Mstn Ii - Lecture 35

Front 1

functional units of the pancreas:

Back 1

Islets of Langerhans

Front 2

Outer rim of Islets:
Interior rim:
Interspersed between:

Back 2

outer: alpha cells - glucagon
interior: beta cells - insulin
interspersed between alpha and beta: delta (d) cells - somatostatin

Front 3

Insulin and Glucagon:

Back 3

insulin produced from beta cells can be made available to the alpha cells that make glucagon. When the insulin binds, glucagon production is inhibited (paracrine relationship).

Front 4

When beta cells or insulin receptors on the alpha cells are not functioning properly:

Back 4

hyperglucagonemia - blood glucose levels will be raised to abnormally high levels.

Front 5

Glucagon and beta cell:

Back 5

- bind to beta cells
- stimulate beta cell production of insulin

Front 6

Somatostatin and alpha and beta cells:

Back 6

- inhibit both the alpha and beta cells

Front 7

somatostatin's autocrine fashion

Back 7

- inhibit itself

Front 8

glucagon levels are too high:

Back 8

glucagon stimulates both somatostatin and insulin release to prevent high glucagon levels from getting carried away.

Front 9

Insulin inhibits:

Back 9

alpha cells - glucagon

Front 10

C peptide connects to the A and B chain by:

Back 10

2 basic amino acids

Front 11

When insulin binds to its receptor:

stimulate:

Back 11

- stimulate the uptake of AA, K and Phosphate into the cell by mobilizing carrier channels.
- stimulate pyruvate dehydrogenase
- stimulate protein synthesis

Front 12

when insulin binds to its receptor:

inhibit:

Back 12

- inhibit: lipolysis by inhibiting the hormone sensitive lipase enzyme causing free fatty acids to be stored as fats
- inhibit protein degradation
- inhibit gluconeogenesis (b/c insulin wants to store, not liberate glucose),
- inhibit the conversion of AA -> glucosse

Front 13

with GLUT transporters, glucose is taken up into the cell through:

Back 13

facilitated diffusion

Front 14

Eating:

Back 14

increased glycogenesis
increased lipogenesis
increased protein biosynthesis

Front 15

fasting:

Back 15

glycogenolysis
lipolysis
gluceoneogenesis
ketogenesis

Front 16

predominantly protein based meal:

Back 16

- AA mildly stimulate insulin release
- AA also have a direct effect to stimulate glucagon secretion
- together, the mild rise in insulin is not enough to suppress glucagon release
- insultin stimulates the uptake of AA's into the cells. Once the AA's are in the cells and proteins are produced, glucagon then stiumulates the AA's to be used for gluconeogenesis.
- blood levels eventually go up during a protein meal, even though it takes more time

Front 17

Brain's uptake of glucose:

Back 17

does not need insulin to take up glucose into nerve cells (insultin-independent)

Front 18

cells that require insulin for the up take of glucose:

Back 18

resting liver
muscle
fat

insulin is not technically required to uptake glucose into the liver, but the liver requires insulin to utilize it.

Front 19

glucagon ensures that:

Back 19

as glucose is taken up by the tissues, the same amount is repalced back into circulation through glycogenolysis etc.

Front 20

increase in stress:

Back 20

increased sympathetic input into the Iselts, stimulating adrenergic receptors on the alpha and beta cells to inhibit insulin and increase glucagon, respecitively

Front 21

exercise causing increase in GLUT transporters:

Back 21

sliding filaments of activated exercising muscle cause the GLUT transporters to migrate to the cellular membrane

Front 22

Famine:

Back 22

- low adequate substrate: insulin inhibition of alpha cells declines -> more glucagon secretion
- stimulate gluconeogenesis -> but not too frequently, b/c you will degenerate lean muscle mass. To avoid this: glucagon stimulate ketogenesis in liver.

Front 23

primary ketone bodies:

Back 23

acetoacetic acid
beta-hydroxybutyric acid

derived from lipolysis and the breakdown of fatty acids into acetyl-CoA

Front 24

excess ketones can create:

Back 24

metabolic acidosis

Front 25

feeding:

Back 25

GI tract detects food -> release GI hormones (CCK, secretin, gastrin etc) before glucose is even detected in the blood
-> release of these hormones signals the release of insulin from the pancrease -> Anticipatory Rise of Eating

Front 26

Anticipatory rise of eating:

Back 26

GI hormones signal the release of insulin from the pancreas even before glucose is detected in the blood

increase the efficiency of insulin, avoid wasting glucose

Front 27

Type 1 diabetes:

Back 27

juvenile (insulin dependent)

- children exposed to infectious conditions
- some have molecular structures that mimic the antigens/structure of beta cells
- overreact to the infectious antigen and thus end up attacking not only the antigen but also their own beta cells.
- wiping out the Beta cells, you lose all ability to produce insulin and undergo hyperglucadonemia

Front 28

Type II diabetes:

Back 28

adult onset (non insulin dependent)

overtime, the insulin receptors down regulate in response to excess insulin - as a result of overexposure of the beta cells to glucose
- impaired production of insulin but still sufficient amounts to prevent ketoacidosis

uncontrolled type II diabetic will not have ketoacidosis, but a type I diabetic might

Front 29

amino acids in circulation and glucagon

Back 29

amino acids in circulation, under the influence of glucagon will stimulate gluconeogenesis.

Front 30

protein breakdown liberates:

Back 30

phosphate and potassium out of the cells into the bloodstream

with no insulin, very little potassium and phosphate is re-taken up into the cell

Front 31

presence of glucose in tubules:

Back 31

- osmotic effect to draw water into the tubules excreting more water and electrolytes. -> hypovolemic state

Front 32

hypovolemic state:

Back 32

decreased cardiac output and hypotension - renal blood flow and function are reduced.

inability of the kidney to excrete hydrogen ions (metabolic acidosis)

Front 33

ketoacidosis:

Back 33

FF's are made available for ketogenesis - metabolic acidsosis

metabolic acidosis coupled with the inability to scecrete hydrogen ions - impairs neuronal function and could result in coma.. death

Front 34

coma due to acidosis occurs in:

Back 34

type I diabetic...

Front 35

type II diabetic, H+ ion and acidosis:

Back 35

in type II, some inability to excrete H+ ion and a slight acidosis.

won't see a significant ketoacidosis, b/c there's just enough insulin being produced to restrain glucagon so you don't develop a major ketoacidosis.

Front 36

osmotic diuresis

Back 36

type II more likely to suffer from the osmotic diuresis and the loss of excessive body water. This causes a loss of fluid out of the brain cells impairing brain function -> not enough to kill, since not aggravated by ketoacidosis

hyperosmotic coma

Front 37

cataracts:

Back 37

glycosylation of the lens of the eye

Front 38

kidney failure:

Back 38

glycosylation of the basement membrane of the kidney

Front 39

A1C hemoglobin

Back 39

glycosylation of hemoglobin = A1C hemoglobin -> cannot release oxygen to the peripheral tissues.

Front 40

gangrene and amputations:

Back 40

excess glucose can bind to red blood cells and decrease their deformability, so they cannot slip through capillaries.

decreased blood supplyl to peripheral tissues -> pangrene and amputation

Front 41

glycosylation of insulin receptor:

Back 41

making it less responsive to insulin