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R2CellRespireRegW11 - Regulation of Cellular Respiration...

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Unformatted text preview: Regulation of Cellular Respiration Regulation of Cellular Respiration & Metabolism in Humans Metabolism Metabolic Pathways: a summary Balance of all reactions that involve energy transformations. • Catabolic (“breaking down”): exergonic – Hydrolysis of polymers into monomers (energy substrates). – Cellular respiration of energy substrates into CO 2 coupled with the synthesis of ATP. • Anabolic (“building up”): endergonic – Dehydration synthesis of polymers for energy-storage or structure; coupled to the hydrolysis of ATP. Uncoupling Proteins Aerobic Respiration Uncoupling proteins (UCP) in inner mitochondrial membrane of mammals q Allow some H + leakage, bypassing ATP- synthase . ß Burn fuel stores without generating ATP ß May be important in regulating %body fat ß May also be important in reducing formation of dangerous Reactive Oxygen Species (ROS) ßH +-leakage is activated by O 2–. ßO2– + 2H +Æ H 2O2 Æ H2O + 1/2O2 q In brown (thermogenic ) fat, UCP1 causes heat generation by burning high-caloric lipid fuel without producing ATP Cellular Metabolism Cellular Metabolism Glucose-6-Phosphate 1. Glucose-6-Phosphate 2. Glucose Glucose 2. 5. = hepatocytes only! Heyer Catabolic pathways: 1. Glycogenolysis 2. Glycolysis 3. Pyruvate Oxidation 4. Krebs Cycle 5. Lipolysis 6. ß- Oxidation 7. Proteolysis 3. 6. 7. 4. 4. Regulation of Cellular Respiration Cellular Metabolism Glycogenesis and Glycogenolysis 1. Glucose Glucose-6-Phosphate •  Glucose-6-phosphate cannot leak out of the cell. •  Skeletal muscles generate glucose-6-phosphate for own glycolytic needs. •  Only Liver contains the enzyme glucose-6phosphatase that can remove the phosphate group and produce free glucose. 2. 3. Intermediate pathways: 1. Glucophosphatase 2. Pyruvate Reduction/ Lactate Oxidation 3. Deamination = hepatocytes only! Uses of Different Energy Sources ⇑⇑ATP→ inhibits F-6-P-kinase ∴ F-6-P → back to G-6-P →  alternate pathway → G-1-P →  glycogenesis ⇑⇑ATP→ inhibits Krebs Cycle enzymes ∴ acetyl-CoA → alternate pathway →  fatty acid synthesis →  lipogenesis Metabolic Pools Gluconeogenesis & the Cori Cycle 4)  3 5)  6)  •  Heyer Lactic acid produced by anaerobic respiration in muscle is released into the bloodstream and delivered to the liver. LDH converts lactic acid to pyruvic acid. Gluconeogenesis: (“creating new glucose”) Pyruvic acid converted to glucose-6-phosphate: G-6-P can be used either for 7A- liver glycogenesis or 7B- can be converted to free glucose and released into the bloodstream. 7A 7B 6 & 7B 6 only occur in liver! 2 Regulation of Cellular Respiration Interactions of Liver, Fat & Muscle Maintenance of circulating energy substrates •  Fasting or low-carbohydrate diet amino acids glucose lactic acid glycerol ketone bodies fatty acids Muscle Fuel Consumption During Exercise 1.  2.  3.  4.  5.  At rest: mostly from aerobic resp. of plama fatty acids. Start exercise: anaerobic resp. of plasma glucose; start muscle glycogenolysis. blood flow & O2 delivery ➠ aerobic resp. of muscle triglycerides. Gluconeogenesis plasma glucose from Cori Cycle. Lipolysis in adipose tissue plama fatty acids for continued aerobic resp. Krebs Cycle Lactate Oxidation Heyer Lipogenesis Gluconeogenesis Balance Between Anabolism and Catabolism •  The rate of deposit and withdrawal of energy substrates, and the conversion of one type of energy substrate into another; are regulated by hormones. •  Antagonistic effects of insulin, glucagon, GH, T3, cortisol, and epinephrine balance anabolism and catabolism. Oxygen Debt Following anaerobic respiration, increased O2 consumption continues to support aerobic oxidation of lactate back to pyruvate. (Reverse of pyruvate reduction. — Uses same LDH enzyme.) Insulin: the primary anabolic hormone Insert fig. 19.4 • glycolysisATP • glycogenesis • lipogenesis 3 Regulation of Cellular Respiration Insulin: the primary anabolic hormone Regulation of Insulin Action •  ↑Blood glucose ⇒ ↑insulin •  ↑Blood amino acids ⇒ ↑insulin ↑Blood amino acids –  If high protein/low carb diet ⇒ ↑blood amino acids/↓blood glucose; ⇒ both ↑insulin and ↑glucagon ⇒ ↓blood amino acids without ↓blood glucose •  Parasympathetic nervous system: rest-and-digest ⇒ ↑insulin •  Intestinal hormones –  ↑Osm of chyme⇒ ↑GIP/GLP-1/CCK ⇒ ↑insulin ↑Cellular uptake of amino acids Amino Acids ↓Blood amino acids • glycolysisATP Protein • protein synthesis The Catabolic Hormones — antagonistic to insulin action •  “anticipates” ↑blood glucose & amino acids •  ↑insulin faster from ingested glucose than from intravenous glucose! •  Adipose hormones –  Enlargement of fat cells ⇒ ↑insulin resistance factor [TNFα] ⇒ ↓insulin sensitivity •  Obesity aggravates diabetes –  Atrophy of fat cells ⇒ ↓TNFα⇒ ↑insulin sensitivity •  Weight loss ⇒ more efficient lipogenesis ⇒ regain lost fat Antagonistic Hormones 1.  Glucagon: blood glucose homeostasis 2.  Epinephrine: acute stress response –  fight-or-flight 3.  Cortisol [glucocorticoid]: chronic stress response –  general adaptation syndrome [GAS] i.  Glucagon and Epinephrine bind to different receptors, but both receptors produce cAMP as a second messenger. Thus they activate the same catabolic enzymes producing the same response. ii.  Glucocorticoids bind to an intracellular DNA-binding receptor to activate genes for a long-term response. Regulation of Insulin and Glucagon Secretion Absorptive & Postabsorptive States Glucagon stimulates catabolic enzymes. Heyer 4 Regulation of Cellular Respiration Diabetes mellitus Diabetes Mellitus: Type I: destruction of ß-islet cells ⇒ insulin deficiency Type II: inactivation of insulin receptors ⇒ insulin resistance Type II Diabetes Mellitus Oral Glucose Tolerance Test •  Measurement of the ability of β cells to secrete insulin. •  Ability of insulin to lower blood glucose. •  Normal person’s rise in blood [glucose] after drinking solution is reversed to normal in 2 hrs. Insert fig. 19.8 cAMP-mediated Catabolic Response Heyer •  Slow to develop. •  Genetic factors are significant. •  Occurs most often in people who are overweight. •  Decreased sensitivity to insulin or an insulin resistance. Insert fig. 19.12 –  Obesity. •  Do not usually develop ketoacidosis. •  May have high blood [insulin] or normal [insulin]. Chronic Stress Response 5 Regulation of Cellular Respiration Glucocorticoids work via nuclear receptors: change gene expression / long term effects Other Important Metabolic Hormones •  Thyroxine Growth Hormone Fat/carb catabolism to support protein anabolism Synopsis of metabolic hormone action –  Adjusts basal metabolic rate (BMR) •  Makes electron transport system less efficient at producing ATP. •  Cells must ⇑glycolysis & ß-oxidation to meet energy demands. “Wasted” energy released as heat. –  Very important in juvenile development to stimulate growth and mental development. •  Anabolic Steroids (androgens) –  At puberty, stimulates protein synthesis for enhanced growth of muscle, bones, and secondary sexual characteristics. •  But also stimulates final maturation of bones, preventing further growth. •  Chorionic Somatomammotropin (hCS) –  Produced by the placenta. GH-like and Prl-like activity. –  GH-like activity: ⇑lipolysis / ⇓glucose utilization in maternal tissues ⇒ ⇑blood fatty acids & glucose available to the fetus. •  “Diabetes of pregnancy” –  Prl-like activity: Also stimulates growth of mammary glands. Heyer 6 ...
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