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Anatomy & Physiology III > Topic 2, L1 & 2 - Nutrition, Metabolism and Energy Balance II > Flashcards

Topic 2, L1 & 2 - Nutrition, Metabolism and Energy Balance II Flashcards

1
Q

Hypoglycemia

A

Low blood sugar

  • Since the brain needs glucose to function, can go into coma (not enough fuel)
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2
Q

Increase in blood glucose levels above homeostatic range …

A

Sensed by pancreas → Releases insulin to stim absorption of glucose from blood by liver / excess glucose can also be stored as glycogen → Glucose also absorbed by tissue cells for their use to produce energy → Some glucose will be taken up by fat cells, stored as triglycerides
(all occurs in the absorptive state)

[ net effect = fall in glucose ]

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3
Q

Decrease in blood glucose levels below homeostatic range …

A

Sensed by pancreas → Releases glucagon to tell body to tap into glucose reserves (glycogen) that were stored during the absorptive state to break them down & release that glucose back into the blood stream

[ net effect = rise in glucose ]

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4
Q

Overview of the Pancreas

A

Triangular gland located partially behind stomach with both exocrine & endocrine cells

  1. Acinar cells (exocrine) produce enzyme-rich juice for digestion
  2. Pancreatic islet cells (islets of Langerhans) contain endocrine cells
    - Alpha (α) cells produce glucagon (hyperglycemic hormone – raises blood glucose levels)
    - Beta (β) cells produce insulin (hypoglycemic hormone – lowers blood glucose levels)
    - Delta (D) cells secrete somatostatin(suppresses release of both glucagon & insulin, slows rate of food absorption / energy secretion along GI tract)
    - F cells produce pancreatic polypeptide [ PP ] (inhibits gallbladder contraction, regulates production of pancreatic enzymes)
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5
Q

How & when is insulin secreted ?

A

Insulin is synthesized as proinsulin, which is then modified. It will be secreted in the case when :

  • Blood glucose levels increase / exceed normal range
  • Blood levels of amino acids and fatty acids increase
  • ACh is released by parasympathetic nerve fibers
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6
Q

What are the effects of insulin on metabolism?

A
  • Accelerates glucose uptake / absorption (all target cells)
  • Stimulates glycogen formation (skeletal muscle fibers, liver cells)
  • Stimulating amino acid absorption & protein synthesis (all target cells)
  • Stimulates ffa absorption & triglyceride formation (adipocytes)

So, its net effects are :
↓ Blood glucose / ↑ Glycogen storage
↓ Blood amino acids & FFA (fatty acids)

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7
Q

3 ways Insulin lowers blood glucose levels

A
  1. Enhances membrane transport of glucose into fat + muscle cells
  2. Inhibits breakdown of glycogen to glucose
  3. Inhibits conversion of amino acids or fats to glucose
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8
Q

How & when is glucagon secreted ?

A

Glucagon is a potent hyperglycemic agent, and its secretion is triggered by :
- Decreased blood glucose levels
- Rising amino acid levels
- Sympathetic NS

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9
Q

What are the effects of glucagon on metabolism?

A
  • Stimulates breakdown of glycogen (skeletal Muscle Fibers & liver Cells)
  • Stimulating breakdown of triglycerides (adipocytes / fat cells)
  • Stimulates production & release of glucose (liver cells)

So, net effects are :
↑ Blood glucose / ↓ glycogen storage
↑ Blood amino acids & FFA

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10
Q

3 ways Glucagon raises blood glucose levels

A

Targets liver to :
1. Break down glycogen into glucose
2. Synthesize glucose from lactic acid and other noncarbohydrates
3. Release glucose into blood

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11
Q

Whether glucose is absorbed by the digestive tract or manufactured and released by the liver, ____________________________________________________

A

very little glucose leaves the body once it has entered the bloodstream

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12
Q

Diabetes Mellitus (DM)

A

Group of metabolic diseases characterized by high levels of blood glucose resulting from defects in insulin production, insulin action, or both

  • Complex disorders of CHO, fat and protein metabolism
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13
Q

DM & Kidneys

A

The kidneys reabsorb virtually all glucose, so glucose does not appear in the urine. However, in diabetes mellitus, glucose accumulates in the blood and urine as a result of faulty glucose metabolism

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14
Q

Type 1 DM

A

Autoimmune destruction of pancreatic β-cell (insulin producing cells) which causes absolute insulin deficiency since beta cells are the sole insulin producing source in the body

Results from hyposecretion OR hypoactivity of insulin (insulin is ABSENT)

  • Requires daily insulin injections / can be multiple times a day

if there is NO INSULIN = Cannot pull glucose from bloodstream into ECF into cell bc there is no insulin signal

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15
Q

Type 2 DM

A

More common

  • Produces normal amounts of insulin initially but their tissues don’t repond efficiently – insulin resistance_

Insulin is PRESENT, but its effects are deficient

  • Causes an interference with insulin binding to target tissue [ we can have receptor + hormone + everything we need, but it binds but does nothing else (put key into lock, but not unlock, glucose cannot move into system) ]

Treatment : Non-insulin type therapies, oral hypoglycemics

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16
Q

In either case of DM, blood glucose levels remain _____ after a meal because glucose is _____________________________________.

A

high, unable to enter most tissue cells

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17
Q

What is the function of glucose transport proteins ?

A

Facilitate movement of glucose into cells

Insulin binds to its receptor → Initiates signal transduction cascade → Tells vesicles to move from within cytoplasm of cell via exocytosis & insert transporters into plasma membrane to allow glucose to move into the cell via

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18
Q

What happens in the absence of insulin ?

A

If we have no insulin, we may still have all components needed for transport pathway → BUT nothing that tells glucose transporters to insert into cell membrane

Transport proteins are not embedded in plasma membrane of target cell (actually in secretory vesicles within cell tself) → USELESS (we need to get them to move from out of the cell into plasma membrane)

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19
Q

What are the consequences of insulin deficiency ?

A

Effects on liver, skeletal muscle, adipose tissue

[ see table ]

  • Polyuria. Excessive glucose in the blood leads to excessive glucose in the kidney filtrate where it acts as an osmotic diuretic (that is, it inhibits water reabsorption by the kidney tubules). The end result is polyuria, a huge urine output that
    decreases blood volume and causes dehydration.
  • Polydipsia. Dehydration stimulates hypothalamic thirst centers, causing polydipsia, or excessive thirst.
    *
    Polyphagia. Polyphagia refers to excessive hunger and food consumption, a sign that the person is “starving in the land of plenty.” Although plenty of glucose is available, the body cannot use it. Instead, the body breaks down protein and fat to supply energy, and this is thought to stimulate appetite.
    When sugars cannot be used as cellular fuel, more fats are mobilized, resulting in high fatty acid levels in the blood, a condition called lipidemia. In severe cases of diabetes mellitus, blood levels of fatty acids and their metabolites (acetoacetic acid, acetone, and others) rise dramatically. The fatty acid metabolites, collectively called ketones (ke’tonz) or ketone bodies, are organic acids. When they accumulate in the blood, the blood pH drops, resulting in ketoacidosis, and ketone bod-
    ies begin to spill into the urine (ketonuria).
    Severe ketoacidosis is life threatening. The nervous system
    responds by initiating rapid deep breathing (hyperpnea) to blow offcarbon dioxide frorn the blood and increase blood pH. (We will explain the physiological basis of this mechanism in Chapter 22.) Serious electrolyte losses also occur as the body rids itself of excess ketone bodies. Ketone bodies are negatively charged and carry positive ions out with them, so sodium an
    abdominal pain and possibly vomiting. If untreated, ketoaci- dosis disrupts heart activity and oxygen transport, and severe depression of the nervous system leads to coma and death.
    The opposite condition to diabetes mellitus is hyperinsulin- isn,, or excessive insulin secretion. It causes low blood glucose
    levels, or hypoglycemia.This condition triggers the release of hyperglycemic hormones, which cause anxiety, nervous- ness, tremors, and weakness. Insufficient glucose delivery to the brain causes disorientation, progressing to convulsions, unconsciousness, and even death. In rare cases, hyperinsu- linism results from an islet cell tumor. More commonly, it is caused by an overdose of insulin and is easily treated by ingesting sugar.
20
Q

Gluconeogenesis

A

Production / synthesis of glucose from non-carbohydrate sources (non-sugar substrates)

21
Q

Glycogenolysis

A
22
Q

What are the metabolic consequences of Type 1 DM ?

A

When sugars cannot be used as fuel, as in DM, fats are used, causing lipidemia (high levels of fatty acids in blood)

Fatty acid metabolism (lipolysis) results in formation of ketones (ketone bodies)
- Ketones are byproducts of betaoxidation (there is so much acetyl-CoA floating around → overwhelms citric acid cycle, so converted into temp storage)
- As they are acidic, their build-up in blood can cause ketoacidosis, as well as ketonuria (their presence in urine, which can cause pulling of cations with them)

Untreated ketoacidosis causes hyperpnea, disrupted heart activity and O2 transport, & severe depression of the NS that can possibly lead to coma and death [ Mainly consequence of TYPE 1 DM, in type 2, we have some insulin around that is usually enough to prevent ]

23
Q

What is the opposite condition to diabetes mellitus ?

A

Hyperinsulinism – Excessive insulin secretion causing low blood glucose levels ( hypoglycemia )

  • Symptoms include anxiety, nervousness, disorientation, unconsciousness, even DEATH
  • Treatment : Sugar ingestion
24
Q

What are the risk factors for Type 2 DM ?

A

Age, obesity, hypertension, physical inactivity, pregnancy & family history

25
Q

What are the consequences of obesity ?

A
  • Adipose tissue secretes hormones that can decrease insulin sensitivity
  • Increased FFAs/ TGs & cholesterol :
    – Interferes with intracellular insulin signalling
    – Decrease tissue responses to insulin
    – Alters incretin actions (GIP, glucagon lipopeptide)
    – Promotes inflammation (inc in inflammatory chemical release)
    – Increases inflammatory cytokines that cause insulin resistance & are toxic to beta cells
26
Q

GIP

A

[ Glucose-dependent insulinotropic peptide OR gastric inhibitory peptide ]

  • Produced in duodenal mucosa, stimulated by fatty chyme
  • Targets stomach to inhibit HCl production (minor effect) & pancreas for insulin release
27
Q

Metabolic Role of the Liver

A
  • Hepatocytes carry out ~500 metabolic functions
  • Processes nearly every class of nutrient
  • Play major role in regulating plasma cholesterol levels
  • Stores vitamins + minerals
  • Metabolizes alcohol, drugs, hormones, and bilirubin
  • Production of coagulation / clotting factors
28
Q

Liver – Carbohydrate Metabolism

A

Particularly important in maintaining blood glucose homeostasis

Functions :
- Converts galactose + fructose into glucose
- Stores glucose as glycogen when blood glucose levels are high
- In response to hormonal controls, preforms glycogenolysis & releases glucose back to blood
- Preforms glyconeogenesis by converting amino acids + glycerol into glucose when glycogen stores are exhausted & blood glucose levels are falling
- Converts glucose to fats for storage

29
Q

Liver – Fat Metabolism

A

Major responsibility

Functions :
- Primary body site of beta oxidation [ breakdown of fatty acids into acetyl CoA ]
- Converts excess acetyl CoA to ketone bodies for release to tissue cells if citric acid cycle becomes overwhelmed
- Stores fats
- Synthesizes lipoproteins for transport of fatty acids, fats & cholesterol in blood
- Synthesizes cholesterol from acetyl CoA ; catabolizes cholesterol into bile salts, which are then secreted in bile

30
Q

Liver – Protein Metabolism

A

Essential for life (eg. clotting protein synthesis, ammonia disposal)

Functions :
- Synthesis of urea to remove ammonia from body (inability to do so like in cirrhosis or hep allows ammonia to accumulate n blood)
- Synthesizes most plasma proteins except for antibodies & some hormones (inability to do so like in cirrhosis causes edema)
- Deaminates amino acids for their conversion to glucose OR for ATP synthesis
- Transamination : Interconversion of nonessential amino acids

31
Q

Liver – Vitamin / Mineral Storage

A
  • Stores vit A (1 - 2 years supply)
  • Stores sizable amounts of vit D & B12 (1 - 4 months supply)
  • Stores iron (other than iron bound to hemoglobin, most stored in liver as ferritin)
32
Q

Liver – Biotransformation Functions

A
  • Metabolizes alcohol, drugs + other toxins by inactivating them for excretion by the kidneys & preforms reactions that may result in products which are more active, changed in activity, or less active
  • Processes bilirubin resulting from RBC breakdown & excretes bile pigments in bile
  • Metabolizes bloodborne hormones that can be excreted in urine
33
Q

Cholestrol Metabolism

A
  • Not used as an energy source
  • Structural basis of bile salts (without we can’t emulsify / digest fats), steroid hormones (estrogen, testosterone) & vitamin D
  • Major component of plasma membranes (20 - 25 % of lipids, provides stability to phospholipid bilayer)
  • 15% is ingested, the rest made in body, primarily by liver
  • Lost from body when catabolized or secreted in bile salts that are lost in feces
34
Q

Cholestrol Transport

A

Transport of exogenous & de novo cholesterol requires a diversity of lipoproteins complexes containing triglycerides, phospholipids, cholesterol & protein (since fat doesn’t like aqueous environments)

Lipoproteins : Transport water-insoluble cholesterol & TGs through blood
- Regulate lipid entry / exit at target cells
- All contain triglycerides, phospholipids, cholesterol, protein
- The higher the percentage of lipids, the lower the density

35
Q

Types of transport lipoproteins

A

HDLs (high-density lipoproteins) – Highest protein content, “good cholestrol”, cholestrol carrier found in blood which scoops up excess cholesterol from tissues & takes it back to liver for excretion
- Transport excess cholesterol from peripheral tissues to liver to be broken down + stored into bile
- Also provide chol to steroid-producing organs

LDLs (low-density lipoproteins) – Highest cholesterol content, carries cholesterol from liver to tissues, “bad cholesterol”
- Transport chol to peripheral tissues for membranes, storage or hormone synthesis

VLDLs (very low-density lipoproteins) – Contents are more than half triglycerides, with low density of proteins, carries the triglycerides from liver mostly to adipose tissue
- Transport triglycerides from liver to peripheral tissues (mostly adipose) for STORAGE

more proteins as part of lipoprotein complex = higher density

  • Chylomicrons – Carries absorbed lipids from intestine to liver; have lowest density (lightest), consists almost entirely of triglycerides
36
Q

Cholestrol can trigger process of _______________

A

Atherosclerosis - intermittent blood flow may lead to heart attacks

Ideally, level of HDL should exceed level of LDL floating around in body (imbalances may leas to dislipidemia)

37
Q

Factors Regulating Blood Cholestrol Levels

A

The liver produces cholesterol at a basal level regardless of dietary cholesterol intake – Restricting dietary cholesterol does not markedly reduce blood cholesterol levels

More important effect is relative amounts of saturated and unsaturated fatty acids :
Saturated fatty acids stimulate liver synthesis of cholesterol & inhibit cholesterol excretion from body (full compliment of H ions)
- Diet high in sat. fats INCREASES blood cholesterol level due to increased disposition of fat in liver which then increases amount of Acetyl CoA floating around in liver –> Then used to produce cholesterol (indirect mechanism)

Unsaturated fatty acids enhance excretion of cholesterol into bile salts (double H bonds leaves unoccupied spaces)

Trans fats - Healthy fats that have been taken + made saturated, made to last longer & taste better
- Worse effect on cholesterol levels than saturated fats; increase LDL (bad) & reduce HDL (good)

38
Q

OTHER Factors Regulating Blood Cholestrol Levels

A

Unsaturated omega-3 fatty acids (found in cold-water fish) have lower proportions of saturated fats & cholesterol
- Make platelets less sticky & help prevent spontaneous clotting
- Have antiarrhythmic effects on heart
- Can lower BP

Stress & cigarette smoking – Lowers HDL levels

Aerobic exercise & estrogen – ↑ HDL levels & ↓ LDL levels

Body shape
- “Apple” – Fat carried on upper body is correlated with high cholesterol & LDL levels
- “Pear” – Fat carried on hips and thighs is correlated with lower cholesterol & LDL levels (usu women)

39
Q

What are characteristics of the thyroid gland ?

A

Butterfly-shaped endocrine gland in anterior neck on the trachea, just inferior to larynx
- Secretes thyroid hormone
- Huge blood supply

Consists of :
- Isthmus – Median mass connecting two lateral lobes
- Follicles – Hollow spheres (holes) lined with epithelial follicular cells that produce glycoprotein thyroglobulin
- Colloid – Fluid of follicle lumen containing thyroglobulin & iodine (precursor to thyroid hormone)
- Parafollicular cells – Produce hormone calcitonin hormone which contributes to regulation of blood calcium

40
Q

What is the thyroid hormone ?

A

The body’s major metabolic hormone

Found in 2 forms :
- T4 (thyroxine) – Major form (93 - 95 % of TH released) that consists of 2 tyrosine molecules with 4 bound iodine atoms
[ Most converted to T3 at tissue level since it is 4x more potent than T4 ]

  • T3 (triiodothyronine) – Form that has 2 tyrosines with 3 bound iodine atoms, present in blood at much smaller quantities but persists for much longer & faster acting

Both are iodine-containing amine hormones

41
Q

What are the effects of the thyroid hormone ?

A

Affects virtually every cell in body (almost every cell has a receptor for it)

Functions like a steroid hormone receptor, even tough made of amino acids :
- Enters target cell + binds to intracellular receptors within nucleus
- Triggers transcription of various metabolic genes

Effects include :
- Increased basal metabolic rate (60 - 100%) & increased heat production as a byproduct (calorigenic effect)
- Regulates tissue growth + development → Critical for normal skeletal & NS development + reproductive capabilities
- Maintains BP by increasing adrenergic receptors in blood vessels

42
Q

Look at TH table

A
43
Q

How is TH synthesized ?

A
  • T3 and T4 are stored in the follicles lumen until triggered for release by TSH
  • Amounts sufficient for 2-3 months

7 steps involved in synthesis of TH :
1. Thyroglobulin (lipoprotein) is synthesized + discharged into follicle lumen
- each mol contains 70 thyrosine amino acids –> foundation of TH synthesis

  1. Iodide is trapped iodide ions (I–) are actively taken into cell & released into lumen
  2. Iodide oxidized – Electrons are removed, converting it to iodine (I2)
  3. Iodine is attached to tyrosine in colloid – Mediated by peroxidase enzymes
    - Monoiodotyrosine (MIT) – Formed if only 1 iodine attaches
    - Diiodotyrosine (DIT) – Formed if 2 iodines attach
  4. Iodinated tyrosines link together to form T3 and T4
    - If 1 MIT and 1 DIT link, T3 is formed
    - If 2 DITs link, T4 is formed
  5. Colloid is endocytosed by follicular cells
    - Vesicle is then combined with a lysosome
    - Lysosomal enzymes cleave T3 and T4 from thyroglobulin
  6. Hormones are secreted into bloodstream
    - Mostly T4 secreted, but T3 is also secreted
    - T4 must be converted to T3 at tissue level
44
Q

What is the role of iodine in TH synthesis ?

A

Iodine - ingested in the form of iodides is necessary for the formation of T3/T4

Iodide from the GI → the blood and is trapped in the thyroid follicles that actively pump iodide from the blood into the interior of the cells

The rate of iodide trapping is influenced by TSH

45
Q

Transport of TH

A

T4 & T3 transported by thyroxine-binding globulins (TBGs)

  • Both bind to target receptors, but T3 is 10 times more active than T4
  • Peripheral tissues have enzyme that to convert T4 to T3 (- 1 iodine)
46
Q

Negative feedback regulation of TH release

A

Falling TH levels stimulate release of thyroid-stimulating hormone (TSH)
- Rising TH levels provide negative feedback inhibition on TSH
- TSH can also be inhibited by GHIH (growth-hormone inhibitory hormone), dopamine & increased levels of cortisol + iodide

Hypothalamic thyrotropin-releasing hormone (TRH) can override the negative feedback during pregnancy (TH needed to promote growth of foetus) or exposure to cold

47
Q

Regulation of TH secretion

A

Hypothalamus – Releases TRH [ thyroid-releasing hormone ] that will act on the anterior pituitary

Anterior Pituitary – Releases TSH [ thyroid-stimulating hormone ] which will tell thyroid gland to release thyroid hormones into bloodstream

When level of thyroid hormones reaches homeostatic range, we shut system down → We do not want to be releasing TH all the time

T3 & T4 feedback and tell anterior pituitary to stop releasing TSH & hypothalamus to stop secreting TRH

Anatomy & Physiology III (8 decks)

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