a&p 600 final review > Metabolism 2 > Flashcards

Metabolism 2 Flashcards

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1
Q

Lipoproteins

Transport by lipoproteins

A
  • Most lipids are nonpolar and hydrophobic
  • Made more water-soluble by combining them with proteins to form lipoproteins
  • Lipoproteins are spherical with an outer shell of proteins, phospholipids, and cholesterol surrounding fats
  • Proteins in outer shell called apoproteins
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2
Q

Lipoproteins

Lipoproteins categorized and named according to

A
  • Density (ratio of lipids to proteins)
  • High density = more proteins
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3
Q

Lipoproteins

Examples of lipoproteins are:

A
  • Chylomicrons
  • Very low-density lipoproteins (VLDLs)
  • Low-density lipoproteins (LDLs)
  • High-density lipoproteins (HDLs)
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4
Q

Lipoproteins

Chylomicrons

A
  • Forms in small intestine mucosal epithelial cells
  • They enter villi and eventually lacteal and are carried by lymph into venous blood
  • Transport dietary lipids to:
  • skeletal muscle for usage
  • cardiac muscle for usage
  • adipose tissue for storage
  • liver
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5
Q

Lipoproteins

Very low-density lipoproteins (VLDLs)

A
  • Formed in hepatocytes
  • Transports triglycerides to adipocytes
  • Become LDLs once triglycerides are removed
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6
Q

Lipoproteins

Low-density lipoproteins (LDLs)

A
  • “bad cholesterol”
  • Carry 75% of total cholesterol in blood
  • Deliver to body cells for repair of cell membranes and synthesis of steroid hormones
  • When in excess, the LDL will deposit cholesterol in and around smooth muscle in arteries forming fatty plaques that increase risk of coronary artery disease
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7
Q

Lipoproteins

High-density lipoproteins (HDLs)

A
  • “good cholesterol”
  • acts to remove excess cholesterol from body cells and blood
  • deliver to liver for elimination, removed in bile salts
  • HDL prevents accumulation of cholesterol in the blood so a high HDL level is associated with a decreased risk of coronary artery disease
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8
Q

Cholesterol

2 sources of cholesterol in the body

A
  • Present in foods
  • does not have a large impact on total blood cholesterol
  • Endogenous cholesterol
  • made in liver
  • trans fats and saturated fats have the biggest impact on circulating cholesterol
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9
Q

Health Applications

Indicators of potential cardiovascular problems

A
  • Total cholesterol above 200 milligrams/deciLiter
  • High LDL:HDL ratio
  • High levels of cholesterol in circulation
  • Most of the cholesterol is going into the tissues and staying instead of returning to the liver
  • Excess cholesterol can accumulate as plaques in blood vessels, causing hypertension, heart attacks and strokes
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10
Q

Lipid Catabolism:

Lipolysis

A
  • Lipolysis is the breakdown of lipids
  • Lipid catabolism in which lipids are broken down into pieces that:
  • Can be converted to pyruvate – WHAT HAPPENS TO PYRUVATE?
  • Can be channeled directly into the citric acid cycle
  • Either route can generate ATP
  • If the demand for energy is low, triglycerides are stored in adipocytes
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11
Q

Lipid Catabolism: Lipolysis

Triglycerides consist of

What hormone inhibits lipolysis

A
  • Triglycerides consist of glycerol and 3 fatty acids
  • Glycerol and fatty acids can each generate ATP
  • Breakdown must occur for muscle, liver, and adipose tissue to oxidize fatty acids for ATP
  • Enhanced by epinephrine and norepinephrine, cortisol, thyroid hormones
  • Insulin acts to inhibit lipolysis
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12
Q

Lipid Catabolism: Lipolysis

  • Glycerol is converted to
A
  • glyceraldehyde 3-phosphate (glycolysis intermediate) and eventually pyruvate (yields 2 ATP)
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13
Q

Lipid Catabolism: Lipolysis

  • Fatty acids are catabolized to
A
  • acetyl-C o A through beta-oxidation in the mitochondrial matrix
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14
Q

Lipid Catabolism: Lipolysis

  • Both pyruvate (from glycerol) and acetyl-CoA (from fatty acids) can enter
A
  • Citric Acid Cycle
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15
Q

Lipid Catabolism: Lipolysis

For each step in beta-oxidation, the cell
gains

A
  • 13 ATP
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16
Q

Lipid Catabolism: Lipolysis

Excessive beta oxidation, with a lack of glucose, results in the formation

A
  • of ketones in the liver
  • Heart, brain, and RBCs can use ketone bodies to generate ATP
  • Brain and RBCs heavily rely since they cannot use beta oxidation
  • Excessive ketones can lead to ketosis and/or ketoacidosis, of which the latter damages tissue
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17
Q

Lipid Catabolism: Lipolysis

  • Lipid catabolism is useful because:
A
  • Beta-oxidation is very efficient
  • Excess lipids can be easily stored as triglycerides
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18
Q

Lipid Catabolism: Lipolysis

  • Lipid catabolism is useful because:
  • However:
A
  • Cannot provide large amounts of ATP quickly
  • Difficult for water-soluble enzymes to access the insoluble droplets
  • Well suited for chronic energy demands during stress or starvation
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19
Q

Lipid Anabolism:

Lipogenesis

A
  • Liver cells and adipose cells synthesize lipids
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20
Q

Lipid Anabolism: Lipogenesis

  • Begins with
A
  • acetyl-CoA
  • Almost any organic substrate (lipids, amino acids, carbohydrates) can be converted to acetyl-CoA
  • Occurs when more calories are consumed than needed for ATP production
  • Excess dietary carbs, proteins, and fats are ALL converted to triglycerides
  • Essential fatty acids
  • Cannot be synthesized; must be obtained from diet
  • Examples: linolenic acid (omega-3 fatty acid) and linoleic acid (omega-6 fatty acid)
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21
Q

Review

What is a chylomicron?

A
  • Transports dietary lipids to adipose tissue for storage
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22
Q

Review

What is a very low density lipoprotein (VLDL)?

A
  • Forms in hepatocytes and contains endogenous lipids
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23
Q

Review

What is a low-density lipoprotein (LDL)?

A
  • Carries 75% of total cholesterol in blood. When in excess, LDL will deposit cholesterol in and around arteries forming fatty plaques
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24
Q

Review

What is a high density lipoprotein (HDL)?

A
  • Acts to remove excess cholesterol from body cells and blood and transports it to the liver for elimination
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25
# Review What is the term referring to the breakdown (catabolism) of lipids?
* Lipolysis
26
# Review What is the term referring to the formation of lipids?
* Lipogenesis
27
# Protein Metabolism Amino acids are either
* oxidized to produce ATP or used to synthesize new proteins * Excess dietary amino acids are not excreted but converted into glucose (gluconeogenesis) or triglycerides (lipogenesis)
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# Protein Catabolism * Protein from worn out cells are
recycled, can be converted to other amino acids and reformed to make new proteins or enter CAC
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# Protein Catabolism * Before entering CAC, amine group must be removed (deamination) | **Where does deamination occur and what does it produce**
* Occurs in hepatocytes * Produces ammonia, liver converts to urea, excreted in urine
30
# Protein Anabolism Protein synthesis is carried out using
* ribosomes (translation) using free amino acids
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# Protein Anabolism * Amino acids are either:
* Essential * Cannot be synthesized in the body, need to be acquired (diet) * Nonessential
32
# Protein Anabolism * Essential amino acids | How many essential amino acids/where do humans get them
* **9** essential amino acids in the human * Must be present in the diet because they cannot be synthesized * Complete proteins contain sufficient amounts of all essential amino acids * beef, fish, poultry, eggs * Incomplete protein does not * leafy green vegetables, legumes, grains
33
# Protein Anabolism * Nonessential amino acids | How are they synthesized
* **11** other nonessential amino acids can be synthesized by body cells using amination and transamination * Transamination is transfer of amine group from one amino acid to a ketoacid to form a new amino acid
34
# Review What happens to excess dietary amino acids?
* They are not excreted but are converted into glucose or triglycerides
35
# Metabolic Adaptations * There are two general patterns of metabolic activity
1.. Absorptive state * ingested nutrients are entering the blood stream 2.. Postabsorptive state * absorption of nutrients from GI tract complete
36
# Metabolic Adaptations * During the absorptive state
* ingested nutrients are entering the blood stream * Glucose readily available for ATP production * Effects of insulin dominate
37
# Metabolic Adaptations * During postabsorptive state
* absorption of nutrients from GI tract complete * Energy needs are met by stored fuels in the body * Nervous system and red blood cells depend on glucose so maintaining steady blood glucose is critical
38
# Absorptive State When does Absorptive State occur/What is the primary regulating hormone
* Time following a meal, when nutrient absorption is occurring * Typically continues for ~ 4 hours * Insulin is primary regulating hormone
39
# Absorptive State * Insulin stimulates:
* (1) glucose uptake and glycogenesis * (2) amino acid uptake and protein synthesis * (3) triglyceride synthesis
40
# Postabsorptive State When does it occur/what happens/hormones used
* About 4 hours after the last meal, absorption in small intestine nearly complete * Blood glucose levels start to fall * Metabolic activity focused on mobilizing energy reserves and maintaining blood glucose (80-120 mg/dL) * Coordinated by several hormones * Glucagon, epinephrine, glucocorticoids, growth hormone
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# Postabsorptive State * Glucocorticoids
* stimulate the mobilization of lipid and protein reserves * these effects are enhanced by growth hormone.
42
# Postabsorptive State * Glucagon
* stimulates glycogenolysis and gluconeogenesis, primarily in the liver * The release of glucose by the liver and the shift away from glucose metabolism by other tissues stabilizes blood glucose levels
43
# Postabsorptive State * Epinephrine
* important in stimulating glycogenolysis in skeletal and cardiac muscle, and lipolysis in adipocytes.
44
# Postabsorptive State * Production of glucose is increased by:
* Breakdown of liver glycogen * Lipolysis * gluconeogenesis using lactic acid, glycerol and/or amino acids
45
# Postabsorptive State * Blood glucose is conserved by:
* Oxidation of fatty acids, lactic acid, amino acids, ketone bodies and breakdown of muscle glycogen
46
# Postabsorptive State * Blood lipid levels decrease | Response is?
* Response is release of fatty acids by adipocytes
47
# Postabsorptive State * Blood amino acid levels decrease | Reponse is?
* Response is amino acid release by skeletal muscles and other tissues
48
# Postabsorptive State * Blood glucose levels decrease | Reponse is?
* Response is glucose release by liver
49
# Postabsorptive State * Catabolism of lipids and amino acids in liver produce acetyl-CoA | Leads to formation of?
* Leads to formation of ketone bodies * Diffuse into blood and are used by other cells as energy source
50
# Fasting and Starvation * Fasting: * Starvation:
* Fasting: going without food for many hours or a few days * Starvation: implies weeks or months of food deprivation or inadequate food intake * During these times, nervous tissue and RBC’s continue to use glucose for ATP production * The most dramatic metabolic change that occurs is the increase in formation of ketone bodies by hepatocytes from excess fatty acid metabolism * Can be used as an alternative fuel source
51
# Energetics * Metabolic rate
* overall rate at which metabolic reactions use energy * Some energy used to make ATP, some is lost as heat
52
# Energetics * Basal metabolic rate (BMR)
* Common benchmark for energetics studies * Defined as the minimum resting energy expenditure of awake, alert person
53
# Energetics * Basal metabolic rate (BMR) | measured when? average person has? factors that affect?
* measured when body is in quiet, resting, fasting condition * Average person has BMR of 70 Calories per hour (1680 Calories per day) * Various factors can affect BMR * Size, weight, level of physical activity * Food intake must be adequate to support activities
54
# Thermoregulation: Heat Balance * The body’s metabolic activities generate heat (a form of energy)
* 40% of energy is used to form ATP * 60% percent is released as heat
55
# Thermoregulation: Heat Balance * Can be measured as temperature and can expressed as a calorie
* calorie (cal): amount of energy required to raise 1 gram of water 1°C * Kilocalorie (kcal) or Calorie (Cal) is 1000 calories
56
Thermoregulation: Heat Balance | Normal range for internal body temp
* Despite wide fluctuations in environmental temperatures, homeostatic mechanisms maintain normal range for internal body temperature * Core temperature (37°C or 98.6°F) versus shell temperature (1-6°C lower) * Important to maintain to keep proper function and structure
57
# Thermoregulation: Heat Balance * Mechanisms of heat transfer:
1. Radiation 2. Convection 3. Evaporation 4. Conduction
58
# Thermoregulation: Heat Balance Radiation
* Heat energy transfer as infrared radiation * Example: the heat from the sun * More than 50% of body heat loss indoors is via radiation
59
# Thermoregulation: Heat Balance Convection
* Result of heat loss due to air movement * Warmer air rises away from the body, replaced by cooler air * Accounts for about 15% of body’s heat loss indoors
60
# Thermoregulation: Heat Balance Evaporation
* Water changing from liquid to vapor absorbs 0.58 Calorie per gram of water * Cools the surface of the skin
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# Evaporation Insensible perspiration
* (from alveoli and skin) * About 20–25 milliLiters per hour (relatively constant) * Accounts for about 20% of body’s heat loss indoors
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# Evaporation Sensible perspiration
* (from sweat glands) * Can excrete up to 2–4 liters per hour
63
# Thermoregulation: Heat Balance Conduction
* Direct transfer of energy through physical contact * Generally not an effective mechanism of gaining/losing heat
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# Thermoregulation: Heat Balance * If core temperature declines
* blood vessels of dermis constrict (reduces heat loss by radiation and convection) * contraction of arrector pili (reduces heat loss by radiation and convection) * release of thyroid hormones, epinephrine and norepinephrine increases cellular metabolism (generates heat) * Shivering (generates heat)
65
# Thermoregulation: Heat Balance * If core body temperature is too high
* dilation of skin blood vessels (heat loss through radiation and convection) * stimulate sweat glands (heat loss through evaporation) * decrease metabolic rate (generates less heat)
66
# Appetite Regulation * Involves two areas of the hypothalamus with opposite effects (stimulating one inhibits the other)
1. Feeding center (involved with hunger) 2. Satiety center (involved with food satisfaction) ## Footnote * These areas are affected by multiple factors, including social factors, psychological pressures, and dietary habits
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# Appetite Regulation * Regulation of appetite can occur on two levels
1. Short-term regulation 2. Long-term regulation
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# * Short-term regulation of appetite * Stimulation of satiety center
* Elevated blood glucose levels * Hormones of digestive tract (such as CCK) * Stretching of digestive tract wall
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# Short-term regulation of appetite Stimulation of feeding center
* Neurotransmitters * Example: neuropeptide Y, or NPY, from hypothalamus * Ghrelin * Hormone secreted by gastric mucosa when stomach is empty
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# Long-term regulation of appetite * Stimulation of the satiety center
* Leptin * Peptide hormone secreted by adipocytes * Stimulates satiety center and suppresses appetite * Effects are gradual
71
# Metabolic Syndrome * a grouping of conditions that occur together that increase your risk of cardiovascular disease, stroke, and type II diabetes | * Defined as:
* Central obesity And * Two of the following: * Hypertension: systolic > 130 or diastolic > 85 mmHg * Increased triglycerides * Reduced HDL cholesterol * Raised fasting blood glucose
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# Metabolic Syndrome * Epidemiology
* estimate of 25% of adult population worldwide
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# Metabolic Syndrome * Risk factors:
* Sedentary lifestyle * Poor diet * High BMI * Genetics * Smoking * Socioeconomic status * Education
74
Familial Hypercholesterolemia (FH)
* A group of genetic mutations leading to high LDL cholesterol independent of diet * Common: 1 in 200 people
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# Familial Hypercholesterolemia (FH) * Increases the risk of cardiovascular as much as 20 times if untreated
* Men with FH get coronary heart disease up to 10 to 20 years earlier * Half of men with untreated FH will have a heart attack or angina before they turn 50 * For some it will be as early as their 20s * In women, coronary heart disease appears up to 20 to 30 years earlier * About 30% of untreated women will have a heart attack before they turn 60
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# Familial Hypercholesterolemia (FH) * Treatment and prognosis
* Excellent prognosis if treated early and managed properly * Treatment: * Statin * Other cholesterol lowering medications`
77
Type II Diabetes
* Chronic condition resulting in insulin resistance * Cells no longer appropriately respond to insulin * Leads to increased blood glucose levels * Eventually insulin production may slow and become insulin dependent
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# Type II Diabetes * Complications
* Cardiovascular disease * Nerve damage in periphery * Other nerve damage * Arrhythmias, digestive upset, ED * Kidney disease * Eye damage * Skin conditions * Slow healing
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# Type II Diabetes * Treatment
* Healthy eating * Regular exercise * Weight loss * Possibly, diabetes medication or insulin therapy * Metformin * Sulfonylureas (glyburide)
80
# Ketoacidosis
* Acidification of blood due to ketone body production * Leads to ketosis
81
# Ketoacidosis * Occurs when
* glucose supplies are limited * Fatty acid and amino acid catabolism in liver leads to acetyl-CoA production and generation of ketones
82
Gout
* Condition involving insoluble uric acid crystals * Purine bases of RNA catabolized into uric acid * Categorized as nitrogenous waste (contains nitrogen) * Normal uric acid levels 2.7–7.4 milli grams/deciLiter * With higher concentrations, body fluids are saturated, and insoluble crystals form
83
# Gout gouty arthritis
Crystals accumulate in joints, especially the great toe, causing gouty arthritis * Painful condition may persist for several days then disappear for days or years

a&p 600 final review (8 decks)

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