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26 Cards in this Set

  • Front
  • Back
3 kinds of somatic signaling
neuronal (nerve-> nerve synapse-> nerve #2)
endocrine (cell->blod stream ->target receptors)
neuroendocrine (a little of both properties)
2 kinds of hypothalamic neurons
1. Neruosecretory- terminals in posterior pituitary and hormones there released into general circulation
2. neurotrophic- termials in median eminence that travel through the portal system into the anterior pituitary)
hypothalamic integration, amplificaiton and feedback
hypothalamus integrates signals (temp, stress, ect) and releases the porper signal in response.
hypothalamic signals (peptides) have a large (10^6) amplification in signal. hormones in different organs respond to the hypothalamus and inhibit further release of original signal
4 hypothamamic peptide hormones and their general function
sommatostatin- role in controling growth (via inhibition of GH)
LHRH- role in cyclicity and sexuality via LH,FSH
vasopressin- or ADH, controls the Na and K resrption and secretion as well as blood volume
GHRH- stimilated growth via GH
AA difference between oxytocin and ADH
oxytocin- the lucys, N-...I..L...-C

ADH- N...P...R...-C
TSH nobel winner and his AA findings
Shally- pyroGlu-His-Pro

proline is usually modified too
synthesis site
type of hormone
role in obesity
role in diabetes
interation with insulin
receptor site of synthesis
Amineo acid hormone made in adipose tissue that is a chemical marker for fed state of the body. Alterations in the receptor (made in the hypothalamus) can lead to DM while alterations in the AA sequence can lead to obisity. Leptin can crosstalk with insulin via downstream signaling of IRS-2 and PI-3K pathway shared by insulin and leptin.
NPY function and melanocortin
high levels of NPY stimulate the feeding function. NPY stimulates orexigenic neurons and Melanocortin stimulares anorexogenic neurons
serine 3 of grelin can be modified with 8-carbon fat thats activates ghrelin makin it a sensitive indicator of feeding and FA metabolism. Just before feeding, ghrelin increases.
diabetes and the similarity to starvation
starvation and diabetes have the same concentrations of insulin and glucagon
effects of insulin
1.increased glucose uptake by the liver, adipose cells and muscle
2.glycogen synthesis (over breakdown)
3.gycolysis (and ACoA production)
4.Fatty acid synthesis (from increased ACoA)
5.TG synthesis
6.increased glucose transporter GLUT-4
7.stimulation of hexokinase and increased expression
8. Stimulation of glycogen sythase and inhibition of glycogen phosphorylase
9. Increased PFK-1 and Pyruvate dhydrogenase
10. Increased ACoA carboxylase
11. increased lipoprotein lipase
effects of glucagon
decreased glycogen sythase
increased glycogen phosphorylase
decreased PFK-1
increased FBPase-2
decreased PKase
Increased PEP carboxykinase
Increased TAG Lipase
Mechanism of diabetes
1. cells think that the decreased glucose inside is from a fasting
2. Krebs intermediates like OX are diverted into gluconeogenesis
3. all the while, FA from adipose tissue is oxidized to ACoA
4. ACoA buildup in the presence of no OX leads to ketone bodies
5. ketones are relseased as fuel for the squash
4 consequnces of insulin deficiency in glucose uptake, production, TAGs and ketogenesis
decreased glucose uptake in adipose and muscle leading to hyperglycemia, osmotic diuresis and dehydration
increased liver produciton of glucose
elevated FFA levels in blood and ketoacidosis
3 cardiovascular effects of diabetes
inhibition of vasodialation, increased smooth muscle vasculature, and increased thrombognesis

all of these are pro-CVAs
Define: glycation
elaborate on mechanistic implications in blood
Glycation is the post-translational modificaiton of proteins by the open form of glucose. glycation leads to increasing the half life of proteins in the blood stream and leads to accelrated arterial changes and athersclerotic suseptabiliy
mechanism of kidney disease in diabetes
diabetes increases the blood glucose concentation. the renal response to increased glucose is to excrete it in the urine. the glomerulus basement membrane thickens to the increased GFR. function decreases and uremia and abluminuria is the final straw and indicates that there is irreversable damage
Define: Kimmelsteil-Wilson nodules
Diabetic nephropathy (nephropatia diabetica), also known as Kimmelstiel-Wilson syndrome and intercapillary glomerulonephritis, is a progressive kidney disease caused by angiopathy of capillaries in the kidney glomeruli. It is characterized by nodular glomerulosclerosis. It is due to longstanding diabetes mellitus, and is a prime cause for dialysis in many Western countries.
visual disease in diabetes
advanced glycosylated end-products lead to cateracts, increased glucose in the blood leads to crecsent-shaped visual field and glaucoma. diabetes leads to neovascularization in the vireous, eventual hemorrhage as well as clot contraction leading to retinal detachment
hypothamamus intregrates signals form which 4 sources
reticualr activating substance (sleep)
limbic system (emotion)
potical system (vision)
thalamus (pain)
anterior pituitary vs posterior pituitary
Anterior pituitary gets hormales from median eminence via portal system and acts in response to stress, reproduction, lactation and metaboic rate and growth
Posterior pituitary resonds to levels of blood and blood Na concentration as well as thirst and urine volume
Neurophysins role
No physiological role, but thier absence leads to continual association of oxytocin and ADH with thier secreting vescicle. Neurophysin I is associated with ADH and Neurophysin II is associated with Oxytocin
AHD binging to VA-1 receptors leads to____
ADH binding to VA-2 receptors leads to _____
4 stimulators of AHD secretion
Increased osmolarity of blood
increased Na in CSF
decreased blood volume
increased temperature
4 inhibitors of ADH secretion
increased blood volume
decreased temperature
decreased Na in CSF
decreased osmolarity of the blood