Chapter 24 Flashcards
Carbohydrate uses in the body
Glucose - fuel used by cells to make ATP
Neurons and RBCs - entirely on glucose
Excess converted to glycogen or fat
Fructose and galactose converted to glucose by liver before circulation
Lipids
Triglycerides (neutral fats)
Saturated fats in meat, dairy foods, and tropical oils; trans fats
Unsaturated fats in seeds, nuts, olive oil, and most vegetable oils
Cholesterol in egg yolk, meats, organ meats, shellfish, milk
Liver makes ~85% cholesterol
Uses of Lipids in the Body
Help absorb fat-soluble vitamins
Fuel of hepatocytes, skeletal muscle
Myelin sheaths, membranes
Protection, insulation, fuel storage
Prostaglandins – smooth muscle contraction, BP control, inflammation
Cholesterol stabilizes membranes; precursor of bile salts, steroid hormones
What’s a complete Protein
Contain All 20 amino acids (eggs, milk, meats, soybeans)
Uses of protein in the body
Structural materials Keratin (skin); collagen and elastin (connective tissue); muscle proteins Functional molecules Enzymes, some hormones Amino acids can be burned for energy
All-or-none rule
All amino acids needed must be present for protein synthesis
Nitrogen balance
Rate of protein synthesis equals rate of breakdown
Positive nitrogen balance - synthesis exceeds breakdown (normal in children, pregnant women, tissue repair)
Negative nitrogen balance - breakdown exceeds synthesis (stress, burns, infection, injury, poor diet, starvation)
Hormonal controls
Anabolic hormones (GH, sex hormones) accelerate protein synthesis and growth Adrenal glucocorticoids (released during stress) protein breakdown; conversion of amino acids to glucose
Anabolism
synthesis of large molecules from small ones
Ex. Amino acids proteins
Catabolism
hydrolysis of complex structures to simpler ones
Ex. Proteins amino acids
Cellular respiration
Catabolism of food fuels capture of energy (ATP)
Enzymes shift high-energy phosphate groups of ATP to other molecules (phosphorylation) which are activated to perform cellular functions
Oxidation
Loss of Hydrogen
Reduction
Gain of Hydrogen
Equation for oxidation of glucose
C6 H12 06 + 6O2 = 6Co2 + 6H2O + ATP
Coenzymes
act as electron acceptors
NAD+ (H) [has electrons] & FAD
Substrate-level phosphorylation
High energy phosphate group directly transferred to ADP, twice in glycolysis, once in Krebs Cycle.
Oxidative Phosphorylation
Makes most of the ATP with Chemiosmotic pressure, with a buildup of proton concentration to build a gradient.
Glucose enters cell by
Facilitated Diffusion and is phosphorylated to Glucose-6-phosphate
How is glucose trapped in cell?
Most cells can’t reverse the action of glucose entering the cells, also the concentration gradient of glucose is always higher outside of cell so doesn’t want to leave.
What cells can reverse the entering of glucose?
Intestine, kidney, liver cell
Step 1: Glycolysis
Occurs in cytosol (anaerobic)
Starts with Glucose
Ends with 2 pyruvic acid, 2 NADH+H, net 2 ATP.
Sugar Activation
Phosphorylation activates glucose converted to fructose-1 & 6-bisphosphate
Sugar Cleavage
6-bisphosphate from Sugar activation is cleaved into 2 pieces
Sugar Oxidation
Removal of Hydrogen
Step after Glycolysis
Anaerobic - NADH gives H+ back to pyruvic acid reducing it to lactic acid
Aerobic - Krebs Cycle in Mitochondria
Transitional Phase
Convert each pyruvic acid to acetyl CoA in 3 steps.
- A carboxyl group is removed from pyruvate releasing Co2.
- NAD+ is reduced to NADH - oxidation reaction
- An acetyl group is transferred to coenzyme and resulting to Acetyl CoA
Krebs Cycle (citric acid cycle)
Occurs in mitochondria
Results in 8NADH +H+, 2 FADH2, 6Co2, 2 ATP
Electron Transport Chain
Occurs in folds of mitochondria
Complexes alternately reduce and oxidize as pick up and pass electrons to oxygen and form H2O.
Hydrogen ion pumped to intermembrane space by respiratory enzymes complexes I, III & IV creates electrochemical proton gradient (change in pH) This is called oxidative phosphorylation
Chemiosmosis
uses the proton gradient created by respiratory enzyme complexes I, III, IV, to synthesize ATP by having protons diffuse back through the matrix via a ATP synthase that creates and electrical current which creates the ATP
Glycogenesis
Glycogen formation via glycogen synthase when glucose supplies exceed need for ATP synthesis
Mostly in liver and skeletal muscle
Glycogenolysis
Glycogen breakdown via glycogen phosphorylase in response to low blood glucose
Only by hepatocytes, some kidney and intestinal cells
Carbo loading
Carbohydrate-rich diet for 3-4 days; decreased activity - muscles store more glycogen - improved endurance
Gluconeogenesis
Glucose formed in liver from glycerol and amino acids when blood glucose levels drop
Protects nervous system and against damaging effects of hypoglycemia
Why is glucose easily converted to Fat?
Because once it is converted to Acetyl CoA, it can then build up and if too many than can go to fat stores instead of back to glucose.
Lipid Metabolism
Greater energy yield than from glucose or protein catabolism
Most products of fat digestion transported in lymph as chylomicrons
Hydrolyzed by endothelial enzymes into fatty acids and glycerol
Lipogenesis
Glucose easily converted to fat because acetyl CoA is
Intermediate in glucose catabolism
Starting point for fatty acid synthesis
Lipolysis
Stored fat glycerol, fatty acids for fuel
Oxaloacetic acid necessary for complete oxidation of fat but converted to glucose if carbohydrates deficient
Acetyl CoA is then converted by in liver to ketone bodies
Ketosis
Accumulation of ketones in blood Ketones acidic - metabolic acidosis Breath smells fruity Rapid breath to release CO2, raise pH Common in starvation, dieting, diabetes Ketone bodies excreted in urine
Protein Metabolism
• Proteins deteriorate, so continually broken down and replaced
•Amino acids recycled
– new proteins
• Protein not stored in body
–When dietary protein in excess, amino
acids are oxidized for energy or
Converted to fat for storage
3 steps of Oxidation of Amino Acids
Transamination - an amine group is switched from amino acid to Keto Acid.
Oxidative Deamination - Amine group of glutamic Acid is removed as ammonia and combined w/ Co2 to form Urea - urine
Keto Acid Modification - The keto acid formed during transamination are altered so they can easily enter the krebs cycle pathways.
Absorptive State
Just Fed, anabolism exceeds catabolism
Carbohydrates during Absorptive State
Glucose major fuel, glucose converted to glycogen or fat. synthesized fat & protein released to blood for storage by adipose as VLDL’s.
Triglycerides during Absorptive State
Lipoprotein lipase catalyze lipids of chylomicrons in muscle and fat tissue. Most glycerol and fatty acids converted to triglycerides for storage. Triglycerides used by adipose tissue, liver, skeletal, cardiac muscle as energy.
Amino Acids during Absorptive State
To many - deaminate and used as ATP synthesis or stored fat. Aminos used in protein synthesis.
What is happening Postabsorptive State
Under fed, catabolism of fat glycogen, and proteins exceeds anabolism. GOAL: maintain blood glucose, promotes use of fats for energy, save glucose for organs that need it most.
Adipose tissue
It is innervated by sympathetic nervous system and supplies glucose if blood levels low.
What do lipoproteins do?
Transport water - insoluble cholesterol and triglycerides in blood. Regulate lipid entry/exit at target cells.
Roles of HDLs (GOOD)
Transport excessive cholesterol protein from peripheral tissues to liver to be broken down and secreted into bile and provide cholesterol to steroid-producing organs.
Roles of LDLs
Transport cholesterol to tissues for membrane storage or hormone synthesis
Roles of VLDLs
Transport triglycerides from liver to peripheral tissues (mostly adipose)
Saturated Fatty Acids
Stimulate liver synthesis of cholesterol, inhibit cholesterol excretion from body. No double bonded carbons, solid at room temperature.
Unsaturated Fatty Acids
Enhanced excretion of cholesterol enhancing cholesterol excretion to bile.
What do Omega-3-Fatty Acids do?
Lower saturated fats and cholesterol, make platelets less sticky, help prevent spontaneous clotting, antiarrhythmic effects on heart, lower blood pressure.
Long term regulators of food intake
Insulin & Leptin
Leptin
Hormone secreted by fat cells in response to increased body fat mass. Indicator of energy stores. Rising the level of leptin has led to weight loss (idea)
Basal Metabolic Rate
The energy need to perform essential activities.
Recorded as kilocalories per square meter of body surface per hour (kcal/m2/h)
BMR increases as ratio of body surface area to volume increases
Decreases with age
Males have higher BMR
Increases with temperature or stress
Thyroxine increases oxygen consumption, cellular respiration, and BMR
Physical training has little effect on BMR
Short Term regulators of food intake
• Neural signals from GI tract
High protein content of meal increases
and prolongs afferent vagal signals
Distension sends signals along vagus
nerve that suppress hunger center
- Rising blood glucose
- Elevated blood amino acid levels
- Blood levels of fatty acids
Total metabolic rate (TMR)
Rate of kilocalorie consumption to fuel all ongoing activities
Increases with skeletal muscle activity and food ingestion (food-induced thermogenesis)
Normal body temperature
37C (98.6F) Optimal enzyme activity Increased temperature denatures proteins and depresses neurons Children <5 convulsions 41C(106F) ~43C (109F) - limit for life
Mechanism of Heat Transfer
Evaporation - heat loss from water to body
Radiation - loss of heat by infrared rays
Conduction - transfer by direct contact
Convection - transfer of heat to air (wind blowing)
Insensible Heat Loss
Accompanies insensible water loss from lungs, oral mucosa, and skin
Sensible Heat Loss
When body temp rises and sweating increases, water evaporates
Related to Body temp, the Hypothalamus receives afferent input from what?
Peripheral thermoreceptors in shell (skin) Central thermoreceptors (some in HT) initiates appropriate heat-loss and heat-promoting activities.
Heat-promoting mechanisms
Increase metabolic rate via Epinephrine and Norepinephrine.
Chemical thermogenesis
Enhanced thyroxine release
Brown adipose tissue.
Hyperthermia
Elevated body temp, tell HT to begin heat stroke
Heat Exhaustion
Heat related collapse after hard exercise dehydration and low BP. Heat-loss mechanisms still functional, may turn to heat stroke.
Hypothermia
Low body temp, shivering stops
can progress to coma and death at 21˚ c
Controlled Hyperthermia
Fever
What causes the symptoms of fever
Injured cells start releasing chemicals
How does fever affect they hypothalamus
Resets the internal thermostat higher, temperature rises.
PKU
Phenylketonuria - cells cannot use the amino acid phenylalanine. Neurotoxins in blood, brain damage, retardation.
