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Fuel Homeostasis General Physiology Biology 346 Tony Serino, Ph.D.
Biology Department Misericordia University
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Energy Metabolism Metabolic Rate (MR) –total rate of energy use in body (Kcal/min) -calorie = amount of heat needed to raise 1g of water one degree Celsius -1 Kcal (1000 calories) = 1 C (nutritional calorie) BMR –(basal MR) MR of conscious, relaxed person hours after eating standardized for STP, diet and body size; represents the minimum energy required for individual to remain alive Estimated by heat production, O2 consumption, or CO2 produced
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Lavoisier’s direct calorimeter
Direct Calorimetry Lavoisier’s direct calorimeter Change in temperature in the exit water directly measures the heat produced by the animal
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Indirect Calorimetry Open Respirometer
Measures subjects uptake of O2 per unit time (Vo2)
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Measuring basal metabolic rate
Basal metabolic rate (BMR)- metabolic rate in a fasting, rested, bird or mammal (endotherm). Specific dynamic action: energy required to digest a meal. Standard metabolic rate (SMR)- metabolic rate in a fasting, rested, poikilotherm at a given temperature. MR is often difficult to assess in animals due to large variations in diet, respiratory quotient is used instead
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Respiratory Quotient (RQ)
RQ is the ratio of O2 used to CO2 produced Carbohydrates (CH2O): In complete oxidation of a carbohydrate, one oxygen is used to oxidize the carbon to form one CO2 Therefore, The RQ for carbohydrates = 1 C6H12O6 + 6 O2 = 6 CO2 + 6 H2O RQ = 6 volumes of CO2/ 6 volumes of O2 = 1 RQ protein = 0.8, RQ fat = 0.7
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Specific dynamic action
anphys-fig jpg
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Metabolic Rate vs. Animal Size
Total energy consumed by an animal increases with body size, but when rate is plotted against body mass a reciprocal function is seen
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The smaller the animal the higher the MR per gram of body mass
Each class (reptiles, birds, mammals, etc) of organism follows this pattern, but on separate curves
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Unicellular organisms, endotherms, and ectotherms, all have metabolic rate related to body mass at a slope of 0.75. RQ
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Rubner’s surface rule Mass-specific metabolic rate increases with decreasing body size because of increased surface area to mass (volume) ratio, ie., not a linear increase. Great surface area means more potential for heat loss; remember heat loss = heat production for constant body temp. Surface area increases as square of linear dimension; volume increases as cube of linear dimension, therefore slope of log VO2 vs log Mb should be 2/3 or 0.67.
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Problems with surface rule
Slope of relationship between VO2 and Mb = 0.75 not 0.67. Same slope for poikilothermic animals and single cell organisms. No reason to think that these animals must keep heat loss = heat production.
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SA = # of sides * area of each side (l * w)
Volume = L * w * d (each side dimension cubed)
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Acquisition of Energy and Nutrients
GI tract mechanically and chemically digests food into their chemical “building blocks” for absorption into internal environment Proteins into amino acids CHO into monosaccharides Fats into fatty acids and glycerol Most absorbed material is first processed by the liver
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Review of Metabolic Pathways
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Nutritional States of the Body
Absorptive State Body is assimilating nutrients and is able to use the energy of this food to survive Lasts about 4 hours (represents time for food to pass through small intestine) Post-absorptive State (Fasting State) Occurs after meal fully absorbed
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Absorptive State (LDLs)
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Absorptive State Summary
Energy source for body is absorbed glucose Glucose utilization is favored (burn or store) Glycogenesis in skeletal muscles and liver: (Glucose glycogen) Lipogenesis in adipose and liver: (FA fat; also excess AA and glucose converted to FA in liver) Skeletal muscle and liver favor protein anabolism: (AA protein) Dominated by insulin
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Post-Absorptive State
(HDL)
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Post-Absorptive State Summary
Body energy provided by stored reserves Glycogenolysis in muscle and liver releasing glucose to blood (glycogen glucose) Protein catabolism (esp. in muscle) puts AA in blood Gluconeogenesis in liver (creation of glucose from non-glycogen sources) Lactate, pyruvate, glycerol, and AA Lipolysis (breakdown of fat FA and glycerol) FA used as energy source by most cells except brain Liver can combine Co-A with FA to form ketones Dominated by glucagon
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Fuel Homeostasis Regulated by Pancreas
Both an exocrine and endocrine gland Located in middle of upper right abdominal quadrant Islets of Langerhans secrete hormones b-cells secrete insulin a-cells secrete glucagon d-cells secrete somatostatin f-cells secrete PP (pancreatic polypeptide)
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Insulin Regulation Secretion stimulated by: Inhibited by:
Increase blood glucose Increase blood AA Increase GI hormone levels in blood Increase parasympathetic activity Inhibited by: Decrease blood glucose Increase sympathetic activity Somatostatin
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Insulin Effects Message: increase glucose utilization
Increase uptake of glu in all cells except brain and liver (increase glucose transporter proteins) Increase FA and AA uptake Increases glycolysis, glycogenesis, lipogenesis, and protein synthesis Net: decrease glu, AA and FA in blood; increase fat , glycogen and protein production
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Glucagon Regulation Secretion stimulated by: Inhibited by:
Decrease blood glucose Increase blood AA Increase sympathetic stimulation Epinephrine secretion Inhibited by: Increase blood glucose Increase parasympathetic stimulation Somatostatin secretion
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Glucagon Effects Increases cytoplasmic cAMP which triggers kinase activity to activate enzymes Increases lipolysis, glycogenolysis, gluconeogenesis Net: increases blood glucose, FA, glycerol and ketones Most cells survive on FA and ketone metabolism (glucose sparing action)
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Exercise Effects Essentially a Fasting State but protein sparing
Skeletal muscle differs from normal response: Increases uptake and use of glucose No protein catabolism (after excerise; increase protein synthesis
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Diabetes Disease state characterized by polyuria, polydipsia, polyphagia Diabetes Insipidus –triggered by decrease production of ADH in post. pituitary Diabetes Mellitus –due to hyposecretion secretion of insulin or insulin hyporesponsiveness Type I (Insulin dependent or Juvenile) results from loss of b-cells in pancreas (maybe autoimmune disease) (10% 0f diabetics) Type II (insulin independent or Adult onset) results from loss of insulin membrane receptors in target tissues (Ab attachment to receptor or a chronic down regulation) (90% of diabetics) Chronic islets stimulation may result in hypertrophy and cell death; and thus insulin dependency
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Organ Response to Insulin Deficiency
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Control of Body Hunger
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