MOVESCI 340 QUESTIONS AND ANSWERS LATEST UPDATE
100% CORRECT A+ GRADED. Buy Quality Materials!
Type 1 diabetes
(childhood onset) beta cells are destroyed, own immune cells digest their insulin,
autoimmune or failure of beta cells (we don't make enough insulin)
Type 2 diabetes
the signal is not received appropriately; blood glucose levels remain pretty much the
same and doesn't clear out like insulin sensitive; sedentary lifestyle you become more
susceptible (obesity epidemic increases)
Steroid-derived hormones
derived from cholesterol, originate from testes, adrenal cortex, and ovaries; "lipid-
derived hormones"; not very soluble in blood, so need carriers to help solubility; can
diffuse across plasma membrane freely and bind to a receptor in the cell. Longer half
life.
Examples of steroid-derived hormones
aldosterone, cortisol, testosterone, and estrogen
Polypeptide hormones
hydrophilic and lipophobic, need a receptor to get into cells; freely soluble in blood, they
don't need a carrier
Examples of polypeptide hormones
insulin and glucagon
Amine hormones
all derived from the amino acid tyrosine; shared properties with steroid and polypeptide
Examples of amine hormones
epinephrine and throxin (thyroid)
Speed of peptide and how it correlates to what it is used for
Peptide hormones are stored in vesicles (regulatory secretion); fast acting; this is
important because maintain plasma glucose levels
Speed of steroid and how it correlates to what it is used for
slower onset, but longer duration; this is good for growth, formation of new bone, regrow
tissues and cell; need to induce cell proliferation
4 hormonal effects
modify protein synthesis rate; change enzyme activity (ex. allosteric modulator changes
the shape of protein and the way it acts);alter plasma membrane transport via second
messenger system (ex. insulin receptor); induce secretory activity
Pathway of a steroid hormone
freely diffuses (lipid loving), gets in and binds to steroid receptor in the cytoplasm, the
hormone-receptor complex translocates to the nucleus and can bind to sites on the
chromatin. This activates mRNA transcription to make more proteins.
Why do we keep steroid hormones in the cytoplasm?
Because we need to keep cell growth under control, otherwise could lead to things like
cancer
, What hormones are not lipid soluble?
insulin, glucagon, epinephrine, norepinephrine and peptide hormones
How do receptors on plasma membrane work?
They cannot diffuse through the plasma membrane, so they bind to a receptor on the
plasma membrane and effect the first messenger which activates the second
messengers in the cytoplasm. (action is linked by G protein, an enzyme complex)
Signal transduction
activates an enzyme complex, go from 1 --> molecules that are signaled and then those
ten activate another 10 each and so on.
Humoral stimuli
changes in ECF composition; capillary blood contains high glucose, insulin is secreted
from the pancreas, target cells absorb more glucose from the blood, low blood sugar
levels inhibit insulin release
Hormonal stimuli
changes in circulating hormone levels; ACTH is released from the anterior pituitary
gland, leads to activation of the adrenal cortex (negative feedback on ACTH release)
Neural stimuli
neural stimulation of a neuroglandular junction; a direct stimulation for a response to
adrenal medulla, that secrete epinephrine
What factors determine hormone levels?
quantity synthesized, rate of catabolism/secretion into blood, quantity of transport
proteins present, changes in plasma volume
explain the mechanism through which exercise training can improve glucose
homeostasis in individuals with insulin resistance (through contraction)
Exercise reduces insulin secretion (beneficial because resistance leads to an abnormal
amount of insulin release); stimulates AMPK, reactive oxygen, nitric oxide and CaMK to
phosphorylate AS160 and remove its inhibition effect on Glut 4
Insulin
mediates glucose metabolism, affects fat synthesis, facilitates protein synthesis,
stimulates glucose transporter (GLUTS), secreted by beta cells
Glucagon
increases blood glucose, increases glycogenolysis in the liver, secreted by Islets of
Langerhans
How exercise training can mediate blood glucose levels (glucose uptake): Liver
increases insulin sensitivity
How exercise training can mediate blood glucose levels (glucose uptake):
Adipose Tissue
decreases abdominal adiposity, increases insulin receptor density, increases GLUT 4,
leads to an increase in glucose uptake
How exercise training can mediate blood glucose levels (glucose uptake):
Pancreas
decrease in hyperinsulinemia, leads to decreased abdominal adiposity
How exercise training can mediate blood glucose levels (glucose uptake):
Skeletal Muscle
increases muscle glucose deliver, increase in insulin receptors, GLUT 4, increase in
glucose storage, increase in glycogon synthase
100% CORRECT A+ GRADED. Buy Quality Materials!
Type 1 diabetes
(childhood onset) beta cells are destroyed, own immune cells digest their insulin,
autoimmune or failure of beta cells (we don't make enough insulin)
Type 2 diabetes
the signal is not received appropriately; blood glucose levels remain pretty much the
same and doesn't clear out like insulin sensitive; sedentary lifestyle you become more
susceptible (obesity epidemic increases)
Steroid-derived hormones
derived from cholesterol, originate from testes, adrenal cortex, and ovaries; "lipid-
derived hormones"; not very soluble in blood, so need carriers to help solubility; can
diffuse across plasma membrane freely and bind to a receptor in the cell. Longer half
life.
Examples of steroid-derived hormones
aldosterone, cortisol, testosterone, and estrogen
Polypeptide hormones
hydrophilic and lipophobic, need a receptor to get into cells; freely soluble in blood, they
don't need a carrier
Examples of polypeptide hormones
insulin and glucagon
Amine hormones
all derived from the amino acid tyrosine; shared properties with steroid and polypeptide
Examples of amine hormones
epinephrine and throxin (thyroid)
Speed of peptide and how it correlates to what it is used for
Peptide hormones are stored in vesicles (regulatory secretion); fast acting; this is
important because maintain plasma glucose levels
Speed of steroid and how it correlates to what it is used for
slower onset, but longer duration; this is good for growth, formation of new bone, regrow
tissues and cell; need to induce cell proliferation
4 hormonal effects
modify protein synthesis rate; change enzyme activity (ex. allosteric modulator changes
the shape of protein and the way it acts);alter plasma membrane transport via second
messenger system (ex. insulin receptor); induce secretory activity
Pathway of a steroid hormone
freely diffuses (lipid loving), gets in and binds to steroid receptor in the cytoplasm, the
hormone-receptor complex translocates to the nucleus and can bind to sites on the
chromatin. This activates mRNA transcription to make more proteins.
Why do we keep steroid hormones in the cytoplasm?
Because we need to keep cell growth under control, otherwise could lead to things like
cancer
, What hormones are not lipid soluble?
insulin, glucagon, epinephrine, norepinephrine and peptide hormones
How do receptors on plasma membrane work?
They cannot diffuse through the plasma membrane, so they bind to a receptor on the
plasma membrane and effect the first messenger which activates the second
messengers in the cytoplasm. (action is linked by G protein, an enzyme complex)
Signal transduction
activates an enzyme complex, go from 1 --> molecules that are signaled and then those
ten activate another 10 each and so on.
Humoral stimuli
changes in ECF composition; capillary blood contains high glucose, insulin is secreted
from the pancreas, target cells absorb more glucose from the blood, low blood sugar
levels inhibit insulin release
Hormonal stimuli
changes in circulating hormone levels; ACTH is released from the anterior pituitary
gland, leads to activation of the adrenal cortex (negative feedback on ACTH release)
Neural stimuli
neural stimulation of a neuroglandular junction; a direct stimulation for a response to
adrenal medulla, that secrete epinephrine
What factors determine hormone levels?
quantity synthesized, rate of catabolism/secretion into blood, quantity of transport
proteins present, changes in plasma volume
explain the mechanism through which exercise training can improve glucose
homeostasis in individuals with insulin resistance (through contraction)
Exercise reduces insulin secretion (beneficial because resistance leads to an abnormal
amount of insulin release); stimulates AMPK, reactive oxygen, nitric oxide and CaMK to
phosphorylate AS160 and remove its inhibition effect on Glut 4
Insulin
mediates glucose metabolism, affects fat synthesis, facilitates protein synthesis,
stimulates glucose transporter (GLUTS), secreted by beta cells
Glucagon
increases blood glucose, increases glycogenolysis in the liver, secreted by Islets of
Langerhans
How exercise training can mediate blood glucose levels (glucose uptake): Liver
increases insulin sensitivity
How exercise training can mediate blood glucose levels (glucose uptake):
Adipose Tissue
decreases abdominal adiposity, increases insulin receptor density, increases GLUT 4,
leads to an increase in glucose uptake
How exercise training can mediate blood glucose levels (glucose uptake):
Pancreas
decrease in hyperinsulinemia, leads to decreased abdominal adiposity
How exercise training can mediate blood glucose levels (glucose uptake):
Skeletal Muscle
increases muscle glucose deliver, increase in insulin receptors, GLUT 4, increase in
glucose storage, increase in glycogon synthase
