Nutrition Metabolism and Energy Balance II Flashcards
Regulation of Blood Glucose:
Insulin (hypoglycaemic): Released when blood glucose is high, stimulates by pancreas:
- Glycogen formation in the liver.
- Glucose uptake by cells, lowering blood glucose.
Glucagon (hyperglycemic): Released when blood glucose is low, stimulates:
- Glycogen breakdown in the liver, raising blood glucose.
Normal Blood Glucose: ~90 mg/100 ml.
Insulin promotes glucose uptake by cells by binding to insulin receptors on the cell membrane, triggering a signaling cascade that facilitates the translocation of glucose transporters to the cell surface.
Liver: Converts sugars/fats to glucose/fat.
Detoxifies alcohol and drugs.
Stores vitamins and iron.
Pancreas: Triangular gland behind stomach
Exocrine (Acinar cells): Produce digestive enzymes
Endocrine (Islets of Langerhans):
Alpha cells: Glucagon (raises blood sugar)
Beta cells: Insulin (lowers blood sugar)
Delta cells: Somatostatin
F cells: Pancreatic polypeptide
Diabetes Mellitus (DM): metabolic diseases.
Diabetes Mellitus (DM): High blood glucose
Cause: Insulin production/action defects
Affects: Carbohydrate, fat, and protein metabolism.
Type 1 DM: Autoimmune destruction of pancreatic β-cells → absolute insulin deficiency.
Type 2 DM: Insulin resistance → pancreas produces insulin, but cells don’t respond properly.
Insulin Mechanism:
Without insulin: Glucose can’t enter cells.
With insulin: GLUT4 transporters move glucose into cells.
Consequences of Insulin Deficit:
High blood glucose: Liver breaks down glycogen; muscles break down proteins.
Fat breakdown (lipolysis) → ketone bodies → ketoacidosis (low pH).
Symptoms: Polyuria, polydipsia, polyphagia, ketonuria, dehydration
Type I DM: Fats used for fuel, causing lipidemia and ketone formation
Ketones: Cause ketoacidosis, ketonuria, coma, death, hyperpnea, heart problems, O2 transport issues, depression of NS.
Hyperinsulinism: Excess insulin causes hypoglycemia
Symptoms: Anxiety, disorientation, unconsciousness, death
Treatment: Sugar ingestion
Type 2 DM Risk Factors:
age, obesity, hypertension, PI, FI
Obesity: Decreases insulin sensitivity.
Increased FFAs/TGs → insulin resistance and β-cell damage.
Hyperinsulinism:
Excess insulin → hypoglycemia (low blood glucose).
Symptoms: Anxiety, confusion, unconsciousness.
Treatment: Sugar ingestion.
Liver Functions:
~500 metabolic roles
Process nutrients, regulate cholesterol
Store vitamins, minerals
Metabolize alcohol, drugs, hormones, bilirubin
Carbohydrate Metabolism:
Glucose homeostasis: Converts galactose/fructose to glucose.
Glycogenesis: Stores glucose as glycogen; releases glucose via glycogenolysis when blood glucose is low.
Gluconeogenesis: Converts amino acids and glycerol to glucose when glycogen is exhausted.
Converts glucose to fats
All by liver
Fat Metabolism:
Beta oxidation: Breakdown of fatty acids to acetyl-CoA.
Ketone production: Converts acetyl-CoA to ketone bodies for energy.
Cholesterol synthesis: Liver Converts acetyl-CoA to cholesterol and bile salts.
Lipoproteins: Synthesizes lipoproteins for transporting fatty acids, fats and cholesterol in blood.
Most cells are capable of some fat metabolism, but the liver is primary.
Protein Metabolism:
Urea synthesis: Removes ammonium from the body.
Plasma proteins: Synthesizes clotting proteins, albumin, etc.
Amino acid metabolism: Deaminates amino acids for glucose/ATP production.
Transamination of nonessential amino acids
Vitamin/Mineral Storage:
Stores vitamins A, D, B12, and iron as ferritin (except for Fe bound to hemoglobin).
Biotransformation:
Detoxification: Metabolizes alcohol, drugs, and toxins for excretion.
Bilirubin: Processes bilirubin from RBC breakdown and excretes in bile.
Cholesterol Metabolism:
Cholesterol Sources:
Liver (synthesis) - de novo
Diet (animal-based foods) -exogenous
Not an energy source
Used for bile salts, hormones, and vitamin D
15% ingested, rest made by liver
Lost in bile salts/feces
Cholesterol synthesis: 85% made by the liver, used for bile salts, steroid hormones, and cell membranes.
Cholesterol transport: Through lipoproteins (HDL, LDL, VLDL, chylomicrons).
Types of transport
Lipoproteins:
HDLs: Transport excess cholesterol to the liver.
LDLs: Transport cholesterol to tissues.
VLDLs: Transport triglycerides to tissues.
Chylomicrons: Transport dietary fats.
Lipoproteins:
Transport cholesterol/TGs
Regulate lipid entry/exit
Contain lipids and protein
More lipids = lower density
Regulation of Blood Cholesterol:
LDL: High levels = atherosclerosis risk.
HDL: High levels are protective.
Dietary impact:
Saturated fats increase LDL production, inhibit excretion.
Unsaturated fats help excrete cholesterol in bile.
Trans fats increase LDL and decrease HDL.
Omega-3 fatty acids lower blood pressure and improve cholesterol.
Factors Influencing Cholesterol:
Body shape: “Apple” shape (abdominal fat) → higher LDL, “Pear” shape (hip/thigh fat) → lower LDL.
Exercise & hormones: Regular exercise and estrogens increase HDL, lower LDL.
Neural Signals: Vagal nerve and GI tract communication play a role in appetite regulation.
Thyroid Gland Overview:
Location: Butterfly-shaped gland in the anterior neck, on the trachea below the larynx.
Structure:
Isthmus: Connects the two lobes.
Follicles: Produce thyroglobulin.
Colloid: Fluid with thyroglobulin and iodine (precursor to thyroid hormones).
Parafollicular cells: Produce calcitonin (Lowers blood calcium by inhibiting bone resorption).
PTH: Increases blood calcium by stimulating bone breakdown and enhancing kidney/intestinal absorption.
Cortex produces aldosterone (Na⁺/K⁺ balance), cortisol (stress), and sex hormones; medulla releases epinephrine/norepinephrine (stress response).
Aldosterone: Regulates Na⁺ and K⁺ balance.
ANP: Lowers blood pressure.
Cortisol: Increases glucose and supports stress response.
Imbalances:
Aldosteronism: High blood pressure, low potassium.
Cushing’s: Muscle loss, high blood sugar.
Addison’s: Fatigue, low blood pressure.
Textbook
Thyroid Hormones:
T4 (Thyroxine): Major form, contains 4 iodine atoms, converted to T3 in tissues.
T3 (Triiodothyronine): Active form, contains 3 iodine atoms.
Both are lipid-soluble amine hormones.
Both - Enter cells, bind to nuclear receptors, and trigger metabolic gene transcription.
Functions of Thyroid Hormone:
Increases basal metabolic rate (BMR) and heat production (calorigenic effect).
Regulates tissue growth and development (important for skeletal, nervous, and reproductive systems).
Maintains blood pressure (increases adrenergic receptors).
Effects of Imbalance:
Hyposecretion: Low BMR, weight gain, cold intolerance, mental dullness, low heart rate.
Hypersecretion: High BMR, weight loss, heat intolerance, irritability, high heart rate.
Thyroid Hormone Synthesis:
Thyroglobulin is made and stored in follicles.
Iodine is absorbed and oxidized.
Iodine attaches to tyrosine (MIT, DIT).
T3 (MIT + DIT) and T4 (DIT + DIT) are formed.
Iodide from GI → blood → trapped in thyroid follicles
Hormones released into blood, T4 converts to T3 in tissues.
Thyroid Hormone (TH):
T4 & T3 are transported by TBGs; T3 is more active than T4.
Negative Feedback: Low TH stimulates TSH; high TH inhibits it.
Hypersecretion of TH (Graves’ Disease):
Cause: Autoimmune, antibodies mimic TSH
Symptoms: High metabolism, sweating, rapid heartbeats, weight loss
Exophthalmos: Protruding eyes
Treatment: Surgery or radioactive iodine
TH Hyposecretion:
Myxedema (Adults):
Symptoms: Low metabolism, dry skin, puffy eyes, cold intolerance, constipation, sluggishness
Cretinism (Congenital):
Symptoms: Intellectual disability, short stature, thick tongue/neck
Energy Balance:
Energy intake must equal energy output for stable body weight. Homeostasis.
Obesity (BMI > 30) increases risks like diabetes, heart disease, and osteoarthritis.
Food Intake Regulation:
Short-term: Gut signals, blood nutrients, and hormones (e.g., ghrelin increases hunger, leptin decreases hunger).
Long-term: Leptin adjusts hunger based on fat stores. Leptin resistance occurs in obesity.
-Leptin Protects against weight loss during nutritional deprivation
Regulation of Food Intake:
Main factors:
Neural signals, hormones, blood nutrients
Secondary: Body temperature, psychological factors
Hypothalamus areas:
ARC, LHA, VMN
Hunger neurons:
ARC releases NPY and agouti-related peptides, increasing appetite via orexins from LHA
Satiety neurons:
ARC releases POMC and CART, suppressing appetite via CRH from VMN
Metabolic Rate:
BMR: energy body needs to perform its
most essential activities.
Factors Influencing BMR:
Age/Gender: Decreases with age; males have higher BMR
Body Temperature: Increases with temperature
Stress: Increases BMR
Thyroxine: Boosts oxygen consumption, respiration, and BMR
Hyperthyroidism: Increased BMR, weight loss, muscle atrophy.
Hypothyroidism: Slowed metabolism, weight gain, cognitive issues.
TMR: Total energy use including activity and food digestion.
Metabolic rate:
▪ Directly: calorimeter measures heat liberated into water chamber
▪ Indirectly: respirometer measures oxygen consumption (directly
proportional to heat production)
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▪ total heat produced by chemical reactions and mechanical
work of body
Body Temperature Regulation:
Heat is generated during metabolism to maintain body temperature (~37°C).
Core: Organs, regulated
Shell: Skin, fluctuates
Best Indicator: Rectal temp
Mechanisms of Heat Exchange:
Radiation: Heat loss through infrared rays (50% of body heat loss).
Conduction: Heat transfer between objects in direct contact (e.g., skin and hot water).
Convection: Heat transfer to surrounding air (15–20% of heat loss).
Evaporation: Heat loss through evaporation of water (sensible and insensible heat loss).
Heat Balance:
Heat production: Basal metabolism, muscular activity (shivering), thyroid hormones, and epinephrine.
Heat loss: Radiation, conduction, convection, and evaporation.
Hypothalamus and Thermoregulation:
Thermoregulatory Centers:
Heat-loss center: Activated when temperature rises.
Heat-promoting center: Activated when temperature drops.
Heat-Promoting Mechanisms:
Vasoconstriction and shivering to conserve heat.
Non-shivering thermogenesis (mainly in infants).
Heat-Loss Mechanisms:
Vasodilation and sweating to release heat.
Voluntary: Wearing lighter clothing or reducing activity.
Hyperthermia:
Heat Stroke: Body temperature above ~41°C, leading to hypothermic failure and potentially fatal positive feedback.
Hypothermia:
Caused by prolonged cold exposure; symptoms include slowed vital signs, drowsiness, and ultimately coma or death below 21°C.
Weight would likely increase due to loss of satiety signals and constant hunger.
Fever:
Cause: Infection, cancer, allergies, or CNS injuries.
Mechanism: Pyrogens from macrophages raise the hypothalamic set point, triggering heat production and increasing body temperature.
Hypothermia
Low body temp, vital signs slow, leads to coma/death.
Fever
High temp from infection, boosts immunity.
Metabolic Disorders
PKU: Can’t process phenylalanine.
Galactosemia: High galactose, brain issues.
Glycogen Storage: Enzyme missing, organ enlargement.
Metabolic Syndrome
5 risk factors: waist, BP, glucose, triglycerides, HDL decrease. Increases heart disease and diabetes risk. all increase
Age-Related Changes
Slower metabolism, muscle loss, weight gain.
Clinical Terms
Appetite: Desire for food.
Familial Hypercholesterolemia: High cholesterol, early heart disease.
Pica: Eating nonfood items.
Protein Malnutrition: Marasmus (calorie), Kwashiorkor (protein).
Skin-Fold Test: Measures body fat.
Adrenal Gland Hormones:
Aldosterone: Regulates blood pressure.
Cortisol: Increases glucose and fat breakdown.
Androgens: Affect libido and hair growth.
Epinephrine/Norepinephrine: Increase heart rate.
Imbalances:
Aldosteronism: High blood pressure.
Addison’s: Low cortisol.
Cushing’s: High cortisol.
Pheochromocytoma: Excess catecholamines.
Pineal Gland:
Melatonin: Regulates sleep and rhythms.
Obestit: Weight loss drugs (e.g., semaglutide) and bariatric surgery (e.g., gastric bypass) help reset the body’s weight set point.
