Ch06 b
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This document discusses how different organs regulate metabolism to maintain energy balance. The liver regulates sugar and fat storage and breakdown. The kidneys help produce glucose during starvation. Hormones like epinephrine, insulin, and glucagon signal the liver and muscles to store or release sugars and fats. Prolonged starvation causes the body to use ketone bodies instead of glucose for fuel. Uncontrolled diabetes occurs when cells cannot respond to insulin signals, leading to high blood sugar and dangerous ketone production. Dieting aims to mimic controlled starvation for weight loss but requires supervision.
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Ch06 b
- 1. Metabolic interrelationship Chapter 6: Integration, Specialization, and Regulation of Metabolism
- 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
- 4. Food pyramid Fig. 24-2, p.668
- 5. Review of metabolism Glycolysis Gluconeogenesi s The pentose phosphate pathway Β oxidation and fatty acids synthesis Amino acids degradation and synthesis The citric acid cycle Oxidative phosphorylatio n
- 9. Brain
- 10. Muscle
- 11. Liver
- 12. 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
- 13. Kidney Overall reaction in kidney: Glutamine → α-ketoglutarate + Functions NH4+ : to filter out the waste During starvation, the product urea from the α-ketoglutarate enters bloodstream gluconeogenesis : to concentrate it for (kidneys generate as excretion much as 50% of the body’s glucose supply) : to recover important metabolites (glucose) α-ketoglutarate : converted to malate : to maintain the blood (TCA cycle) pH : pyruvate (oxidized to CO2) or via OAA to PEP : converted to glucose via gluconeogenesis
- 17. Hormones reacts as the intercellular messengers Hormones transported from the sites of their synthesis to the sites of action by the bloodstream Fig. 24-5, p.671
- 18. 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
- 20. 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. 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.
- 32. During prolonged starvation or fasting, 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 Dieting – to lose excess weight. Diet forced the body to follow the same adjustment like starvation or fasting but a more moderate or controllable pace. Dieting is not free of problems, therefore it is advisable to undergo diet under supervision of physician or nutritionist.
Notes de l'éditeur
- 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 24.5 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.
- 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.