Flashcards in Hormonal regulation of metabolism Deck (43):
what tissues are for fuel storage
1. liver and muscle: carbohydrates; glycogen
2. adipose: lipids; triglycerides
3. tissue and blood proteins: protein (no other storage form)
what is the fuel usage time line
after 8 hr; liver glycogen is depleted
after 24 hr; TGs provide energy for all tissues except for the brain and RBC; protein degradation provides glucose for brain
Several days: OAA depleted as shunted for gluconeogenesis; AcCoA builds up as FA's oxidized; Ketone bodies used as alternative fuel.
what insures brain function
glucagon; releases fuel from liver glycogen and adipose tryglycerides.
adipose, liver and muscle
what are longer term metabolic control hormones
2. Thyroid hormone
- first is steroid hormone
-second behaves like steroid hormone
-last two made by adipose tissue and are protein hormones
as fat stores increase adiponectin ___ whereas as fat stores increase leptin increases
what does stress trigger
cortisol secretion; responds to hypothalmic/pituitary signals Hypothalamus secretes CRH into portal system, anterior pituitary secretes ACTH into systemic circulation, adrenal cortex responds with secretion of cortisol.
Where does ACTH come from
a large precursor protein: made by a gene called Pro oplomelanocortin (POMC) gene
What are features of cortisol
fuel mobilizer, elevates blood glucose, mobilizes fat, inc muscle protein catabolism, is well known for its anti inflammatory effects
what is cushings syndrome
excess cortisol; weight gain of upper body and trunk, skin changes inc darkening of the skin and easy bruising, excess hair growth/acne in women, personality changes/mood swings and fatigue.
what is addisons disease
cortisol deficiency; changes in BP or heart rate, chronic diarreah, darkening of the skin, paleness, extreme weakness and fatigue. Loss of apetite and mouth lesions on the buccal mucosa
what happens if you have hyporthyroidism
cold sensitive, weight gain, fatigue, constipation, depression, brittle hair, and nails
congenital hypothyroidism: cretinism
what is hyperthyroidism
heat sensitive, weight loss, exopthalmia, insomnia, diarrehea, tremor
what is leptin
the "set point" hormone. when it gets knocked out you are hungry all the time. as fat tissue biulds up, more leptin produced to shut off hunger response
what kind of receptor does leptin use
what does leptin and insulin inhibit
production of oriexgenic neuropeptide Y which is a neurotransmitter that activates hunger response.
leptin and insulin activate:
anorexigenic peptides which are derived from proopiomelanocortin (POMC)
Receptor that responds to leptin is called
JAK/STAT receptor --> goes to nucleus and ponds to POMC and causes them to be inc in transcription
Receptors bind and dimerize and recruit JAK kinase to them phosophorylates a transcription factor which goes into nucleus and activates:
what is adiponectin
opp of leptin. Less FAT more adiponectin. Gets turned on as you lose weight thus low levels in obseity. Related to type 2 diabites. Inc sensitivity to insulin.
what is a receptor for adiponectin
AMPK; major target for diabetic drugs. Impt in blood glucose regulation. Inc fatty acid and glucose uptake. Inc beta oxidation. Decreases gluconeogenesis and fatty acid synthesis. In summary, it inhibits energy consuming processes and activates energy producing processes
what is a target for AMPK
acetyl CoA carboxylase which is first enzyme inv in FA synthesis and inactivates it.
Excerise and AMP Kinase increases what
mobilize glut 4 transporters in membrane which lowers blood glucose levels. This is impt for diabetics
what is the signaling mechanism for bacterial products
what is the signaling mech for glucocorticoids
what is the signaling mechanism for cytokines
what is the signaling mechanism for thromboxane A2
what is the signaling mechanism for nitric oxide
what are toll receptors activated by
PAMPs such as lipopolysaccharide or flagella proteins; activates two major proinflammatory transcription factors: AP-1 and NFkB
what is the NFkB pathway
IkB kinase phophorylates IkB which is inhibitor of NFkB. But when IkB gets phosphorylated it gets ubiquinated and degraded then NFkB enters the nucleus and enhances the expression of inflammatory proteins.
what are some NFkB regulated genes
many interleukins, tumor necrosis factor alpha, cyclooxygenase, nitric oxide synthase, inhibitors of apoptosis, cyclin D and MMPs
what do glucocorticouids do
go into nucleus and repress NFkB and AP-1 binding (you wont get inflammatory response) but enhance STAT
what do glucocorticoids decrease transcription of
3. inducible enzymes
4. adhesion molecules
what do glucorticoids increase transcription of
3. MAPK phosphatase
4. beta 2 adrenergic receptors
what is pathway for thromboxane A2 receptor and angiotensin II?
G protein (Gq)--> phospholipase C --> hydrolyzes phosphatidylinositol - 4,5 bisphosphate --> releases DAG and inositol 1, 4, 5, triphosphate (IP3) --> opens up Ca++ channels and DAG activates PKC
what are some phospholipase C/IP3 mediated hormones
4. thryotropin releasing hormone
5. gonadotropin releasing hormone
6. thromboxane A2
7. Angiotensin II
what is the receptor enzyme guanylate cyclase
its a hormone receptor; no G protein required. Ultimately activates cGMP dependent protein kinase (PKG). its important in BP regulation. important for smooth muscle and ion channels
what are two types of guanylate cyclase
1. integral membrane proteins: activated by atrial natriuretic factor (ANF) and E. coli endotoxin
2. cytosolic protein with associated heme: activated by nitric oxide (NO)
which aa is precursor for NO
ANF goes to 2 places:
1. Kidneys: ANF binds type 1 GC receptor --> inc cGMP levels-->activates PKG which enhances Na+ channels which gets excreted and water gets excreted as well.
2. ANF receptors in vasculature, PKG targets Ca+ channels, which lowers cystolic Ca levels and dec smooth muscle contraction
Both even decrease BP
first gas to be recognized as hormone.
-short half life
what is the basis for nitroglycerin's action
NO: angina due to ischemia in area of heart muscle. Nitroglycerin is slowly degraded to NO which binds guanylate cyclase and inc cGMP levels which activates PKG which results in low cystolic Ca which causes relaxation of heart muscle