BackMetabolism, Energy Balance, and Temperature Regulation: Study Notes for Anatomy & Physiology
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22.1 Appetite and Satiety
Feeding and Satiety Centers
The hypothalamus contains centers that regulate hunger and satiety, controlling food intake through complex interactions of neural and hormonal signals.
Feeding Center: Stimulates hunger and food intake.
Satiety Center: Inhibits hunger after eating.
Control Factors: Include blood glucose levels, hormones (e.g., leptin, ghrelin), and psychological factors.
Glucostatic vs. Lipostatic Theory
Glucostatic Theory: Hypolthalamus regulates by blood glucose levels; low glucose stimulates hunger.
Lipostatic Theory: Long-term regulation of food intake is based on body fat stores; hormones like leptin signal fat reserves.
Chemical, Neural, Psychological, and External Factors
Chemical: Nutrient levels, hormones.
Neural: Hypothalamic pathways, vagus nerve signals.
Psychological: Emotions, stress, learned behaviors.
External: Social cues, food availability.
22.2 Energy Balance
Energy Input Equals Energy Output
Energy balance is the relationship between energy intake (food) and energy output (work and heat).
Total energy=energy stored+ intake+output
First Law of Thermodynamics: Energy cannot be created or destroyed, only transformed.
Energy Intake: Consists of food consumed, measured in kilocalories (kcal).
Energy Output: Biological work and heat; output takes two forms: external work (movement) and internal work (cellular processes).
Types of Biological Work:
Mechanical work (muscle contraction)
Chemical work (biosynthesis and storage)
Short-term storage (ATP)
Long term (glycogen stored in the liver and skeletal muscles, fat stored in adipose tissue)
Transport work (moving molecules across membranes)
Oxygen Consumption Reflects Energy Use
Direct Calorimetry: Measures heat produced by the body to estimate energy expenditure.
Indirect Calorimetry: Estimates energy use by measuring oxygen consumption and carbon dioxide production.
Metabolic Energy Content of Nutrients
Carbohydrate: 4 kcal/g
Protein: 4 kcal/g
Fat: 9 kcal/g
Total Kilocalories: Determined by multiplying grams of each biomolecule by their energy content and summing.
Measuring Metabolic Rate
Methods: Direct calorimetry, indirect calorimetry, measuring oxygen consumption, and estimating from activity levels.
Many Factors Influence Metabolic Rate
Basal Metabolic Rate (BMR): Energy expenditure at rest, in a fasting state.
Resting Metabolic Rate (RMR): Similar to BMR but less strict conditions.
Influencing Factors: Age, sex, genetics, hormones, body composition, temperature.
Diet-Induced Thermogenesis: Increase in metabolic rate after eating.
Voluntary Control: Physical activity and food intake.
Energy Is Stored in Fat and Glycogen
Daily Energy Requirement: Expressed in kilocalories per day.
Glycogen vs. Fat Storage: Fat stores more energy per gram and is less accessible than glycogen, which is quickly mobilized.
Glycogen Storage: Mainly in liver and skeletal muscle; liver stores ~100g, muscle stores ~400g.
22.3 Metabolism
Metabolism Defined
Metabolism encompasses all chemical reactions in the body, including energy production, storage, and use.
Anabolic Pathways: Build complex molecules from simpler ones (e.g., protein synthesis).
Catabolic Pathways: Break down complex molecules to release energy (e.g., glycolysis).
States of Metabolism: Fed (anabolic) and fasted (catabolic).
Ingested Energy May Be Used or Stored
Fates of Biomolecules: Used for energy, stored, or used for biosynthesis.
Nutrient Pools: Amino acid pool (proteins), free fatty acid pool (lipids), glucose pool (carbohydrates).
Regulation: Plasma glucose concentration is most tightly regulated.
Key Metabolic Terms
Glycogenesis: Formation of glycogen from glucose.
Glycogenolysis: Breakdown of glycogen to glucose.
Gluconeogenesis: Formation of glucose from non-carbohydrate sources.
Lipogenesis: Formation of fat from non-lipid precursors.
Lipolysis: Breakdown of fats to fatty acids and glycerol.
Push-Pull Control of Metabolic Reactions
Push-Pull Control: Simultaneous regulation of opposing pathways (e.g., synthesis and breakdown) to maintain homeostasis.
Fed State- influenced by insulin results in net glycogen synthesis
Fasted State- influenced by glucagon, net glucose synthesis
Example: Insulin promotes glycogenesis (push), glucagon promotes glycogenolysis (pull).
22.4 Fed-State Metabolism
Carbohydrates Make ATP
Glucose Absorption Path: Intestine → blood → cells via facilitated diffusion and insulin-regulated transporters.
Fates of Absorbed Glucose: Used for ATP production, stored as glycogen, or converted to fat.
Glucose Storage
Unused Glucose: Stored as glycogen in the liver and muscle.
Amino Acids Make Proteins
Amino Acid Absorption Path: Intestine → blood → cells for protein synthesis or energy.
Fates of Absorbed Amino Acids: Protein synthesis, energy production, or conversion to fat/glucose.
Fats Store Energy
Dietary Fat Absorption: Fats absorbed as chylomicrons, enter lymph, then bloodstream.
Triglyceride Processing: Lipoprotein lipase converts fatty acids and glycerol; fatty acids used for energy or stored, glycerol converted to glucose in liver.
Triglyceride synthesis
Glycerol is made from glucose through glycolysis
FA are made when 2-carbon acyl units from acetyl-CoA are linked
One glycerol + 3 FA makes triglyceride
Glucose Transport in Adipose and Skeletal Muscles
Insulin binds to receptor tyrosine kinase
Signal transduction cascade
Exocytosis
Glucose enters the cell
Lipoprotein Complexes: Transport lipids in blood; targeted to tissues via apolipoproteins.
LDL vs. HDL: LDL delivers cholesterol to tissues; HDL removes excess cholesterol.
22.5 Fasted-State Metabolism
Glycogen Converts to Glucose
Primary Glycogen Supply: Liver glycogen supplies blood glucose for several hours.
Glycogenolysis: Most muscle glycogen converted to glucose-6-phosphate, then to pyruvate/lactate; liver glycogen converted to glucose for release into blood.
Proteins Can Be Used to Make ATP
Deamination: Removal of amino group from amino acids before entering energy pathways.
By-product: Ammonia, converted to urea for excretion.
Gluconeogenesis: Amino acids converted to glucose in liver.
Lipids Store More Energy than Glucose or Protein
Fatty Acid Oxidation: Fatty acids undergo β-oxidation in mitochondria, producing acetyl-CoA for the citric acid cycle.
Potential Dangers: Excessive β-oxidation can lead to ketone body production and metabolic acidosis.
22.6 Homeostatic Control of Metabolism
The Pancreas Secretes Insulin and Glucagon
Islets of Langerhans: Contain α cells (glucagon), β cells (insulin), D cells (somatostatin), PP cells (pancreatic polypeptide).
Neural Control: Parasympathetic stimulation increases insulin secretion; sympathetic stimulation inhibits it.
Insulin-to-Glucose Ratio Regulates Metabolism
Dominant Hormone: Insulin in fed state, glucagon in fasted state.
Effects: Insulin promotes glucose uptake and storage; glucagon promotes glucose release.
Fluctuations: Glucose, insulin, and glucagon levels vary throughout the day based on food intake and fasting.
Insulin Promotes Anabolism
Signal Transduction: Insulin binds to the receptor tyrosine kinase, activates intracellular pathways for glucose uptake.
Target Tissues: Adipose, muscle, liver.
Effects: Increases glucose uptake, glycogen synthesis, fat synthesis, protein synthesis.
Regulation: Increased blood glucose stimulates insulin secretion.
Glucagon Is Dominant in the Fasted State
Stimulus: Low blood glucose.
Primary Target: Liver.
Effects: Stimulates glycogenolysis, gluconeogenesis, and lipolysis.
22.6 Diabetes Mellitus
Diabetes Mellitus Is a Family of Diseases
Characterization: Chronic hyperglycemia due to insulin deficiency or resistance.
Diagnosis: Glucose tolerance test.
Type 1 vs. Type 2: Type 1 is autoimmune destruction of β cells; type 2 is insulin resistance.
Symptoms: Polyuria, polydipsia, polyphagia, muscle wasting, metabolic acidosis, increased ventilation, hyperkalemia.
Treatment: Type 1: insulin therapy; Type 2: lifestyle modification, oral medications, sometimes insulin.
Type 2 Diabetics Often Have Elevated Insulin Levels
Reasons: Insulin resistance leads to compensatory hyperinsulinemia.
Ketosis: Rare in type 2 due to residual insulin activity.
Therapy: Diet, exercise, medications (e.g., metformin), sometimes insulin.
Metabolic Syndrome Links Diabetes and Cardiovascular Disease
Metabolic Syndrome: Cluster of conditions (obesity, hypertension, dyslipidemia, insulin resistance) increasing risk for diabetes and heart disease.
Criteria: Central obesity, high triglycerides, low HDL, high blood pressure, high fasting glucose.
PPARs: Nuclear receptors regulating lipid and glucose metabolism.
22.7 Regulation of Body Temperature
Body Temperature Balances Heat Production, Gain, and Loss
Metabolic Efficiency: Lower in obesity due to increased energy storage.
Homeothermic: Humans maintain a stable internal temperature.
Normal Range: 36.5–37.5°C
Influencing Factors: Time of day, activity, environment, hormones.
Highest Temperature: Late afternoon/early evening.
Heat Gain and Loss Are Balanced
Internal Heat Production: Metabolism, muscle activity.
External Heat Input: Environmental temperature, radiation.
Types of Heat Loss: Radiation, conduction, convection, evaporation.
Body Temperature Is Homeostatically Regulated
Thermoneutral Zone: Range where body does not need to expend energy to maintain temperature.
Physiological Challenge: Extreme hot or cold temperatures.
Integrating Center: Hypothalamus.
Thermoreceptors: Located in skin and core body regions.
Heat Loss Mechanisms: Sweating, vasodilation.
Heat Production Mechanisms: Shivering, non-shivering thermogenesis.
Alterations in Cutaneous Blood Flow Conserve or Release Heat
Sympathetic Neurons: Regulate blood vessel diameter; vasodilation increases heat loss, vasoconstriction conserves heat.
Sweat Contributes to Heat Loss
Sweat Gland Anatomy: Coiled tubular glands; sweat is mostly water, with some electrolytes.
Neural Control: Sympathetic cholinergic neurons stimulate sweat production.
Heat Loss: Evaporation of sweat cools the body.
Body Temperature Variation and Fever
Physiological Causes: Exercise, circadian rhythm.
Pathological Causes: Infection, inflammation.
Fever: Elevated body temperature due to resetting of hypothalamic set point; caused by pyrogens.
Biomolecule | Energy Content (kcal/g) | Main Storage Form | Accessibility |
|---|---|---|---|
Carbohydrate | 4 | Glycogen | High |
Protein | 4 | Muscle Protein | Low |
Fat | 9 | Triglycerides | Low |
Key Equations:
First Law of Thermodynamics:
Energy Expenditure (Indirect Calorimetry):
Metabolic Rate:
Additional info: Some explanations and table entries were expanded for clarity and completeness based on standard Anatomy & Physiology curriculum.