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44 Cards in this Set

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Cortisol as a glucose counter regulatory hormone
under normal conc. cortisol effects carb metabolism but barely. It helps adjustment to fasting.

cortisol maintains enzymes required for gluconeogenisis and lipolysis
Glucose counter reulatory hormones
glucagon (main one)
symp system
cortisol
GH
GH primary responsiblity
stimulates protein synthesis and bone growth
GH affects on carb and lipid metabolism
GH has minor effects on carb and lipid metabolsim. GH affects carbs and lipid metabolism when plasma levels are hi or lo. At hi levels GH has anti insulin effects and it makes adipocyes for sensitive to lipolytic stimuli and increases gluconeogenisis by liver and decreases muslce and adipocytes sensitivy to insulin.

it overall decreases glucose uptake by cells
hormone levels during fasting
insulin is lo (decreases)
glucagon hi (increase)
GH hi (increase)
cortisol normal
what happens to glycogen during fasting
glycogen stores in liver and muscle are depleted so plasma glucose declines
during fasting what do metabolic substrate shift to?
lipolysis products
fa
glycerol
ketones
describe glucose uptake by liver, adipocytes, muscle, and brain during fasting
glucose uptake by liver, adipocytes, and skeltal m. decreases

glucose uptake by brain remains normal
what happens during fasting

5 main things
1. glucose uptake by liver, adipocytes, muscle decreases but brain glucose uptake remains constant

2. glycolysis is decreased in liver and skeletal m.

3. lipolysis increases. tissue shift to use fa for metabolism

4. breakdown protein

5. glycerol from lipolysis and aa (alanine) from protein catabolism undergo gluconeogenisis
what happens after 3days of fasting?
1. decrease in insulin MORE

2. use more fa

3. increase ketone conc. for brain bc no more glucose left. increase ketones decrease protein catabolism bc now brain is using ketones.
Problem with ketone synthesis
can cause metabolic acidosis
how long can fat stores provide body with metabolic substrate
60 days then death occurs
hypoglycemia
lo blood sugar in postabsorptive state
sympotoms of hypoglycemia
due to lack of glucose in brain

headaches
confusion
dizziness
incoordination
slurred speech
convulsions
coma if below 40 mg/dL
effects of symp stimulation due to lo blood glucose (hypoglycemia)
tachycardia
trembling
nervousness
sweating
anxiety
2 things that can cause hypoglycemia
increased blood insulin

defect in glucose counter regulatory systems
how can blood insulin be increased to cause hypoglycemia
insulin secreting tumors

drugs causing insulin secretion

overdose of insulin

drugs (beta adrenergic, ethanol)
how can pt get a defect in glucose counter regulatory systems to cause hypoglycemia
inadequate glycogenolysis or gluconeogenisis due to liver disease

glucagon defiency

cortisol defiency
criteria for diagnosis of diabetes
fasting plasma glucose of more than 140 mg/dL or plasma glucose over 200 mg/dl 2 hrs after glucose meal
% of people with Type I diabets
9%
2 peaks of incidence for diabetes I
first at puberty

second peak around 40
Type I diabetes
lack of insulin due to destruction of pancreatic beta cells

autoimmune disease
plasma glucose with type I diabetes
plasma glucose is 300-400 mg/dl but could be up to 1000 mg/dl. since glucose does not enter the cell, the cell thinks its starving so it increases lipolysis, making fa, glycerol and ketones

ketones cause diabetic ketoacidosis with leads to problems w/ neural function
what is seen with type I diabetes pts.
see hi glucose levels, hi triacylglyceride levels due to lipolysis and lo insulin
what is in Type I diabetes pts urine?
glucose and ketones bc saturation of renal transporters

glycosurea
polyuria
seen with type I and II diabetes

when osmotic diuresis and loss of electrolytes and nutrients cause dehydration
polydipsia
seen mainly with type I diabetes

it is excessive thirst bc increase urine flow and lossof water
why do you see wieght loss in people with Type I diabetes although polyphagia is occuring?
due to loss of glucose and nutrients in the urine
therapy for type I diabetes
insulin injection
insulin pump
insulin pump/glucoe monitor
insulin inhalation
who are main pts who get diabetes type II
90% are overwieght and 80% are obese
type II diabetes
insulin is made BUT target tissue is unresponsive to insulin. cells decrease glucose uptake and decrease glycogen synthesis. This is due to obesity

some loss of insulin occurs bc beta cells are not as sensitive to glucose
why do pts w/type II diabetes not lose wieght?
bc not enough glucose is excreted in urine
only time ketosis occurs in type II diabetes
stress or trauma from infections
symptoms of type II diabetes
polyuria,thirst,blurred vision, parethsis, and fatigue
therapy for type II diabete
excercise
drugs
how does excersice help type II diabetes pts?
weight reduction w/excercise. insulin responsiveness increases w/ excercise. excercise increases the number of glucose transporters in skeletal m.
non insulin dep. diabetes
Type II
drugs to treat type II diabetes
sulfonylureas

biguanides

GLP-1 agonist

amylin agonist
how does sulfonylureas help Type II diabetes
stimulates secretion of insulin from pancrease by closing K channel
how does biguanides help type II diabetes pts?
inhibits hepatic gluconeogenisis so more glucose wont be released
how does GLP-1 agonist help diabetes II pt?
enhances glucose stimulated insulin release and decrease release of nutrients from tummy
symptoms of type I diabetes
polydipsia
weightloss
polyphagia
blurred vision
polyuria
effects of chronic elevated glucsoe levels
atherosclerosis bc lipid circulation

kidney failure

peripherial vascualr disease

neuropathies

infection

retinopathies cause blindness
what causes chronic abnormalities of diabetes mellitus
due to non enzymatic glycoslyation of proteins caused by chronic elevated gllusoe levels

mainly due to damage to vasculature and narrowing of caps