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87 Cards in this Set

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How does glucagon increase blood glucose levels?
(what 3 processes?)
1.Stimulation of hepatic glycogenolysis -> blood glucose levels can double within minutes
2.Stimulation of hepatic gluconeogenesis (via increased amino acid uptake)
3.Stimulation of lipolysis in fat tissue in very high concentrations
Which type of diabetes is potentially reversible?
Diabetes type 2
Two types of hormones (in terms of where originate):
1. Tissue hormones - produced by individual endocrine cells; not in large glands
2. Glandular hormones - e.g. cytokines
Which 2 organ systems produce the most hormones?
1. CNS (brain)
2. GI
What are endocrines or hormones? functions?
Produced in a gland and secreted directly into circulation w/o ducts

chemical messangers, regulators of homeostasis and metabolic pathways, etc.
autocrine hormones
affect cell of production
Are endocrine hormones present in high concentrations?
No, always in extremely low concentration (pg - ug/ ml), which why they are difficult to detect.
4 Types of hormones in terms of chemical structure?
(e.g. peptide hormones, and ? )
1. peptide hormones (like insulin)
2. steroid hormones (e.g. vit.D)
3. amines (e.g. dopamine, epinephrine)
4. eicosanoids (e.g. prostaglandins)
which hormone type is most common?
peptide hormones
what hormones are hydrophilic?
peptide hormones
which hormones are lipophilic?
steroid hormones
What is term Dr. Zeigler uses for parts of hormone precursor which are cleaved off during protein/peptide synthesis? Are these cleaved off pieces ever active on their own?
pre-pro sequences; can be active compounds also!
What are differences between nervous and endocrine system?
endocrine system is slower to react, much slower, because it relies on chemical messengers

also endocrine system responds to INTERNAL stimuli; while nervous system responds to external ones.
How long (approx.) does it take protein hormone to be produced?
~45-60 minutes
How long does it take for protein hormone to be released?

How are hormones released so quickly, when protein synthesis takes so long?
2-5 minutes

* b/c after prepro seq. cleaved off, hormone stored in secretory granule or vesicle where can secrete immediately upon stimulation via exocytosis

* also hydrophilic so dissolves easily in plasma
What type of hormones made in adrenal cortex:
A. peptide hormones?
B. steroid hormones?
C. amines?
D. eicosanoids?
* hormones made in adrenal cortex are steroid h's
e.g. mineralocorticoids (aldosterone) and glucocorticoids (cortisol).
* also a secondary site of androgen synthesis.
True or false: Protein hormones generally have longer half-life then steroids.
False, b/c proteases are found everywhere in tissues, esp. concentrated in blood flow of liver&kidney.
Steroid Hormones are derived
from ? In one sentence, describe how made.
Steroid Hormones are derived
from Cholesterol

* stimulus activates enzymes -> starts a series of 3 conversions to produce steroid hormones
How are steroid transported in plasma?
What % of bound?
* not hydrophilic, are lipophilic, so need to attach to carrier (like albumin) in plasma

1-10% are in free form=active; rest is bound=inactive (acts as a hormone reserve in plasma)
Why is half life of steroids extended (last longer than peptide hormones)?
* binding to albumin helps protect steroids from degradation and quick destruction in liver (longer half-lives -> hours to days)
* also makes "reservoir" in circulation
How are most steroids metabolized?
glucuronidation in liver
How tissues get cholesterol?
Flows around body in what form?
* from diet (although can be converted from Acetyl CoA)
* TriG and cholesterol all condensed into VLDL
* LPL off loads cholesterol in tissues making steroids
Receptor location for hydrophilic hormones?
Describe these receptors; are they complex?
* Cell membrane (cannot diffuse through); so receptor on surface of membrane
* most of these receptors are very large and complex w/external binding portion and internal transducing portion
Receptor location for lipophilic hormones:
* Cytoplasm or Nucleus; receptor inside target cell b/c lipophilic hormones have no problem entering cell to bind to it
All hormones affect their target tissues by forming first a ________ , which alters the activity of their target cells.
HORMONE - RECEPTOR complex
We know number of particular receptor can increase and decrease; which is more common: up regulation or down regulation?
down regulation
What is example of up regulation of receptor number?
Example: Aldosterone (steroid) initiates synthesis of enzyme ATPase in its target cells -> stimulates Na/K pumps
True or false: Antagonist does opposite action of hormone.
False, antagonist simply blocks binding of hormone to receptor.
Lipophilic hormones induce protein synthesis, w/newly formed proteins being mostly enzymes, which now stimulate or inhibit certain metabolic pathways = ?
= METABOLIC EFFECT
In following example: which represents the secondary messanger?
cAMP

Note: The first messenger (= hormone) remains outside of its target cell b/c cannot enter, but transmits its message via cAMP = second messenger
phosphorylation is usually stimulatory or inhibitory event?
stimulatory
This an example of a _______feedback loop: effect of plasma glucose levels on glucagon secretion
NEGATIVE FEEDBACK LOOP
What is stimulated (to start) if glycogen stores are full?
lipogenesis, creation of fat
What cells are not affected by insulin? (examples)
glucose independent cells

neurons, retina, lens, blood
cells, pancreatic B cells, kidney,
GI mucosa, placenta
?% of body cells contain insulin
receptors
80% of body cells contain insulin
receptors = insulin-sensitive tissues
Where is insulin receptor located?
what type of mechanism?
* its a protein, so on cell membrane
- called a tyrosine kinase
* 2nd messanger mechanism (these are usually G-coupled) but not sure
* insulin binds to external part alpha subunit, and stimulates beta subunits
After insulin – receptor binding (= in
insulin-sensitive tissues): what happens?
Beta parts of receptor become the
activated tyrosine kinase (= second messenger)
-> leads phosphorylation of various enzymes
What is stimulated by insulin binding?
* glucose uptake by GLUTs
* fat uptake and storage in fat tissue via lipoprotein lipase enzyme - extracts fat from VLDL or chylomicrons
* inhibits hormone specific lipase
* inhibits proteases / proteolytic enz. / protein brk.down
* stim. protein temporary storage and synthesis (organ function, growth, clotting factors & albumin in liver)
What happens without w/o insulin, but with circulating chylomicrons?
LDL not active, full of chylomicrons
Glucagon opposes Insulin effects on _____ in the LIVER


Glucagon ____ blood glucose level
Glucagon opposes Insulin effects on carbohydrate metabolism (which were storage, breakdown)

Glucagon INCREASES blood glucose level
How does glucagon increase blood glucose levels?
(by stimulating what 3 processes?)
1.Stimulation of hepatic glycogenolysis -> blood glucose levels can double within minutes
2.Stimulation of hepatic gluconeogenesis (via increased amino acid uptake)
3.Stimulation of lipolysis in fat tissue in very high concentrations
What might stop glucagon from secreting?

What cells are involved?
high blood glucose, like after high carb. meal

(pancreatic alpha cells are insulin-sensitive: high plasma glc -> high insulin ->
glc uptake into alpha cells -> glucagon secretion is inhibited!)
Main signal for glucagon release
HYPOGLYCEMIA -> stimulates glucagon secretion
high plasma amino acid levels ___ glucagon secretion
also stimulate glucagon secretion

but only when blood glc levels are low (A.A. are then channeled into gluconeogenesis)
= IDDM
Type I DM
circulating insulin levels are low
What causes Type I DM?
Causes: islet cell destruction b/o pancreatitis, senile degeneration, autoimmune disease -> hyperglycemia (b/c low insulin; cells can't take up glc.)
Definition of Diabetes Mellitus:
absolute or relative lack of insulin leading to impaired
carbohydrate, lipid and protein metabolism
Non-insulin dependent DM =
Type II DM
Causes of Type II DM?

Insulin resistance?
* something goes wrong with insulin receptors, not binding insulin right, or not enough of them
* insulin present but not responding to it; known as insulin resistance aka "relative" lack of insulin
%2 of ___ suffer from diabetes m.
%2 of burmese cats
Are beta cells of pancreas intact in type 2 diabetes?
yes at first, insulin still being made in excess as way to compensate blas
eventually the beta cells become "exhausted" and type I diabetes develop
Secondary type diabetes or type 3 diabetes
high levels of other hormones like cortisol
high glucagon
Which type of diabetes has normal insulin levels?
Type II DM
Which hormone responds to high osmoregularity in plasma? causes what?
ADH, causes incr. in thirst
two initial clincal signs of diabetes?
1a. rapid weight loss
(b/c of excess lipolysis, proteolysis), 1b. polyphagia (b/c body thinks it's hypoglycemic)
2. glucosuria
What is consequence of excess lipolysis?
Excessive Lipolysis -> FATTY LIVER and KETOACIDOSIS -> diabetic COMA

FYI: Ketones produced when FA broken down in liver. Before this FA are enz. broken down via β-oxidation to form acetyl-CoA. However, if conditions not right for TCA cycle (intermediates not present), A/CoA become ketones instead.. In high lvl. lower pH of blood, leading to 'ketosis'
Glycated Proteins/Acidosis/Proteolysis/Swelling further lead to?
* vascular damage -> microangiopathies / neuropathies
(e.g. glomerula, TIBIAL nerve/cat, retina/humans)
What is consequence of weight loss and proteolysis?
proteolysis -> WEIGHT LOSS, muscle weakness and reduction of organ functions
At what glc. plasma level will glucose start appearing in urine?
if over 180mg/dL
what 2 clinical signs of diabetes usually appear as a result of glycosuria?
1. polyuria
2. polydipsia (incr. thirst)
Does polyphagia (as hypothalamic satiety centre is insulin-dependent) continue?
initially only as hypothalamic satiety centre is insulin-dependent; later anorexia and vomiting following tissue damages a/o acidosis
What tissues get too much glucose with diabetes?

Do do these tissues with excess glucose?
insulin independent tissues (neurons, liver, RBC, etc.)

do not have a lot of glucogen storing ability, also cannot convert to FAs
~form complexes w/proteins -> glycated proteins
Are glycated proteins functional?

Examples?
No

glycated hemaglobin! (A chain more often that B chain), after ~6 wks. of hyperglycemia
What are glycated proteins in plasma called (e.g. glucosa + albumin)?
Time frame? (like when does this start to happen?)
fructose amines

2 weeks
What glycated protein test is most frequently done in vet medicine?
fructose amine test, for detecting glc. & albumin complexes
In the tissues excess glucose is converted into ___ in the lens?
Eventual consequence of this?
sorbitol

H2O acc. in lens, gets cloudy -> nerve damage and blindness
What are animals with diabetes prone to UTI?
tract has lots of sugar in it
which type of diabetes most common in cats?
DM type 2
how would u treat DM type 1?
give insulin
Why do u have to inject insulin?
have to inject all peptide hormones otherwise get degraded by the acid in stomach, etc.
why are steroid able to taken as pills?
lipophilic
what maintenance diet wud you feed animal with diabetes?
high in quality protein, low soluble carbs, low FA (b/c often obesity is cause, and leads to fatty liver), high in fiber
Which type of diabetes is potentially reversible?
diabetes type 2
how would you treat T2 diabetes to begin recovery process and why?
would give insulin along with exercise so BW reduced; this gives exhausted beta cells in pancreas (have churning out extra insulin) a chance to recover and make insulin again on own
What must be functional in animal to recover?
(unanswered questions)
* Beta cells can't be completely shot
* Need at least some insulin receptors on insulin dep. tissue
>But aren't receptors the source of problem with T2??
What is course of action if animal recovers from T2 diabetes? (What would you watch for?)
* animals blood glucose levels must monitered closely
* if beta cells making insulin again, must reduce or stop insulin supplements
* otherwise can become hypoglycemic
Could you cure/reverse type 1 diabetes?
Theoretically could do pancreas transplant, but normally only done in human medicine
(remember in type 1 is absolute of insulin, so beta cells not functional at all)
How treat diabetes type 3?
(unanswered question)
Secondary DM or Type III ( TRANSIENT DM)
* high levels of other hormones like cortisol, or glucagon
* caused by DM Type II; insulin resistance

Does it fix itself?
What is connection between cortisol and insulin/hyperglycemia?
If glucagon levels really HIGH, which metabolic pathway favored?
lipolysis (2.3.1)
Where is glucagon made?
secreted in pancreatic
α cells AND stomach <- gut glucagon
Half life of glucagon?
5 minutes (it's a peptide - shorter half life than steroid, b/c proteases are everywhere)
How are pancreatic alpha cells and beta cells different aside from the hormones they make?
* Beta cells are insulin independant (they just make it)
* alpha cells are insulin dependent
What happens when insulin binds alpha cells?
(unanswered question)
glucagon secretion stops being released
(remember peptide hormones stored, so inhibiting synthesis..i dont think)
Name two most common health problems affects in ferrets:
1. Adrenal disease - excess sex steroids

2. Insulinoma - tumor in beta cells of pancreas
True or False: Regarding adrenal disease in ferrets, characterized by rise in cortisol & aldersterone.
False!

Ferrets w/adrenal disease have excess sex steroids (estrogens > androgens); but cortisol & aldosterone are normal
Symptoms of Adrenal disease in ferrets?
Ferret with Adrenal Disease:
estrogens > androgens:

symptoms include alopecia, enlarged vulva, prostate hypertrophy, sexual aggression, bone marrow depression (anemia)
True or False: Insulinoma in ferrets causes rapid increase in blood glucose
False!!!

Insulinoma in ferrets causes rapid DROP in blood glucose

because more insulin secreted