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Figure 22.3 Adapted from LL Langley, Homeostasis

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Figure 22.3 Adapted from LL Langley, Homeostasis ABSORPTIVE STATE Dr. Dalay Olson Office: 3-120 Jackson Hall Office Hours Tuesday 1-3pm [email protected] WHAT HAPPENS TO FOOD BETWEEN DIGESTION AND STORAGE? Why do we eat food in the first place?? LEARNING OBJECTIVES 1. Describe the journey of glucose, amino acids from Gut liver peripheral cells where they are used and stored. 2. Explain how glycogenesis and lipogenesis in the liver prevent large spikes of plasma glucose after a meal. 3. Compare and contrast the storage of absorbed TGL vs. TGL from the liver. 4. Describe negative feedback regulation of insulin. 5. Explain how insulin promotes Rx of absorptive state. 6. Describe the relationship btwn diabetes mellitus and hyperglycemia. METABOLISM • Sum of chemical reactions in the body 1. Extract energy from nutrients 2. Use energy for work 3. Store excess energy • Anabolic pathways synthesize larger molecules from smaller ones • Fed state, or absorptive state • Catabolic pathways break large molecules into smaller ones • Fasted state, or postabsorptive state © 2013 Pearson Education, Inc. ANABOLIC CATABOLIC PATHWAYS PATHWAYS • Glycogenesis (glyco-genesis) • Glycogenolysis (glycogen-o- • Formation of glycogen lysis) • Breakdown of glycogen • Lipogenesis (lipo-genesis) • Formation of lipids • Liopolysis (lipo-lysis) • Breakdown of lipids • Gluconeogenesis (gluco- neo-genesis) • Formation of glucose “Genesis” = formation “Lysis” = breakdown INGESTED ENERGY MAY BE USED OR STORED • Ingested biomolecules have three fates 1. Energy to do mechanical work 2. Synthesis for growth and maintenance 3. Storage as glycogen or fat • Nutrient pools are pools available for immediate use • Free fatty acids pool • Glucose pool • Amino acid pool © 2013 Pearson Education, Inc. EXCESS ENERGY CAN BE STORED AS FAT AND GLYCOGEN • Glycogen (glucose polymer) • Stored in liver and skeletal muscles • Rapid source of energy • Fat • Fats have more than twice the energy content of an equal amount of carbohydrate or protein • Energy in fats is harder and slower to access © 2013 Pearson Education, Inc. Fates of Glucose 1. Oxidation 2. Glycogen storage 3. Triglyceride synthesis Fates of Amino Acids 1. Oxidation 2. Protein synthesis 3. Triglyceride synthesis Fates of Triglycerides 1. Storage in the adipose tissue 2. Oxidation (minor) Dietary Fats Intestinal lumen Chylomicrons Vs. Monoglycerides Phospholipids Lipoproteins Cholesterol Free fatty acids (FFA) 1. Where do the lipids apo originate? Intestinal cells 2. Apo protein function CM Chylomicron FFA 3. Where do lipids end up? Lymph Bile Blood Adipose cells duct Apo Proteins CM Lipolysis by lipases lpl FFA Reassemble TG Glycerol to triglycerides storage (TG) CM remnants Most cells HDL-C LDL-C FFA oxidized for energy Liver Cholesterol for synthesis Phospholipids Metabolized Triglyceride Lipoprotein complexes KEY apo = apoproteins Cholesterol + FFA + Lipoproteins lpl = lipoprotein lipase LDL = low-density lipoprotein HDL = high-density lipoprotein Bile salts C = cholesterol FATE OF NUTRIENTS IN THE FED STATE NUTRIENT ABSORBED AS FED-STATE METABOLISM + • Used immediately for energy through aerobic Glucose primarily; pathways* (glycolysis and citric acid cycle) Carbohydrates • Used for lipoprotein synthesis in liver I also fructose and + • Stored as glycogen in liver and muscle galactose (glycogenesis) + • Excess converted to fat and stored in adipose N tissue (lipogenesis) S + • Most amino acids go to tissues for protein Amino acids synthesis* • if needed for energy, amino acids converted U Proteins primarily plus some in liver to intermediates for aerobic small peptides metabolism (deamination) • Excess converted to fat and stored in adipose L tissue (lipogenesis) I Fatty acids, + • Stored as triglycerides primarily in the liver triglycerides and and adipose tissue* (lipogenesis) Fats • Cholesterol used for steroid synthesis or as cholesterol N a membrane component • Fatty acids used for lipoprotein and eicosanoid synthesis * Primary fate Common bile duct Pancreas Pancreatic duct Small intestine (duodenum) Gross anatomy Figure 22.13-2 Part (b) based on data from Orci and Unger, Lancet 2: 1243–1244, 1975 (2 of 2) Exocrine cells Alpha cells secrete glucagon. Endocrine cells D cells Islet of secrete somatostatin. Langerhans Beta cells secrete insulin, amylin. Cells of the islets of Langerhans, which constitute the endocrine pancreas FACTORS THAT CONTROL INSULIN SECRETION 1. Increased plasma glucose 2. Increased plasma amino acids 3. Feed-forward effects of GI hormones 4. Parasympathetic activity 5. Sympathetic activity (inhibition) © 2013 Pearson Education, Inc. INSULIN CAUSES GLUT INSERTION Vander 16-6 pg 562 INSULIN’S CELLULAR MECHANISM OF ACTION Extracellular Insulin binds to tyrosine fluid Insulin kinase receptor. Receptor phosphorylates insulin-receptor substrates (IRS). Second messenger pathways GLUT4 alter protein synthesis and existing proteins. IRS IRS P Transport activity Membrane transport is modified. Second Nucleus messenger pathways Enzymes or Cell metabolism is changed. Transcription factors Changes in metabolism INSULIN PROMOTES ANABOLISM 1. Increases glucose transport 2. Enhances cellular utilization and storage of glucose 3. Enhances utilization of amino acids 4. Promotes fat synthesis © 2013 Pearson Education, Inc. INSULIN IN THE FED STATE Eat a meal Presence Distension Nutrient digestion KEY of GI tract of carbohydrates and absorption Stimulus wall in GI lumen Sensor Input signal Stretch Integrating center Plasma receptors Plasma Endocrine amino Output signal cells of small glucose acids Target intestine Tissue response Sensory Systemic response neuron input α cells of pancreas Incritins CNS β cells of pancreas Parasympathetic output Insulin Liver Muscle, adipose, and other cells Glucose Glycolysis transport Glycogenesis Lipogenesis FIGURE QUESTION Protein synthesis What is the neurotransmitter and receptor for parasympathetic output at ? Plasma Negative glucose feedback DIABETES MELLITUS -Type 1 - characterized by insulin deficiency -Type 2 - known as insulin-resistant diabetes -Characterized by abnormally elevated plasma glucose concentrations, or hyperglycemia -Complications of diabetes affect blood vessels, eyes, kidneys, and nervous system © 2013 Pearson Education, Inc. DIET Carbohydrates Glycogenesis Glucose Fat Lipogenesis stores Excess glucose Glycogen stores Urine Glycogenolysis Glucose pool Range of normal plasma glucose Metabolism in most tissues Brain metabolism © 2013 Pearson Education, Inc. LEARNING OBJECTIVES 1. Describe the journey of glucose, amino acids from Gut liver peripheral cells where they are used and stored. 2. Explain how glycogenesis and lipogenesis in the liver prevent large spikes of plasma glucose after a meal. 3. Compare and contrast the storage of absorbed TGL vs. TGL from the liver. 4. Describe negative feedback regulation of insulin. 5. Explain how insulin promotes Rx of absorptive state. 6. Describe the relationship btwn diabetes mellitus and hyperglycemia..
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