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Transcript
Metabolic Pathways - absorptive GI tract Glucose • Hormonal Control of Blood Glucose Triglyceride Amino Acids Liver Glycogen Fatty acids Glucose α-ketoacids amino acids Glucose energy Glucose protein energy muscle Fatty acids Glucose amino acids Glycogen Triglycerides Fatty acids Triglycerides All tissue adipose Metabolic Pathways - postabsorptive Liver Glycogen 1. Absorptive state is about Glucose storage Blood Glucose • • • Glucose Lactate & pyruvate energy energy glycerol Fatty acids α-ketoacids Glucose Nervous tissue 2. Postabsortive state is about preserving glucose for the nervous system ketones amino acids ketones energy Lactate & pyruvate amino acids Glycogen muscle protein glycerol Fatty acids Triglycerides Glycogen by muscle & liver Triglycerides by adipose All tissues use glucose as the energy source Fatty acids • • Utilizing glucose stores to produce blood glucose Switching other tissues to fat All other tissue adipose 1 Sources of blood glucose 1. Glycogenolysis • • • Breakdown of glycogen to glucose Liver and muscle Muscle is indirect via lactate & pyruvate 2. Lipolysis • Breakdown of trigylcerides in adipose 3. Gluconeogenesis • Production of ‘new’ glucose from any precursor Hormonal Control of Blood Glucose • Endocrine pancreas – Only 2% of entire pancreas, – the rest produces digestive enzymes (exocrine) – Islets of Langerhans • Insulin (β cells) • Glucagon (α cells) • Somatostatin (Δ cells) Hormonal Control of Blood Glucose What controls: • production of glycogen, protein and triglyceride during absorption? • Use of glucose during absorption and the switch to fat postabsorption? • Glucose uptake by liver during absorption and release of glucose postabsorption Insulin • Stimulus for secretion is high blood glucose • Secreted by β cells • Leads to glucose uptake and storage in liver, muscle and fat tissue. • Effect is to ↓ blood glucose 2 Control of insulin secretion Blood glucose ↑ Blood glucose Sympathetic NS or Epinephrine ↑ Blood amino acids GIP from GI tract How does glucose control insulin secretion from β cell? β cells Parasympathetic NS depolarization Glut2 K+ channel glucose Ca++ glucokinase Ca++ dependent release of Insulin containing vesicles Glucose 6 phosphate Glycolysis & Citric acid cycle ATP ↑plasma insulin Effects of Insulin Muscle and Fat Tissue Effects in Muscle & Fat GLUT4 Glycogen synthesis • Insulin initiates transfer of glucose transporters to cell membrane Glucose transporter glucose SNARE dependent transport Glucose transporter ↑ Glucose transporters → ↓ blood glucose → ↑ production of glycogen storage vesicle Insulin 3 Effects of Insulin Liver Effects in Liver • insulin stimulates the synthesis of an enzyme (glucokinase) • Required to ‘trap’ glucose in the cell • initiates glycogen production GLUT2 Glycogen synthesis Glucose transporter glucose X glucose Glucose 6-phosphate glucokinase ‘trapped’ Summary of response to insulin Glucagon ↑ Plasma insulin fat muscle ↑Glucose uptake ↑Amino acid uptake ↑Glycogen & protein synthesis ↑Glucose uptake ↑Triglyceride synthesis liver ↑Glucose uptake ↑Glycogen synthesis ↑Triglyceride synthesis – Secretion stimulated by low blood glucose – Activates enzymes for gluconeogenesis and glycogenolysis – Leads to ↑ blood glucose levels ↓ Plasma insulin muscle ↑ Glucose uptake ↑ Glycogen breakdown ↑ protein breakdown fat ↓ Glucose uptake ↑ Triglyceride breakdown & release of glycerol and fatty acid liver ↑Glucose release into blood due to glycogen breakdown & gluconeogenesis ↑Ketones released 4 Glucagon Control • primarily under inhibitory paracrine control by insulin insulin β α Glucose Regulation Summary • Endocrine pancreas • Secretion of several hormones important for blood glucose regulation • Insulin → glucose uptake and storage – Different effects on liver and muscle & fat • ↑blood glucose → ↑insulin →↓glucagon • ↓ blood glucose → ↓ insulin → ↑ glucagon • Also sympathetic NS can ↑ glucagon release • Glucagon → glucose production • Diabetes • End of Hormones – 2 million Canadians – $9 billion per year health care costs – Insulin isolated by Banting & Best 1922, U of T Dept of Physiology (1923 Nobel Prize) • Type 1 – No or very little insulin produced • Type 2 – Reduced cellular response to insulin • Consequences – – – – Death Blindness Kidney disease Limb amputation 5
