1. Alters plasma membrane permeablitity or membrane potential, or both, by opening or closing ion channels
2. Stimulates synthesis of proteins or regulatory molecules such as enzymes within the cell (growth hormone, testastarone)
3. Activates or deactivates enzymes
4. Induces secretary activity
5. Stimulate mitosis (aids in reproduction of the cell)
lipid soluble hormones. (like steroids). the hormone can go straight through plasma membrane into the cell.
Increase of receptors. Body adjusts to excessive amounts of hormones in the blood by producing more receptors on the target cell for that hormone.
Process that desensitizes the target cells due to prolonged exposure to high hormone concentration.
The target cells respond less vigorously to hormonal stimulation.
Prevents the target cells from overracting to persistently high hormone levels (like insulin resistence).
regulates metabolic activity through hormones
(reproduction, growth and developement, maintenence of electrolyte, water, and nutrient balance of the blood etc.)
secreated by the glads and travel through the blood to work on specific cells
specific cells that respond to specific hormones
eat lots of sugar at frequent intervals
insulin goes up--exessively
stay up for extended period of time
cells become numb to insulin (down-regulation)
pancreas wears out after years (produce less insulin)
patient gets agressive symptoms
correct diabetes early on through
concentration of hormone in blood, determined by
1. rate of release
2. how quickly the hormone is inactivated (and removed from body).
the length of time it takes the blood level of a hormone to decrease by half (half as much hormone in the blood as origonally)
(hormone release) Humoral stimuli
hormone is secreted in direct response to changing blood levels of certain ions and nutrients
Ex. glucose up, insulin up (then glucose uptake--as in, it is stored in the muscles).
(hormone release) Neural stimuli
Nerve fibers stimulate hormone release
Ex. stimulation of the adrenal medulla to release epinephrine (adreniline) during stress
(hormone release) Hormonal stimuli
1 gland releasing a hormone that triggers another gland to release a hormone.
So endocrine glands release their hormones in response to hormones produced by other endocrine glands.
3 types of Hormone Release
1. Humoral Stimulus
2. Neural Stimulus
3. Hormonal Stimulus
Negative feedback system
stimulates hormone secretion--more hormone in blood. Target cells activated in large numbers. sends message back telling glands to cease producing that hormone.
Gland made of exocrine glands and indocrine glands. Behind liver. Secretes hormones. Some directly into the duodium.
Islets of Langerhans
In pancreas. Secrete insulin.
Within islet cells, beta cells
produce insulin. (lighter spot)
Within islet cells, within beta cells--alpha cells
Job is to move glucose out of the blood (where it has little value), into the cells.
body breaks it into glucose in the stomach
glucose moved to blood stream
body recognizes glucose and pancreas secretes insulin
insulin binds to glucose and moves into the cell
hormone secreted by alpha cells. Raises blood sugar levels (so we don't become hypoglycemic). i.e. when we're fasting, haven't eaten for a while, or are exercising.
It does this by breaking down glycogen
carbs that don't spike blood sugar levels. Insulin rises slower. Carbs that spike blood sugar lead to rapid and large amount of insulin which stay in the body longer than the sugar (which is where you crash)
If this is an on going cylce, it CAN be prediabetic.
Treatment of hypoglycemia
Eat foods that don't raise the blood sugar levels rapidly
Eat regularly (small meals)
Blood glucose levels
<110 is normal. >125 is diabetic.
Blood glucose levels chart
(get from powerpoint)
Negative Feedback System
Glucose up, pancreas secretes insulin, moves glucose to cells, blood levels of glucose equalize.
Glucose down, pancreas secretes clucagon, break up glycogen, sugar levels go up.
Autonomic Nervous System 2 Segments
Sympathetic Nervous System
Triggered by stress, exercise etc. Secretes empinephrum, stops insulin production.
Parasympathetic Nervous System
Triggered by sleep or rest. Starts insulin production.
It is what is damaged when you are insulin resistent. When it is triggered, processes within the cell occur that open the protein channels for gulcose.
3 Actions of Insulin
1. Move glucose into the muscle where it promotes glycolysis (break down of glucose that produces ATP and provides short burst of energy)
2. Move glucose into the liver where it can be converted into glycogen (stored until needed).
3. Take glucose out of the blood and move it into the fat.
Insulin and weight gain
more blood glucose
more body fat.
Influence energy metabolism
Help the body reduce stress
regulates blood glucose (process is gluconeogenesis)
Breaks down fat and muscle to create glucose
Negative freedback system
Hypothalamus --> (hormone)
--> anterior pituitary --> (hormone)
--> adrenal cortex --> cortisol (which inhibits the other parts of the system).
Excessive amounts of cortisol excreted (often caused by a tumor on the gland)
Resulting in a loss of muscle and bone protein.
Cushing's Syndrome Symptoms
water and salt retention
distributed to nape of neck
poor wound healing
stretch marks--they look pregnant
Hyposecretion (cortisol) OR Addison's Disease
(genetic--glands just don't work sufficiently)--opposite of Cushing's Syndrome
Decreased glucose and sodium
Raises glucose levels by doing two things
1. Lipolysis (fat--break-down of)
2. Glycogenolysis (break down of glycogen)
secreted by the anterior pituitary gland
both growth-promoting and metabolic actions
increase size and number of cells (muscle and bone)
encourages the use of fats for fuel, thus conserving glucose
Produce more growth hormone but your growth plates haven't fused yet so you grown tall but with normal body proportions
Epiphyseal plates have closed
Englarged bones in hands, feet, face
Pituitary dwartism (hyposecretion)
slowed long bone growth with normal body proportions
Egyptian 1500 BC -- Pulyuria "frequent peeing" identified as a "sugar disease."
Greece 14 AD -- Kidney disease
Diabetes historic diagnosis
Lots of light colored pee
Smelled like "sweet hay"
Tasted like sugar
English physician who first documented the taste of pee.
Called the sweetness of diabetic pee "mellitus."
Early symptoms of diabetes
Boils and carbuncles (because they're secreting glucose in their sweat which attracts bacteria)
Dry bowel movements
Early treatments of diabetes (we had no clue!)
herbs and grains
avoidence of sex
roast meat dripping in fat
very few green vegetables
diet-refrain from foods with sugar/starch
eat meats, and green vegetables
Claude Bernard 19th century
Discovered that glycogen was stored in the liver, overproduction of glucose caused diabetes.
Paul Langerhans 19th century
Discovered "islet cells" in the pancreas (which secrete insulin and glucagon)
1. Eat--worsen disease and shorten life
2. Low calorie diet (starve)--lengthen life a little
Type 1 diabetes caused by...
Insulin Deficiency--your pancreas can't produce enough insulin
What causes a child to get diabetes?
Often it is an immune system problem that killed the beta cells
Insulin Deficiency chart
Milestones in diabetic studies
Thomas Willis--sweet taste
Dr. Dobson--boiled urine (sugar was left)
Thomas Cawley--autopsies--shriveled pancreas
Oscar Minkowski--took pancreas out of healthy dogs--> diabetic symptoms
Sir Edward Albert Sharpeg--discovered insulin
Fredrick Banting/Charles Best--tested with insulin injections
Short acting insulin
(regular, lispro, aspart, glulisine)
inject after eating
works within 5-15 minutes. Peak 1-1.5 hrs. Lasts 3-4 hrs.
Long acting insulin
slow release of insulin into the circulation
given once per day, before bedtime
given twice daily
mixed insulin preparations
Mix of fast and slow acting insulin.
Given before breakfast and dinner.
(trims down the amount of injections from 4 to 2)
Syringe (anywhere where there is loose skin). Rotate the area.
Pen injector devices
Insulin pump--scheduled and set to inject regularly.
(agressive treatment--pancreas transplant, or islet cell transplants)
Diabetes Mellitus: Type 1
Pancreatic islet B cell destruction
Body does not produce sufficient amounts of insulin
100000000 cases per year
90% immune-medicated 10% Idiopathic (i.e. we don't know what causes the destruction of the B cells).
Peaks of incidence in children before school age, again at puberty (Juvenile onset).
Diabetes Mellitus: Type 2
Ciculating endogenous insulin is inadequate to prevent hyperglycemia
OR increased tissue insensitivity (insulin resistence)
2500000000 cases per year (1 million more cases per year)
Obesity, sedentary lifestyle, diet
Predominantly in adults (now more in adolescents).
Located paritally behind the stomach, triangular gland
Aides in digestion
Secretes alpha cells and beta cells
Extremely potent hyperglycemis (1 molecule of glucagon can release 100 million glucose)
1. breaks down glycogen to glucose
2. Synthesis of glucose from lactic acid
(releases clucose into the blood)
Main effest is to lower blood glucose
1. Enhances membrane transport into cells
2. Inhibits breakdown of glycogen to glucose
3. Inhibits conversion of amino acids or fats to glucose
Stimulated by elevated blood glucose levels
Negative feeback system
Etiology of Type 1 Diabetes
Pancreatic B Cell destruction
Circulating insulin is virtually absent
Elevated plasma glucagon and glucose levels in the blood
Causes of Type 1 Diabetes
mom has it 3% risk per child
dad has it 6% risk per child
caucasian most at risk
Idiopathic- (we don't know what caused it)
common in Asian or African
viral infection during childhood, early adulthood, or a mom's pregnancy. Antibodies against virus--attack beta cells. Destroy beta cells.
Diagnose Type 1
Urinalysis (analyze urine)
--Glucosuria (sugar in urine)
--Ketonuria (ketones in urine--from breaking down far for energy)
-- >126 mg/dL (after 12 hour fast)
--Hmoglobin A1C ---Assess diabetic control (blood glucose levels) over the lifespan of the red blood cell (RBC) (120 days)... >6HbA1C
Type 2 Diabetes statistics
25.8 million in 2010
Most patients are 40+ yrs old and obese
> 90% of all diabetes patiens have Type 2
Predominantly seen in adults, but becoming more prevalent in children and adolescents
Does the pancreas produc insulin in type 2?
Yes, enough to prevent ketoacidosis but not enough to prevent hyperglycemia
Does location (distribution) of fat correlate with insulin resistance?
Yes, visceral obesity (abdominal fat) correlate with insulin resistance more than subcontaneous fat.
What makes you more prone to insulin resistence?
Type 2: What is insulin resistance syndrom?
25% of monobese, nondiabetic population has insulin resistance.
Gestational Diabetes Causes
1. Insufficient insulin release (not enough for you and the fetus).
2. Insulin resistance
Gestational Diabetes Risks
Development of DM II later in life
Complication duing pregnancy
Future gestational diabetes
Child at increased risk of obesity and DM II
Daughters at higher risk of gestational and DM II
Higher risk of DM I
Diabetes Insipidus Causes:
1. Failure of release antidiuretic hormone (ADH)
2. Failure ro recognize ADH
ADH conserves water--the lack (or resistance) of ADH lead to polyuria (peeing) and polydipsia (thirst)
Microvascular Diseases (destruction of small vessels)
-Retinopathy--destroy vessels in the eye (patient goes blind)
Macrovascular Diseases (destruction of large vessels)
-Cardiovascular disease (myocardial infaction)
-Cerebrovascular disease (stroke)
How do we get micro/macrovascular diseases?
It starts with GLYCOSYLATION.
amino acids + sugar (which makes glycosylation) --> glycated protein (ADD CHART FROM POWERPOINT) (happens when you have high levels of glucose over a long period of time).
Advanced Glycosylation End Products (AGE's) (product of glycosylation) leads to:
1. Increased vessel permiability (LDL's will penetrate the vessel wall --> Plaque).