Glucose Regulation - 216

endocrine organs role

synthesize and secrete hormones

endocrine hormones are released

into the bloodstream

example of endocrine hormones

insulin, epinephrine

pacrine hormones are release into

adjacent tissues only

pacrine hormone examples

histamine

secretetion of hormone triggered by

concentration of specific substances

neural stimulation

endocrine sequences

charecteristics of hormones

- long half life and likely high ppb (t4 hormone)

what regulates endocrine hormones

negativee feedback

function test used to find:

hormone level

affector substance level

hormone level example

T4

affector substance level example (indirect test of insulin fx)

blood glucose

dysfunctions

hyposecretition

hypersecretition

dysfunctions caused by

- primary endocrine disorder

- signaling disorder

- sequence disorder

causes of hypo secretion ddx

congenital defect

disease/infection/inflammatoin

hypoperfusion

ageing

causes of hypersecretion ddx

genetic

tumours

environmental stimuli (exposure)

signs and symptoms directly related to

excess or deficiet of the expected hormone

primary energy sources

glucose, fatty acids

glucose

readily distributed

most needy system

in the CNS/brain

brain

- requires constant supply of glucose

- cannot store glucose for later

glucose broken down to

carbon dioxide and water

extra glucose

stored as glycogen and triglycerides

where is glycogen stored

liver, muscles

triglycerides stored

in adipose tissue

fall in blood glucose

glycogen breakdown

formation more glucose from other sources

glycogen breakdown

glycogenolysis

what triggers glycogenolysis

glucagon

formation of more glucose from other sources

gluconeogensis

fatty acid distribution

via lymph to circulation

what cannot use fatty acids

- CNS

- RBC

extra fatty acids

stored as triglycerides

triglycerides are broken down into

3 fatty acids, and glycerol

glycerol

glycotic pathway into glucose

fatty acids

not converted into a glucose and cannot be used by the brain for energy

fatty acid metabolism →

ketone metabolite

fatty acids are not converted to

glucose and therefore can't be used by brain

insulin

pancreatic hormone

insulin is synthesized by

beta cells (Langerhans)

action of insulin

glucose cellular uptake

promote storage formation

prevents: glycogen and fat lysis and protein lysis

amino acid cellular uptake

promotes storage formation

glycogen synthesis

triglyceride synthesis

protein synthesis

fat lysis prevention

in order to first use glucose

prevent protein lysis

to preserve tissue

actions of insulin; amino acid cellular uptake;

triglyceride adipose cell uptake

glucagon is synthesized by

alpha cells

glucagon action

the opposite of insulin

glucagon purpose

promotes mobilization of stores

triggered by low plasma glucose levels

promoting mobilization of stores

glycogenolysis

gluconeogenesis

lipolysis

glycogenolysis

glycogen breakdown

gluconeogenesis

amino acid conversion into glucose

lipolysis

triglyceride breakdown

glucagon trigger

low plasma glucose levels

low plama glucose levels occurence

between meals (hypoglycaemia)

glucagon

mobilizes stores and replenishes bg for cellular use

glycemic regulation

optimum Gi delivery from serum to tissues

high blood glucose triggers

pancreas release of insulin

pancreas releases insulin →

- liver produced glycogen

- cells take up glucose from blood

low blood glucose triggers

pancreas release glucagon

pancrease release glucagon stimulates

liver to breakdown glycogen

blood glucose

4-8 mmol/L

insulin synthesis

stimulant is high serum glucose

glucose enters pancreatic beta cells via

glucose transporter

what happens when glycose enters beta cells

metabolized via glycokinase into ATP

what happens after glucose in merabolized

closes k channels on beta cells

closing k channels causes

depolaization

depoalization causes

insulin secretition

what receptors do insulin bind to

tyrosine kinase insulin receptors

insulin receptors activate

kinase enzyme in the cells

kinase enzyme in cells

simulates glucose transporter channels to open

active insulin receptors cause

- signal transduction

- gene expression and growth regulation

signal transduction causes

- glucose channels open

- glucose utilization

- glycogen.lipid/protein synthesis

immediate effects

disabled transport of gluocse into cells

disabled transport of glucose into cells

dysfunction of glucose, fat, and protein metabolism

pathophysiology sequelae

increased glucose in plasma

high solute concentration in renal tubules

ketons

increase glucose in plasma

- high solute concentration

osmotic shift of fluid into circulation

high solute concentration

polydipsia

osmotic shift of fluid into circulation

cellular dehydration

high solute concentration in renal tubules

osmotic shift into filtrate

osmotic shift into filrate

high urine production

high urine production

polyuria

affects of beta cell destruction

hyperglycemia

polydypsia

polyuria

glycosuria

metabolict shift in energy in beta cell destruction

fat for energy- breakdown of triglycreides and glycerol

heptic metabolism of fatty acids

ketones (ketone bodies)

are ketones acidic or basic

acidic

accumulation of ketones

metabolic acidosis and metabolism produces acetone

using fatty acids mainly

ketonuria

changes LOC

acetone

metabolic acisosi

coma

death

oncotic

when proteins influence osmotic pressure increase

exmaples of solutes

sodium

ablumin

urea

glucose

free fatty acids first turn into

acyl coA

acyl coA, and glucose are both changed into

acetylene coA

where does acetyl coA go

- enter the TCA cycle

- synthesizes ketone bodies

where do ketone bodies synthesized in the liver go

into the blood

after reaching the blodo where do ketone bodies go

- form acetone secreted through lungs

- excreted through kidneys

- move into extrahepatic tissue

what do keton bodies do in extrahepatic tissue

converted to acetylene coA and used in citric acid cycle

TCA

citric acid/kreb cycle

reduced glucose uptake consequencies

- energy substitutes

- altered cellular function

energy substitutes

- lipolysis

- proteolysis

lipolysis

fatty acid breakdown

fatty acid breakdown

liver metabolism fatty acids (fatty acid oxidation) producing ketones

proteolysis causes

weight loss, and muscle wasting

altered cellular functions

- insulin resistance

- altered cellular repair

- endothelial dysfunction and decreased angiogenesis

- increased oxidative stress

- risk for clotting

- organ injury