PSL-Last 2 lectures on Endo Flashcards
What are the processes the body utelze during fasted state to build up the energy it needs
those processes are glucogenolysis, lipolysis, and protein degradation
which are considered the catabolic parts of metabolism
How does the body converts thefod it obtains to energy
through anabolic part of metabolism, by glycogenesis, glyconeogenesis, lipogenesis, and protein synthesis
What is metabolism
it is the sum of chemical reaction sin the body which consist of two types of chemical reactions: anabolic and catabolic and each of those two reactions will occur at a state:
the body has 2 states, in the Fed state the body will have anabolic chemical reactions where it builds up macromolecules and in the Fasted state there is catabolic reactions where those build up macromolcules will get broken down to provide body with the energy it needs
When is the body considered in a fast state
3-4 hours after eating
What is the BMR
basal metabolic rate, where individual’s energy expenditure when resting, comfortable temp, and fasted state
What is energy balance
a control caloric intake and exercise
How does glucose get inside cells
using glucose transporters called GLUT and the two most important ones are GLUT 2 and GLUT 4
How are the two GLUT receptores, GLUT 2 and GLUT 4 different
GLUT 2: found in liver, pancreas, and intestines and kidneys, it is a glucose transporter and insulin secretion
GLUT 4: found in adipose tissue and skeletal muscle , it is glucose transporter but it is insulin dependent since more GLUT 4 get glucose in when there is insulin secretion
What are the endocrine cells in pancreas
alpha cells: which make glucogon
beta cells : which makes proinsulin that gets cleaved into C peptide and insulin
gamma cell: make somatostatin which is involved in growth
But the pancreas also contain exocrine cells that produces bicarbonate and proenzymes used for digestion
How does the insulin and glucagon change gears between feeding and fasting states of a cell
the two are antagonists of each other, they will target the same cell but will depends on which receptor will be bound as the insulin binds a receptor ensyme while the glucagon will bind a G receptor protein and as we know, different receptores lead to different cascades of signalling pathway
How is controlling glucose concentration using homeostasis by insulin to glucagon ratio achieved
glucagon is high in fast state and starts dropping after a meal due to increase in insluin which also increase glucose present in cell
in fed state, there is increase in glucose and that glucose needs to into cell and by doing so will cause release of insluin from the pancreatic cell and since insulin is antagonist of glucagon, in fed state, the glucagon levels are low
Other than insluin being high in fed state, what are some of its other characteristics
it is a peptide hormone which binds the receptor tyrosine kinase and its job is to reduce blood glucose levels by taking in that glucose into the cell and will use that glucose to promote formation of glycogen, fat, and protein by promoting anabolic pathways
Steps involved in the mechanism of insulin action
once insluin has ben released, it binds the tyrosine kinase receptor which cause phosphorylation of IRS( insulin receptor substance) which then will cause second messengers pathways to be signalled and those pathways will have affect on receptores and in enzymatic activites of the cell by having GLUT 4 let in more glucose and by increasing in enzymes that will catalyze anabolic pathways so that glucose doesn;t get too much in the cell
What is the exception that will let GLUT 4 receptores be found in the membrane
since GLUT 4 receptores are insluin dependent, if there is no insulin, they are stored inside the cell, but they can also be exocytosed onto teh emmebrane even if there is no insulin because of excercise and be used for energy in muscle cells
How does liver cell uptake glucose without stopping?
liver cells also express GLUT 2 transporters and gluconeogensis happen in the liver so glucose can build up in liver cell but with a mechanism, the liver cell can still uptake glucose: when the insulin binds the tyrosine kinase receptor and activate signalling pathway, that pathway will activate hexokinase enzmye which will convert glucose to glucose 6 phosphate which will keep internal glucose low so more glucose can be taken
What is incretin effect and how is it involved with insulin
incretin effect is the increase in insulin in response to glucose injected into intestine because of incretin hormones whicb are GIP 1 and GLP 1
What are the charactersitics of GIP 1 vs GLP 1
GIP 1: a glucose dependent insulinotropic polyppetide which is released by k cells in small intestines due to nutrients present in intestinal lumen and GIP 1 receptor is G proetin with alpha subunit found on beta cells
CLP 1: is glucagon like peptide which is released by L cells in small and large intestine due to presence of nutrients in intestinal lumen and the GLP 1 receptor is also a G protein with alpha subunit on the beta cells to stimulate insulin release
How does GLP 1 further stimulate the release of insulin from beta cell
since it has a G protein with alpha subunit, when it binds it, it activate the subunit which will adenylyl cyclase to make cAMP that phoisphorylate EPAC and PKA which further causes release of Ca ions to increase exocytosis of insulin
What are regulators of insulin secretions, both stimulations and inhibitions
the stimulations ones are: increase plasma glucose, have the intecrine hormones GIP 1 and GLP 1 released due to nutrients in lumen of the intestines which is also known as feedforward regulation, increases amino acids plasma, and have parasympathatic nervous system impact
inhibitions: sympathatic nervous system
What is role of glucagon release during fasted state
glycogeonolysis, gluconeogenesis, and ketogenesis, it basically targets the liver where all of these occur
What is the main role of glucagon
to prevent hypoglycemia by triggering activation of cascade of signalling moilecules inside hepatocytes where each is transmitting and amplifying fasting signal
How does glucagon promote movement oif glucose out of hepatocytes
since glucose is needed for the body to have energy, glucogan is high since it is in fasted state and needs that glucose in bloodstream and not stored so the glucagon will bind its G receptor and activate a phosphorylase which will cause high glucose concentration in the cell so that it will be chemicallly driven out of cell and into bloodstream where there is low glucose levels
How is cortisol invoved in glucagon and epinephrine
cortisol is always found in body in some amount anf helps glucagon and epinephrine by increasing their effects, it has permessive effects as glucagon needs corticol
what are the regulatores of glucagon secretionb, both teh stimulations and inhibitions
stimulations: decrease plasam glucose, increase plasma amino acids, and a sympathatic nervous system
inhibitions : glucagon like peptode ( GLP 1)
What are teh active hormones that can be cleaved off from a proglycagon
if in alpha cells, it will be cleaved as glucagon but if in L cells and in bran, it will eb cleaved off as GLP 2 and GLP 1
What are the two types of diabetes mellitus and how do they differ
Typpe 1: insulin indepedent diabetes, mostly in kids/youth, it makes up 10% of diabatics, and insulin secretion is reduced or absent so they are treated by insulin in injections or insulin pumps
Type 2 : is noninsulin dependent and mostly affect older population, makes up 90% of diabatics, defect in insulin secretion and target xcell responsivness to insulin is reduced ( 1 glucose caused receptores to desensatize and because unresponsive), treated by diet/excercise/cause translocation of GLUT 4 to membrane and oral hypoglycemics
what is the pituitary gland consist of
2 fused glands, the posterior and an terior pituitary gland
what are the products of posterior pituitary vs anterior pituitary
posterior pituitary: a nueral tissue that secreted 2 nueurohormones: vassopressin and the exytocin
the anterior pituitary is the true endocrine gland tissue that secretes 6 hormones: prolactin, thyrotropin, adrenocorticotropin, grpwth hormone, follicle stimulating hormone, and luteinizing hormone
How is bone mass related to age
as we age, the bone masss is lost and the decrease is greater in females as they have menopause and overall what happens is trhat from baby to adult, the cartilage gets ossified little by little until growth plates are closed so it starts going backward now by losing bone past age of 40
How does the state of the bone as we go fron in untero to adolescent to adult changes
in untero: soft bones with cartilage not fully ossified and active growth plates
in adolesecnt: bone fully ossified and growth plates closing toward end of puberty
in adult: the growth plates cloased and bone loss startes past age of 40
How does bone grow, from being cartilage to being ossified
cartilage is made by chondrocytres amnd these chondrocytes will make the cartilage of the bone, but the very old ones after producing their fair share of cartilage will get disintegrate which allow osteoblasrts to lay new bone on top of the cartilage
When does bone growth cease
when epiphyseal plates fuses
What are characteristics of growth hormone
it consist of 191 amino acids and released from anterior pituitary, is stimulayed by GHRH from hypothalamus and inhibited by somatostatin, acts on the liver to stimulate IGF release which is involved in catabolic processes and IGF causes responses of cartilage growth/increased blood glucose/and bone and tissue growth, its receptor is also a tyrosine kinase
What is the effect of IGF1 on the chondrocytes
it increases their recruitment, their proliferation, and their matrix
What are the three effects of GH
1- glucose sparing: stimulate adipose cells to break down stored fats
2- growth: increase uptake of aa from blood and enhance cellular proliferation and reduces apoptosis
3- disbetogenic- stimulate liver to break down glycogen into glucose and fueling the gorwth effect
What does growth depend on
diet and genetics, hormone and growth factors: growth hormone and IGF1, thyroid hormone, insulin, sex steroids, and cortisol
where thyroid hormone’s effect is strongest during early ages and then starts declining, the growth hormone’s efefct is there after birth and until late puiperty and stops at 20, and the sex steroids effect not happening until later after puiperty until age of 20
What can having too much GH cause
1- giantism if there is too much GH in childhood
2- acromegaly if there is too much GH in adulthood which causes increase in otrher bone structures and tissues since it cannot just expand like in child
What is the source of thyroid hormone
thyroid follicle, C cell, follicular cells, and colloid but is synthesized from iodine and tyrosine
How does tyrosine get made and released into bloodstream
there is a NaI symporter on the follicular cells and that will bring in iodine into the cell with sodium and that iodine gets released into the colloid by pendrin transporter and the folloid cell will also synthesize enzymes and thyroglobulin for the colloid and those get exocytosed into the colloid and one of those enzymes, the thyroid peroxidase will add iodine to the tyrosine and make T3 and T4
then the thyroglobulin will be takesn back into folloid cell by endocytosis and then the incellular enzymes will speprate T3 and T4 from thyroglobulin and that free T3 an T4 will go into circulation
what are the structural components of T3 and T4
T3 consist of 2 tyrosine with 3 iodine added
T4 consist of 2 tyrosine with 4 iodine added
how is thyroid hormone regulated
by the hypothalamus, when there is stimuli received by hypothalamus to release TRH which is a thyrotropin releasing hormone, that will go to the anterior pituitary and cause release of TSH which is a ppetide hormone called thyroid stimulating hormone and the role of this hormone is to activate the G protein cascade acting via adenylate cyclase to stimulate synthesis and activities of enzymes involved in T4 and T3 synthesis and will also activates transcription factors like c-fos, c-myc, and stimulate thyroid growth
What are teh mechanism of actions of thyroid hormones
T3 and T4 circulate in the blood bound to plasma proteins, T3 is 3-5 times more potent than T4 so T4 get converted to T3 in target tissues and both can bind nuclear thyroid receptiores
What are the functions of thyroid hormone
metabolically- affect metabolic rate, oxygen consumption, heat production, peotein degradation, and lipolysis
nervous system- enhances speech, thinking, and reflexes
growth nad development- essential in children, works with GH
cardiovascular- enhances heart rate and contractility, peripheral blood flow, work in part by increasing number of beta adregenic receptores an dother proteins
What is hyperthyroidism and what are the causes/sympotoms/treatment
hyperthyroidism is when there is thyroid hormone excess which is caused by: tumour and thyroid stimulating immunoglobulins(Grave’s disease),
sympotoms are goiter, nervousness, insomina, anxiety, high heart rate, exophthalmos (Grave’s disease), weight loss
treatment- removing part of thyroid gland, drug blocking synthesis of T3 and T4, or blocking conversion of T4 into T3
What is Grave’s disease
an autoimmune disease where the body’s own abnormal antibodies against TSH receptor are produces, the causes are unknown, but it is most common cause of hyperthyroidism and most coomon cause of general thyroid enlargement in developed countries
What is hypothyroidism, what are its causes/symptoms and treatments
it is a thyroid hormone deficiency,
causes- underactive thyroid gland, lack of iodine in diet
symptoms- goiter, slowed HR, slowed speech, fatigue, cold intolerance, cretinism in infants, stuned growth in infants, and weight gain
treatment- exogenous thyroid hormone T4
how does iodine deficiency cause goiter which leads to many health issues
iodine defiency menas there is lack of negative feedback leading to excess TSH stimulation but since they thyroid gland is unable to produce T4 and T3, the TSH keeps stimulating growth of thyroid gland leading to goiter
what are the symptoms of mild deficiency to severse deficiency
mild deficiency- nodular goiter and hyperthyroidism with lower eductability
mid deficiency- causes increased infant mortality, goiter, and hypothyroidism
severe defiuciency- cause mental retardation and poor growth
