Endocrine Physiology Flashcards
1
Q
what is a hormone?
A
any substance formed in very small amounts in 1 specialised organ or group of cells, carried to another organ or group of cells upon which it has a specific physiological effect
2
Q
what are the main hormone producing glands in the body?
A
hypothalamus, pituitary gland, thyroid gland, parathyroid glands, adrenal glands, pancreas, ovaries, testes
3
Q
what are the main 3 ways hormones act on the body?
A
enable and promote development of physical, sexual and mental characteristics; keep certain physiological parameters constant; enable and promote adjustment of physiological adaptations
4
Q
what are the 4 main structural types of hormone?
A
peptide and protein hormones, steroid hormone, amine hormones, arachidonic acid derivatives
5
Q
what are steroid hormones?
A
lipid hormones derived from cholesterol
6
Q
how are steroid hormones mainly transported in the blood?
A
bound to plasma proteins as aren’t water soluble
7
Q
what must happen before bound steroid hormones can interact with the target cell?
A
must be released
8
Q
what are amine hormones derived from?
A
tyrosine or tryptophan
9
Q
what sort of hormones are thyroid hormones?
A
amine hormones
10
Q
what sort of hormones are catecholamines?
A
amine hormones
11
Q
what sort of hormone is thyroxine?
A
thyroid hormone which is an amine hormone
12
Q
what sort of hormone is adrenaline?
A
catecholamine which is an amine hormone
13
Q
what is an example of a hormone that can act as both a neurotransmitter and hormone?
A
dopamine
14
Q
what are arachidonic acid derivatives synthesised from?
A
linoleic acid
15
Q
what do arachidonic acid derivative hormones play a role in?
A
mediation of inflammatory responses
16
Q
how do some non-steroidal anti-inflammatory drugs (NSAIDs) interact with arachidonic acid derivatives?
A
inhibit their mediation of inflammatory responses
17
Q
what do peptide hormones contain that directs the protein to the secretory pathway in the cell?
A
an N terminal sequence
18
Q
what does signal recognition complex binding of peptide hormones cause?
A
translational arrest
19
Q
what happens when peptide hormones bind to the signal recognition complex?
A
translational arrest, signal recognition complex binds to docking protein in ER, signal peptide sequence cleaved from hormone in ER, re-initiation of translation, sometimes additional cleavages required to generate mature hormone from prohormone
20
Q
difference between prohormone and preprohormone?
A
preprohormones have multiple cleavage sites
21
Q
what group do some peptide hormones require the addition of?
A
an amide group at the carboxy terminus
22
Q
where is kisspeptin produced?
A
arcuate and anteroventral periventricular regions of the hypothalamus
23
Q
what does kisspeptin do?
A
stimulates secretion of gonadotrophin releasing hormone (GnRH)
24
Q
what does gonadotrophin releasing hormone do?
A
inhibits release of gonadotropic hormones from pituitary
25
where is gonadotrophin inhibitory hormone produced?
paraventricular and dorsomedial regions of the hypothalamus
26
what sort of hormone are kisspeptin and GnIH?
peptide hormones
27
what is the general mechanism of action of peptide/protein hormones?
bind to cell surface receptors and activate intracellular signalling mechanisms that result in alteration of protein and enzyme activities
28
what is the general mechanism of action of steroid hormones?
bind to intracellular receptors and alter gene transcription
29
how do hormones signal via tyrosine kinase activation?
bind to receptor tyrosine kinases -> dimerisation and auto-activation of tyrosine kinase activity -> protein phosphorylation and biological response
30
how do hormones signal via the G protein/adenylyl cyclase pathway?
hormones bind to specific cell surface receptors and activate G proteins to stimulate (Gs) or inhibit (Gi) adenylyl cyclase- adenylyl cyclase increases intracellular cAMP levels, activates PKA to alter protein activities by phosphorylation
31
how do hormones signal using the DAG/IP3 pathway?
hormones bind to cell-surface receptors and activate G-proteins (Gq) which stimulate phospholipase C to convert PIP2 to IP3 and DAG. IP3 stimulates Ca2+ release from internal stores, DAG activates PKC. Calmodulin activated protein kinase activated, increases protein phosphorylation. Enzymatic activities altered
32
how do hormones signal via cytoplasmic/nuclear receptors?
nuclear receptors have common domain structure consisting of an activation domain (AF1), Zn finger DNA binding domain, and a ligand binding/dimerisation domain. Lipid soluble hormones (steroid or thyroid) cross plasma membrane, bind to nuclear receptors in cytoplasm- allows receptor to dissociate from heat shock proteins and enter nucleus as hormone-receptor complex which brings about changes in gene transcription by binding to a specific hormone response element
33
how is hypothalamus linked to anterior pituitary gland?
prominent blood vessel portal system, no direct neural connection
34
how is the hypothalamus linked to the posterior pituitary gland?
nerve fibres from paraventricular and supraoptic nuclei in hypothalamus pass directly to posterior pituitary where they secrete the hormones they contain into the bloodstream
35
what neurons does the paraventricular nucleus contain?
oxytocin and vasopressin neurons that project to neurohypophysis, neurons that regulate ACTH and TSH secretion, gastric reflexes, maternal behaviour, blood pressure, feeding, immune responses, temperature
36
what hypothalamic hormones control anterior pituitary secretions?
CRH, TRH, GnRH, GHRH, SMS, dopamine
37
what is CRH?
corticotrophin releasing hormone
38
structure of CRH?
41 amino acid peptide hormone
39
function of CRH?
stimulates release of ACTH
40
what is TRH?
thyrotropin releasing hormone
41
structure of TRH?
3 aa peptide hormone
42
function of TRH?
stimulates release of TSH and prolactin
43
structure of GnRH?
10 aa peptide hormone
44
function of GnRH?
stimulates release of LH and FSH
45
what is GHRH?
growth hormone releasing hormone
46
structure of GHRH?
44 aa peptide
47
function of GHRH?
stimulates release of GH
48
what is SMS?
somatostatin (growth hormone inhibiting hormone)
49
structure of SMS?
14 aa peptide
50
function of SMS?
inhibits release of GH, gastrin VIP, glucagon, insulin, TSH, prolactin
51
structure of dopamine?
monoamine
52
function of dopamine?
inhibits release of PRL
53
what is the hypophysis?
the pituitary gland
54
what is the neurohypophysis?
the posterior pituitary
55
what is the adenohypophysis?
the anterior pituitary
56
what is the posterior pituitary?
down-growth of brain
57
what nerves does the posterior pituitary contain?
nerves from the paraventricular and supraoptic regions of the hypothalamus
58
where are the cell bodies of the paraventricular and supraoptic nerves, and where are the nerve endings?
cell bodies in hypothalamus, nerve endings in posterior pituitary
59
where are the hormones stored in the posterior pituitary made?
cell bodies of nerves which are in the hypothalamus
60
what hormones are released by the posterior pituitary?
ADH (vasopressin) and oxytosin
61
which pituitary is part of the brain, posterior or anterior?
posterior
62
how is the anterior pituitary connected to the brain?
hypophyseal portal vessels from the hypothalamus, no nervous connection
63
how are hormones from the hypothalamus delivered to the anterior pituitary?
secreted into the primary capillary plexus, delivered from there in hypophyseal portal vessels to anterior pituitary
64
what are the 6 main hormones secreted by the anterior pituitary?
ACTH, TSH, GH, prolactin, FSH, LH
65
what pattern of hormone release does the anterior pituitary use?
pulsatile
66
what does ACTH stand for?
adrenocorticotropic hormone
67
structure of ACTH?
39 aa hormone
68
what does TSH stand for?
thyroid stimulating hormone
69
structure of TSH?
glycoprotein with 2 subunits
70
target organ of ACTH?
adrenal gland
71
target organ of TSH?
thyroid gland
72
what is GH?
growth hormone
73
structure of GH?
191 amino acids
74
target organ of GH?
various
75
structure of prolactin?
199 amino acids
76
target organ of prolactin?
breast and other tissues
77
structure of FSH?
glycoprotein with 2 subunits
78
target organ of FSH and LH?
gonads
79
structure of LH?
glycoprotein with 2 subunits
80
what do lesions in the hypothalamus produce?
atrophy of some endocrine glands- similar to observed effect of removal of anterior pituitary
81
what does electrical stimulation of hypothalamus lead to in the adenohypophysis?
secretion of anterior pituitary hormones
82
what is the result of transection of the pituitary stalk?
atrophy of some endocrine glands
83
what happens when anterior pituitary transplanted to another site with and without a blood supply connection with hypothalamus established?
without doesn't restore endocrine gland function, with will maintain endocrine gland function
84
what is the effect of adding purified hypothalamic releasing hormones to pituitary explants in cultures?
secretion of anterior pituitary hormones
85
how long is the approximate cycle of circadian rhythms?
24 hours
86
how long is the periodicity of pulsatile rhythms?
less than 24 hours (usually every 30 mins-2 hours)
87
what causes pulsatile rhythms of endocrine secretions?
pulsatile secretion of hypothalamic releasing hormones
88
what do pulsatile rhythms ensure?
no down-regulation of pituitary receptors
89
what is the eventual effect of continuous hypothalamic hormone secretion?
decreased hormone production from the anterior pituitary
90
what additional changes in release patterns do sex hormones show?
changes according to breeding season or oestrous cycle
91
what happens in negative feedback?
hormone produces response in the target cells that feeds back on the endocrine tissue to decrease hormone production
92
what happens in positive feedback? (hormones)
hormone produces response in target cells that feeds back on the endocrine tissue to increase hormone production. hormone production continues until hormone is depleted or feedback from target tissue is removed
93
how are hormones usually measured?
by immunoassays
94
what type of enzyme reaction is needed for an ELISA?
one that catalyses a colour change
95
what type of isotope is needed for an RIRIA (radio-immunoassay RIA)?
a radioisotope
96
what happens in a general ELISA?
sample with unknown amount of hormone immobilised in wells of microtiter plate (often via an antibody), detection antibody covalently linked to an enzyme added forming a complex with the hormone, between each step plate washed to remove antibodies that aren't specifically bound. the antibody/hormone complex is detected by adding enzyme and substrate that catalyses reaction with colour change, higher hormone concentration in original sample= greater visual signal
97
what happens in a competitive ELISA?
the sample containing the hormone to be measured is mixed with fixed amount of the same hormone labelled with the enzyme. greater amount of hormone in sample= greater competition with labelled hormone for binding to the well. the higher the hormone conc. in original sample = the lower the visual signal
98
what characteristics are shared between both ELISA assays?
standard curve generated using pure hormone at known concentrations, comparison with unknown samples must be in linear range of standard curve
99
where are the adrenal glands located?
above each kidney
100
what does the outer cortex of the adrenal gland secrete?
glucocorticoids, mineralocorticoids and small amount of sex steroids
101
what does the zona glomerulosa secrete?
aldosterone (principal mineralocorticoid)
102
what is aldosterone responsible for?
homeostasis of blood pressure, sodium and potassium levels
103
what does the zona fasciculata secrete?
cortisol (principal glucocorticoid)
104
what is cortisol responsible for?
glucose homeostasis and stress responses
105
what does the zona reticularis secrete?
weak androgens (DHEA)
106
what does the inner medulla secrete?
adrenaline and noradrenaline - catecholamines
107
what are adrenal steroid hormones derivatives of?
cholesterol
108
what neurones release CRH, where are they found?
hypothalamic neurones, in paraventricular nucleus of hypothalamus
109
what does ACTH regulate and what doesn't it regulate in the adrenal glands?
stimulates glucocorticoid and sex hormone production from adrenal cortex, doesn't regulate mineralocorticoid or catecholamine secretion
110
what is ACTH derived from?
proteolytic processing of POMC
111
what regulates mineralocorticoid secretion?
renin-angiotensin system and plasma levels of Na+ and K+
112
what are mineralocorticoids responsible for?
conservation of body sodium by stimulating resorption of sodium in the kidney in exchange for potassium
113
what are glucocorticoids responsible for?
changes in carbohydrate, fat and protein metabolism. cortisol has weak binding to mineralocorticoid receptor- at high levels can act like aldosterone
114
when are cortisol levels highest? why?
first thing in the morning, decline during the day. probably reflects the body's response to low blood glucose after overnight fasting
115
what are most of the actions of cortisol aimed at?
dealing with stressful events such as trauma
116
effects of cortisol relating to starvation?
promotes FFA release from adipose tissue, promotes breakdown of muscle and plasma proteins to provide amino acids, promotes gluconeogenesis, increases appetite
117
effects of cortisol relating to inflammation?
inhibits synthesis of substances that cause inflammation
118
effects of cortisol relating to the immune system?
inhibits secretion of interleukins, increases apoptosis of lymphocytes, decreased antibody production
119
what do interleukins do?
released by macrophages, attract lymphocytes to point of infection. promote secretion of CRH, ACTH and cortisol
120
effects of cortisol relating to the fetus?
causes surfactant production, deposition of glycogen in liver, causes intestinal tract to secrete and absorb, acid secretion by stomach, increased filtration rate in kidney, causes T4 -> T3 conversion, in some species causes placenta to change steroid secretions into mother initiating birth
121
effects of cortisol relating to the CNS?
can cross blood-brain barrier, can alter mood (cause euphoria), causes jet-lag
122
effects of cortisol relating to the cardiovascular system?
allows vasoconstrictive actions of catecholamines, adrenaline causes smooth muscle contraction so blood vessel constriction, important in maintaining blood pressure, stimulates erythropoietin synthesis to increase RBC production
123
% of adrenaline vs noradrenaline secreted by the adrenal medulla?
80% adrenaline, 20% noradrenaline
124
actions of catecholamines?
stimulate heart rate, increase heart contractility, CO and systolic pressure, reduce diastolic pressure, piloerection, dilation of pupils, reduced gut motility, increased breakdown of glycogen to glucose in liver, increase glycogen breakdown in liver, reduce gut motility
125
what causes release of catecholamines from the adrenal medulla?
sympathetic nervous stimulation of chromaffin cells
126
what causes hyperadrenocorticism (Cushing's syndrome)?
excessive glucocorticoids
127
what causes Cushing's syndrome?
adrenal gland tumour, increased ACTH, increased CRH, exogenous corticosteroid treatment
128
typical symptoms of Cushing's syndrome?
weight gain, rosy cheeks, skin pigmentation, skeletal muscle wasting, purple abdominal striations, capillary fragility, suppression of immune system, glucose intolerance, hyperglycaemia, insulin resistance
129
how many cases of canine Cushing's are caused by pituitary tumours?
80%
130
signs of canine Cushing's?
pot bellied abdomen- enlarged liver and abdominal muscle weakness, polyuria/polydipsia, muscle wasting over head shoulders, thighs and pelvis, polyphagia
131
symptoms of equine Cushing's syndrome?
excessive hairy coat, polyuria/polydipsia, muscle wasting, sweating
132
what is Addison's disease?
primary hypoadrenocorticism
133
what does primary hypoadrenocorticism result in?
deficiency of both glucocorticoids and mineralocorticoids
134
what causes Addison's disease (primary hypoadrenocorticism)?
destruction of adrenals, autoimmune reaction/inflammatory disease, haemorrhage
135
what does secondary hypoadrenocorticism result in?
deficiency of glucocorticoids
136
what causes secondary hypoadrenocorticism?
lack of ACTH
137
typical symptoms in absence of aldosterone and cortisol?
tiredness, weakness, vomiting, skin pigmentation, eventually hypotension and death
138
symptoms of ACTH production impairment (so cortisol and sex hormone production impairment)?
loss of body hair in females, males get sex hormones from their testes
139
what causes congenital adrenal hyperplasia?
lack of enzyme involved in cortisol production, increases in CRH-ACTH levels to compensate
140
what does congenital adrenal hyperplasia cause?
excessive production of sex steroids, masculinisation of female fetus in utero, precocious puberty caused by excess adrenal androgen, decreased production of mineralocorticoids
141
where is the thyroid gland located?
attached to the trachea just below the larynx, has rich blood and autonomic nerve supply
142
what nerve supply does the thyroid gland receive?
sympathetic and parasympathetic (vagus) nerves
143
what 3 hormones does the thyroid gland secrete?
thyroxine (T4), tri-iodothyronine (T3) and calcitonin
144
what is the histological structure of the thyroid gland?
contain 1000s of follicles- each consists of central colloid filled cavity surrounded by epithelial cells, nerves control blood supply, c cells scattered between follicles
145
where are T3 and T4 in the thyroid gland?
the 2 iodine containing hormones (T3 and T4) are attached to thyroglobulin and stored in the colloid material.
146
what cells secrete calcitonin?
the C cells (parafollicular cells) secrete calcitonin which is involved in regulation of plasma Ca2+ levels.
147
what is the most potent thyroid hormone?
tri-iodothyronine (T3)
148
what enzyme in target tissues and the pituitary converts T4 to T3?
deiodinase enzyme
149
how are the iodine containing thyroid hormones synthesised from tyrosine?
iodine is attached to tyrosine to produce mono-iodotyrosine (MIT) and di-iodotyrosine (DIT). MIT and DIT are coupled to produce T3, DIT and DIT are coupled to produce T4
150
how can thyroxine be converted into T3 and rT3?
removal of an iodine atom
151
what is rT3?
inactive tri-iodothyronine
152
what are the principal steps in synthesis of thyroid hormones?
uptake of iodide from blood by sodium-iodide symporter (SLC5A5) and addition of iodine to exposed tyrosine residues of thyroglobulin protein in the follicles. thyroglobulin internalised into follicular cells by endocytosis and broken down in lysosomes to release T3 and T4 into the circulation
153
what does TSH stimulate in the thyroid gland?
iodide uptake and oxidation to iodine, endocytosis of thyroglobulin and secretion of T3 and T4 into the blood
154
how do thyroid hormones enter cells?
lipophilic so passive entry, also transport mediated entry
155
cellular effects of thyroid hormones?
increase BMR so increase heat production, heat generation by stimulating Na+/K+ ATPase pump, increased cellular respiration, increase number of mitochondria per cell
156
what is the overall effect of thyroid hormones?
increases the substrates for oxidative respiration in the cell
157
what do thyroid hormones effect?
whole body growth, basal metabolic rate and CO
158
effect of calcitonin?
reduces plasma CA2+ levels, inhibits osteoclast activity in bone, inhibits Ca2+ resorption in kidney.
159
effect of parathyroid hormone on calcium regulation?
increases plasma Ca2+ levels
160
effects of thyroid hormones on metabolism?
increase glucose uptake by muscle and adipose, and by GI tract, increase release of FFAs from adipose, increase gluconeogenesis, increase substrates for oxidative respiration, increase CO, T3 enhances effects of catecholamines, GH secretion, CNS development
161
what does T3 do in peripheral thermogenesis?
acts on muscle to stimulate Na+/K+-ATPase, glycerol phosphate dehydrogenase (GPDH), uncoupling protein 2 and SERCA to generate heat
162
what does T3 do in general thermogenesis?
acts at the ventromedial hypothalamus (VMH) to inhibit AMP kinase and increase sympathetic nerve action on brown adipose to generate heat via uncoupling protein 1 (UCP1)
163
what causes hypothyroidism?
iodine deficiency, disease of thyroid, lack of TSH, congenital absence of thyroid
164
symptoms of hypothyroidism?
weight gain, possible goitre, cold extremities, lethargy, muscle weakness, reduced CO and slow pulse
165
long term effects of hypothyroidism?
short stature, lack of thyroid hormone during late fetal life and early post-natal development results in severe mental retardation
166
treatment of hypothyroidism?
oral administration of thyroxine
167
what causes hyperthyroidism?
overactivity of thyroid gland (hyperplasia and thyroid adenomas), autoimmune response (Graves' Disease, causes 50%)
168
symptoms of hyperthyroidism?
weight loss, sweating, tremor, possible goitres, agitation and nervousness, fast heart rate, atrial fibrillation, muscle weakness, rapid growth rate and bone maturation in children, staring eyes, infertility and lack of periods
169
symptoms of feline hyperthyroidism?
weight loss, rapid heart rate, vomiting/diarrhoea, increased water consumption
170
common cause of feline hyperthyroidism?
benign thyroid adenoma
171
treatment for hyperthyroidism?
anti-thyroid drugs to block hormone production, oral thyroxine, surgery, destruction of thyroid by radioiodine treatment
172
what does TRH from the hypothalamus stimulate?
thyrotrophs in anterior pituitary to release TSH
173
when is human fetal growth greatest, what is the survival % after this point?
16-20 weeks gestation, greater than 50% after this point
174
what does an earlier growth spurt mean for final height?
shorter
175
when is the incidence of childhood lymphomas highest?
10 years old
176
3 factors involved in growth?
genetic, environmental (nutrition), physiological (GH)
177
structure of human GH?
191 amino-acid polypeptide with 2 internal di-sulphide bridges (tertiary structure critical for receptor binding)
178
what secretes GH?
somatotrophs in anterior pituitary
179
factors increasing GH release?
GHRH, arginine, lysine, ornithine, ghrelin, gonadal steroids, hypoglycaemia, sleep, exercise, thyroid hormones
180
what releases GHRH?
arcuate neurons in hypothalamus
181
what is used clinically to diagnose GH deficiency?
arginine (should be low in deficiency), hyperglycaemia
182
what is involved in the GH surge at puberty?
gonadal steroids
183
what decreases GH release?
GHIH (somatostatin), GH + IGF1 (negative feedback), lipids, age, thyroid deficiency, hyperglycaemia, dopamine
184
structure of GHIH (somatostatin) and where is it released from?
14 a.a. peptide from periventricular neurons in hypothalamus
185
what is used to treat excess GH?
dopamine agonists
186
effect of GH on bone growth?
stimulates chondrocyte mitosis at the epiphyseal growth plate, stimulates osteoblasts to deposit new bone on surface
187
what hormone limits long bone growth and how?
sex steroids by triggering epiphyseal fusion
188
effect of GHRH?
stimulates somatotrophs in anterior pituitary to produce GH
189
structure of the GHRH receptor?
G-protein coupled receptor that signals via Gs to increase cAMP in somatotrophs
190
what opposes action of GHRH?
somatostatin (GHIH)
191
how can GH exert indirect effects?
via production of somatomedins (e.g. IGF1) by the liver
192
what sort of molecule is IGF1?
somatomedin
193
metabolic effects of GH?
inhibition of glucose uptake by muscle and fat cells, increased lipolysis, increased sodium and fluid retention, increased BMR, hepatic gluconeogenesis, reduced insulin sensitivity, synergistic with cortisol, antagonistic with insulin, increase glomerular filtration rate in kidney and Na+/fluid retention
194
why is GH diabetogenic?
synergistic with cortisol and antagonistic with insulin
195
types of growth factors?
nerve GF, epidermal GF, transforming GF, fibroblast GF, platelet-derived GF, erythropoietin, interleukins
196
what are growth factors usually?
small secreted peptides that act locally to promote growth of specific cell types
197
systemic high gonadal hormone effects?
stimulates GH release- bring about pubertal growth spurt, increased rate of long bone growth
198
local high gonadal hormone effects?
loss of chondrocytes, epiphysial fusion, sex steroids eventually trigger epiphyseal fusion to limit long bone growth
199
effect of excess glucocorticoids on growth?
inhibit growth
200
relationship of insulin and IGFs with growth?
essential for normal growth, especially in utero
201
cause of gigantism?
hypersecretion of GH before puberty
202
cause of acromegaly?
hypersecretion of GH in adulthood
203
most common cause of acromegaly?
pituitary tumour
204
is acromegaly more common in dogs or cats?
cats
205
clinical appearance of acromegaly?
increased cartilaginous growth- so enlarged ears and nose, growth of jaw, enlarged hands, feet and tongue
206
effect of GH deficiency during childhood?
pituitary dwarfs- reduced growth but normal body proportions
207
GH deficiency in childhood treatment?
GH injection
208
difference between pituitary dwarfism and achondroplasia?
in achondroplasia normal body proportions aren't found
209
common cause of achondroplasia?
mutation in FGFR3
210
what is a (kilo)calorie?
energy needed to warm 1 (k)g of water by 1 degree
211
what is basal metabolic rate?
energy required to keep a resting, awake individual alive in a thermoneutral environment
212
what is indirect calorimetry?
measurement of the amount of heat generated in an oxidation reaction by determining the intake or consumption of oxygen or measuring the amount of CO2 released and translating these quantities into a heat equivalent
213
factors that increase BMR?
infection/high temp, high growth rate, pregnancy, lactation, menstruation, large size, high stress, male gender
213
factors that decrease BMR?
low temp, old age, starvation, female gender
214
effect of insulin on energy storage?
promotes it
215
effect of glucagon on energy storage?
decreases it
216
which hormones improve the response of the endocrine pancreas to absorbed nutrients?
GLP-1, GIP and potentially OX
217
what is GLP-1?
glucagon like peptide 1
218
what is GIP?
gastric inhibitory peptide
219
how do GLP-1, GIP and maybe OXM improve the response of the endocrine pancreas to absorbed nutrients?
act on pancreatic islets of Langerhans to stimulate insulin and inhibit glucagon production
220
what cells produce GLP-1?
L cells in GI tract
221
what cells produce GIP?
K cells in duodenum
222
which areas of the hypothalamus regulate food intake?
satiety centre in ventromedial hypothalamus and feeding centre in lateral hypothalamus
223
effect of destruction of the lateral hypothalamus in rats
reduces food intake
224
effect of destruction of the ventromedial nucleus in rats?
induces hyperphagia and obesity
225
what does anoretic mean?
causes appetite suppression
226
what does oretic mean?
causes appetite stimulation
227
what experiment was performed to identify a blood borne satiety factor?
parabiosis experiments in rats- connect obese rat with VMN lesion and normal rat- normal rat stopped eating and died
228
structure of leptin?
16 KDa protein
229
what produces leptin?
white and brown adipose tissue
230
what is the level of leptin in the blood directly proportional to?
amount of adipose tissue in the body
231
effect of mutation in leptin/leptin receptor gene in mice?
hyperphagic, obese, increased risk of developing type 2 diabetes
232
effect of leptin injection in ob/ob and db/db mice?
induces weight loss in ob/ob mice, not in db/db mice
233
structure of ghrelin?
28 a.a. peptide hormone
234
what cells produce ghrelin?
P/D1 cells in fundus of stomach, ε-cells in islets of Langerhans
235
how does ghrelin signal hunger?
stimulates NPY/AgRP neurons in hypothalamus
236
effect of ghrelin on pituitary?
increases GH secretion
237
relationship between ghrelin and insulin levels after each meal?
inverse
238
change in GH secretion when stomach is pretty full (after full meal)
decreases
239
what do anoretic produce?
POMC peptides: MSH, CART
240
what does POMC stand for?
pro-opiomelanocortin
241
what does MSH stand for?
melanocyte stimulating hormone
242
what does CART stand for?
cocaine and amphetamine stimulated transcript peptide
243
what receptors does MSH act on?
melanocortin receptors MC3 and MC4
244
what is the effect of alpha MSH?
suppresses feeding
245
effect of defective MC4R in humans?
leads to obesity
246
what do oretic neurons contain?
NPY and AgRP
247
what is NPY?
neuropeptide Y
248
what is AgRP?
agouti related peptide
249
what is the effect of NPY?
acts on Y receptors to stimulate feeding
250
what is the effect of AgRP?
antagonist of MC3/4 R activity
251
how does leptin cause anoretic effects?
inhibits the activity of NPY/AgRP neurons and increases activity of POMC/CART neurons
252
what signals regulate food intake?
signals from leptin, neuronal pathways, gut peptides, ghrelin
253
how do neuronal pathways provide information about food digestion and stomach distension to the DVC?
via the vagus nerve
254
what is the DVC?
the dorsal vagus complex
255
what gut hormones released from the lower GI tract stimulate satiety?
cholecystokinin (CCK), oxyntomodulin (OXM), PYY, GLP-1
256
what does pancreatic polypeptide do and where is it released from?
stimulates satiety, released from islets of Langerhans
257
what are the medical/pharmalogical treatments for obesity?
eat less, exercise, liposuction (cosmetic), restrict food absorption
258
what does bariatric surgery involve?
reduction of stomach volume using gastric band or gastric bypass surgery- limits amount patient can eat at one time and slows passage of food
259
what is bariatric surgery most effective when combined with?
a malabsorptive technique to bypass part of the digestive tract to reduce absorption
260
effect of bariatric surgery on ghrelin, PYY and GLP1?
reduces ghrelin, increases PYY and GLP1
261
what is Xenecal?
a lipase inhibitor that prevents digestion of lipids
262
side effect of xenecal?
steatorrhea
263
difference in solubility of peptide/protein and steroid/iodine containing thyroid hormones?
peptide and protein are water soluble, steroid/iodine containing thyroid hormones are fat soluble
264
difference in storage of peptide/protein and steroid/iodine containing thyroid hormones?
peptide/protein often substantial in secreting cell in secretory granules, in steroid/iodine containing storage is minimal
265
difference in half life of peptide/protein and steroid/iodine containing thyroid hormones?
short (minutes) and long (hours) respectively
266
target cell-binding site of peptide/protein and steroid/iodine containing thyroid hormones?
p/p target cell-surface receptor to start G protein pathway, s/i target cytoplasmic/nuclear receptor
267
site of action of peptide/protein and steroid/iodine containing thyroid hormones?
plasma membrane and nucleus respectively
268
process of catabolism in peptide/protein and steroid/iodine containing thyroid hormones?
proteases in lysosomes and modification in liver respectively
269
time course of action of peptide/protein and steroid/iodine containing thyroid hormones?
rapid onset and short duration vs long latency and duration respectively
270
difference in transport of peptide/protein and steroid/iodine containing thyroid hormones?
p/p not usually associated with binding proteins, s/i associated with specific binding proteins
