Lecture 12 Flashcards
complication with diabetes causes
the inability to utilized fats due to the low insulin in their system
insulin is known as the hormone of Glutton
insulin surges quickly when a person is eating even a small meal will promote a significant production/ release of insulin
insulin is a protein that
stimulate the uptake of glucose and store it as glycogen.
insulin as an effect on glycogenesis, what is glycogenesis
glycogenesis is the process of glycogen synthesis
if there is too much glucose insulin promotes
the conversion of glucose to fats in adiposites
insulin can increase the up amino acid that
promotes the synthesis in specific cells
insulin is produced by
the B cells found in the islets of langerhann
——- are converted to smaller protein
Preprohormones(proinsulin)
Preprohormones (proinsulin)
has three chains A, B, and C, A and B are linked by disulfide linkage and are biologically active, these are the insulin made by the pancreas, it is short lived, and it is broken down by the kidneys and liver. The C chain is removed at the Golgi network
The insulin receptor is located
on the outside of the cell membrane
IRS
insulin receptor substrate
IRS promotes
the recruitment of glucose transporters
Glucose transporter ( gluts)
there are 7 different transporters. they are located in vesicles and theses vesicles fuse to the membrane to bring the the glut to te surface of the membrane
the gluts allow glucose to go into the cell via
facilitated diffusion
without GLUTS
the cell membrane would be impermeable to glucose, therefore glucose cannot go into the cell
all cells in the body uses Gluts except
Neurons, glucose can diffuse through the neurons because it is the sole source of energy for neurons
in the muscle glucose is stored as
glycogen
During fasting
because there is no insulin the sarcolemma of the muscle cell does not have gluts to take up glucose in the blood
liver promotes polymerization of glucose
through glucogenesis
hepatocytes are
liver cells
hepatocytes take up glucose and promote
glycogenesis ( polymerization of glucose to glycogen )
Glucose kinase
traps the glucose in hepatocytes by phosphorylation
glycogen synthase
it polymerize the phosphorylated glucose to glycogen, this is activated by insulin
liver phosphorylase
participates in glycolysis to break down glycogen into glucose…insulin turn this off
when the liver is saturated, excess glucose
is turned to fatty acid in the liver , then bounded to protein made by hepatocyte, then transferred and stored in the adipocytes
hormone sensitive lipase
embedded in the adipocyte membrane this enzme breaks down fatty acid…. this is also inhibited by insulin, because the body does not want to break down fats and store it at the same time
glycerol is produced
in the adipocytes and insulin promotes its production
when the insulin binds to the receptor
the receptor becomes an active enzyme( tryosine kinase). the insulin receptor comes in pairs and they phosoporylate each other in a form of autophoshorylation. and phosphorylate IRS I II III
hypoglycemic shock
due to low level of glucose neurons are very susceptible to this can lead to neurological problems, cause seizure, fainting and in extreme cases come.
insulin effects on protein
promotes for the uptake of amino acid and conversion to protein
when glucose level in our blood increase
Gluts allows for the entry of glucose into the cell, the increase in glucose cell allows for the making of atp which affect the K channel by closing them leading to depolarization, causing a voltage gating effect allowing for Ca to enter the cell . ca will promote protein trafficking to lead the vesicle with insulin to be exocytosed
Diabetes Melitis
type i juvenile diabetes,occurs in early life,usually manifest in teen years, must be in replacement therapy for insulin for life, must be inject directly into the blood if consumed it will be denatured
insulitis
this is a type of type 1 diabetes,this is an autoimmune disease where the antigen attacks the B cells, the body can make antibodies that can can cause the disease. if the individual had all three antibodies they will most likely get this disease
the antibodies of insulitis
anti insulin, anti GAD( anti glutamic acid carboxylase), and anti IA antigen- attacks beta cells directly.
Diabetes type II
usually caused by defect in glucose transporter, linked to linked to obesity, studies have shown that when an individual exercise and lose the weight the illness goes away. can occur any time throughout ones life , the symptoms are similar to type I
Resistin
hormone produced by the fats and endocrine cell which is an antagonist to insulin, it blocks insulin recptor
symptoms of diabetes
excessive thirst and urination, retinoapathy, cardiopathy, nephropathy, and nervopathy( loss of nerve function)
excessive urination is caused by
glucose accumulates and disrupts the osmotic pressure, glucose is a solute and must be dissolved in water . water that is usually absorbed back is used to dissolve glucose. glucose in this case is a solute diuretic
glucogon
hormone of fasting, primary stimulator is low levels of glucose, aka hypoglycemic hormone, breaks down glucose , promote glucogenolysis, promotes gluconeogenesis , affects glycogon receptor with cAMP as a second messenger, glycogon levelare high when there is low level of glucose
calcium level is steady and essential it is an important electroyle that maintain functions
secondary messenger, transduction mechanism, bone structure, muscle contraction,calcium dependent exocytosis , endocytosis, and calcium dependent blood clotting
majority of Ca is stored in the
bone matrix small amount in the ECF and calicstome
calcium is stored in three way
in a complex with transport protein( this can not be utilized)
in form of a salt
bound with phosphate citrate
absorption of ca is dependent
on vitamin D and PTH( para thyroid hormone )
phosphate is stored in two forms
bisphosphate and dihydrophosphate
phosphate and calcium
usually work together and the used phospate and calcium are excreted though the kindneys
