-keto acid, via urea cycle excreted urea) Glucogenic a.acid – converted to pyruvate / OAA (TCA cycle intermediates) Ketogenic a.acid – converted to ketone bodies
    12. 12. Kidney  Overall reaction in kidney: Glutamine → α- ketoglutarate + NH4+ Functions  During starvation, the α- : to filter out the waste ketoglutarate enters product urea from the gluconeogenesis bloodstream (kidneys generate as : to concentrate it for much as 50% of the excretion body’s glucose supply) : to recover important  α-ketoglutarate : metabolites (glucose) converted to malate : to maintain the blood (TCA cycle) pH : pyruvate (oxidized to CO2) or via OAA to PEP : converted to glucose via gluconeogenesis
    13. 13. Hormones and second messengers Hormones reacts as the intercellular messengersHormones transported from the sites of their synthesis to the sites of action by the bloodstream Fig. 24-5, p.671
    14. 14.  Some typical hormones: - steroids (estrogens, androgens) - polypeptides (insulin and endorphins) - a.acid derivatives (epinephrine and norepinephrine) Hormones help maintaining homeostasis (the balance of biological activities
    15. 15. Table 24-3, p.672
    16. 16. Control system mechanismHormone releasing factor Fig. 24-7, p.673
    17. 17. Fig. 24-8, p.674
    18. 18.  Second messenger e.g cyclic AMP (cAMP) p.676
    19. 19. Fig. 24-9a, p.675
    20. 20. Fig. 24-9b, p.675
    21. 21. Hormones & metabolism The effects of hormones triggered the responses within the cell There are three hormones play a part in the regulation of CHO metabolism Epinephrine, insulin and glucagon Epinephrine: acts on muscle tissue, to raise level of glucose on demand, when it binds to specific receptors, it leads to increased level of glucose in blood, increased glycolysis in muscle cells and increased breakdown of f.acid for energy p.681
    22. 22. Fig. 24-14, p.682
    23. 23.  Glucagon: acts on liver, to increase the availability of glucose, when it binds to specific receptors, it leads to increased level of glucose in blood.
    24. 24. Metabolic homeostasis
    25. 25. Table 24-4, p.685
    26. 26. Metabolic adaptation During prolonged starvation, the brain slowly adapts from the use of glucose as its soul fuel source to the use of ketone bodies, shift the metabolic burden form protein breakdown to fat breakdown Diabetes mellitus is a disease in which insulin either not secreted or doesn’t stimulate its target tissues → high [glucose] in the blood and urine. Abnormally high production of ketone bodies is one of the most dangerous effects of uncontrolled diabetes

    ×