Chamberlin's Study Guide Flashcards
If there were a reduction in insulin levels across all levels of blood glucose levels, how would this change the glucose equilibrium point?
Blood glucose levels would rise. A new set point (higher one) will be established.
(Glucose Regulation - slide 4)
What is the relationship between glucagon and insulin?
When one goes up, the other goes down, and a set point is reached btwn 70-110 mg/dl
(Glucose Regulation - slide 3)
How are decreased insulin levels and insulin resistance related?
End up doing the same thing (blood glucose levels rise)
Glucose Regulation - slide 4
What organ has both endocrine & exocrine function?
pancreas
Glucose Regulation - slide 6
Which cells produce insulin, which produce glucagon, which produce somatostatin?
Insulin - beta cells
Glucagon - alpha cells
Somatostatin - delta cells
(Glucose Regulation - slide 6)
What is the difference between D cells and delta cells?
D cells are found in the stomach, delta cells in the pancreas, both secrete somatostatin into the blood stream.
(Glucose Regulation - slide 6)
What are the two mechanisms glucagon employs to increase blood glucose?
Glycogenolysis & gluconeogenesis
Glucose Regulation - slide 8
What stimulates glucagon secretion and what inhibits it?
Stimulated by - low glucose, amino acids, ACh, EPI, NE
Inhibited by - high glucose, Insulin, Fatty acids
(Glucose Regulation - slide 15)
Why does activation of the sympathetic nervous system stimulate glucagon release?
You need to put as much immediately usable fuel into the circulatory system to provide for the needs of the muscles that will be fleeing or fighting soon.
(Glucose Regulation - slide 15)
What is paracrine secretion?
Secretion into the local area only
Glucose Regulation - slide 15
Which pancreatic hormone utilizes paracrine secretion?
Somatostatin
Glucose Regulation - slide 15
What is the purpose of somatostatin?
To down regulate both insulin and glucagon secretion so that levels of both don’t get out of control
(Glucose Regulation - slide 15)
Why is calming things down important (in regards to somatostatin release)?
So you don’t exhaust nutrients too quickly
Glucose Regulation - slide 15
What stimulates somatostatin’s release?
Glucagon, insulin, & AA
Glucose Regulation - slide 15
What is the most effective most immediate treatment for hypoglycemia?
Glucagon
Glucose Regulation - slide 16
Why does glucagon reduce the uptake of glucose into adipose cells?
Its action is to keep as much glucose as possible in the circulatory system
(Glucose Regulation - slide 16)
What does insulin do?
- Glucose uptake into cells
- Protein, fat, & glycogen synthesis
- Growth & gene expression
- Satiety signal
(Glucose Regulation - slide 9)
What is the function of the IRS?
It’s the receptor that insulin binds to, and subsequently causes glucose channels to increase in number on the cell membrane thus increasing glucose uptake into the cell.
(Glucose Regulation - slide 10)
What does the insulin receptor trigger?
Translocation of GLUT-4 glucose transporter into cell membrane to facilitate glucose absorption
(Glucose Regulation - slide 10)
What are the old antiquated classifications of diabetes?
Insulin & non-insulin dependent
Glucose Regulation - slide 17
Why was it important to change the old classifications of diabetes?
Eventually most non-insulin dependent diabetics will require insulin.
(Glucose Regulation - slide 17)
How do the autoimmune processes of type I & type II DM differ?
Type I - involves destruction of the beta cells in the pancreas
Type II - alteration of IRS &/or GLUT-4 receptors in the target adipose tissue
(Glucose Regulation - slide 17)
If the body chooses to store glucose, what are the 2 primary forms that it is stored as?
Glycogen & TG
Glucose Regulation - slide 11
Where is glycogen normally stored?
Liver & muscle
Glucose Regulation - slide 11
Where are TG normally stored?
adipose tissue
Glucose Regulation - slide 11
Do myocytes normally store fat for later use as energy?
No, they store glycogen
Glucose Regulation - slide 11
Does insulin cause lipogenesis or lipolysis?
Insulin promotes lipogenesis (TG formation & storage) in adipose tissue & liver (it inhibits lipolysis of TG).
(Glucose Regulation - slide 11)
Where are GLUT-2 receptors found?
Beta-cells in the pancreas
Glucose Regulation - slide 12
What is the effect of GLUT-2 receptors on beta cells becoming activated?
Insulin is released from the pancreas
Glucose Regulation - slide 12
Does insulin travel through the pancreatic duct to the duodenum?
No, just the exocrine products (lipase, HCO-).
Hormones are secreted in the vascular system
(Glucose Regulation - slide 12)
In what phase does parasympathetic activity stimulate beta cells?
cephalic phase
Glucose Regulation - slide 20
What is the ultimate function of the interaction between glucagon and insulin?
To keep blood glucose levels into a very narrow range during fasting
(Glucose Regulation - slide 22)
When a person gets hypoglycemia, why does their sympathetic nervous system activate?
To keep the person conscious as the brain relies on glucose alone for energy & on a second-to-second basis
(Glucose Regulation - slide 22)
If stress is causing continuous sympathetic activation, what will happen to the equilibrium point of glucose?
ANS will cause constant glucagon release and the point will shift upward to result in a higher concentration of fasting glucose levels (stress can lead to diabetes in this way).
(Glucose Regulation - slide 21)
Iron & B12 are both absorbed in specific locations, what are they?
Iron - duodenum
B12 - terminal ileum
(Intestinal Secretion - Slide 4)
Where are other nutrients absorbed?
Water Soluble Vitamins (except B12) = Mainly Jejunum (Slide 6)
Fat Soluble Vitamins w/dietary fats = most of small intestine (Slide 7)
Electrolytes/Water = small & large intestine (Slide 8)
For list of specific nutrients and their order of absorption look at: Intestinal Secretion - Slide 4
Do fat soluble vitamins avoid the first pass effect? And what is the first pass effect?
Yes, this is when substances with a high fat content avoid being degraded by the liver by bypassing it & going to the peripheral tissues first.
(Intestinal Secretion - Slide 7)
Where does intestinal absorption occur?
Where does intestinal secretion occur?
Absorption - enterocytes
Secretion - crypts of Lieberkuhn
(Intestinal Secretion - Slide 8)
Daily secretion & absorption of fluid are massive.
About how much fluid is secreted a day by the stomach alone?
By the entire GI system?
stomach - 2L
GI system - 9L
(Intestinal Secretion - Slide 9)
Both small & large intestine absorb water, but do entirely different things with K+, what are they?
Sml intestine - absorbs K+
Lrg intestine - secretes K+
(Intestinal Secretion - Slide 9)
Why does most NaCl & water absorption occur in the duodenum & jejunum and less absorbed in the ileum & colon?
Because the tight junctions in the duodenum & jejunum are more permeable to water & solutes than in the ileum & colon.
(Intestinal Secretion - Slide 10)
If by controlling Cl- and thus controlling Na, how does controlling just one molecule control all other things?
Na follows Cl movement and water follows both.
Mechanisms have developed so that every time a Na+ enters a cell it drags a glucose with it and at the same time expels a H+.
(Intestinal Secretion - Slide 11)
In the jejunum, what is co-transported with glucose?
Na+
Mechanisms have developed so that every time a Na+ enters a cell it drags a glucose with it and at the same time expels a H+
(Intestinal Secretion - Slide 11)
In the ileum and large intestine what is absorbed Na exchanged for and what buffers this system in the lumen?
Absorbed Na is exchanged for secreted H. In the lumen H is buffered by HCO3-
(Intestinal Secretion - Slide 11)
In the duodenum & jejunum, how is Cl- absorbed?
Cl- just diffuses into or around the cells & is absorbed.
Intestinal Secretion - Slide 12
In the ileum & colon how is Cl- absorbed?
Cl- has a special pump, where it is absorbed via an exchange with HCO3-.
(Intestinal Secretion - Slide 12)
True/False. The pump that absorbs Cl- in the ileum & colon via an exchange with HCO3- is the same as the CFTR pump.
FALSE!
(HE WROTE THIS IN ALL CAPS, AND SO WILL I)
(Intestinal Secretion - Slide 12)
What is the difference between the way Cl- is absorbed and secreted?
Absorbed - diffusion through gap junctions
Secreted into a lumen - has to use CFTR
(Intestinal Secretion - Slide 17)
What is does CFTR mean?
cystic fibrosis transmembrane regulator
Intestinal Secretion - Slide 17
About how much water is secreted into the intestine and how much is reabsorbed in a 24 hour period?
secreted - 9000 ml/day
reabsorbed - 8900 ml/day
(Intestinal Secretion - Slide 15)
How much water is lost a day?
100 ml
Intestinal Secretion - Slide 15
Why is secretory diarrhea so deadly?
It causes the CFTR to endlessly secrete Cl- (& water) and it does so down low below the duodenum & jejunum where water could be normally reabsorbed.
You would lose liters & liters of water/day versus 100 ml.
(Intestinal Secretion - Slide 18)
How does secretory diarrhea differ from osmotic diarrhea?
Osmotic diarrhea does not involved the CFTR, but is a water drag situation where the overall water loss is much smaller.
(Intestinal Secretion - Slide 18)
How can losing just 2 BMI points lead to a vast change in heath?
Visceral fat ‘dissolves’ first, lessening intra-abdominal mass effects (i.e. hiatal hernia), and may decrease the likelihood of an autoimmune reaction in the peripheral fat.
(Adiposity - Slide 4)
How does fat storage differ in men & women?
Men tend to store visceral fat first, women peripheral fat first
(Adiposity - Slide 4)
One of two theories about the development of type II DM involves inflammatory cytokines damaging peripheral fat cell receptors.
Which cytokines are thought to cause this damage?
TNF, IL-6, FFAs (free fatty acids)
Adiposity - Slide 10
What receptors are the inflammatory cytokines damaging on the peripheral fat cells in type II DM?
IRS
Adiposity - Slide 11
What is the consequence of damaging the IRS?
GLUT 4 receptors cannot translocate to the cell wall & thus the adipocyte cannot uptake glucose.
(Adiposity - Slide 11)
Why are these IRS damaging cytokines thought to be released?
Because of an immune reaction occurring between visceral fat and bacterial agents in the GI system.
(Adiposity - Slide 11)
Describe the process of TNF (tumor necrosis factor) causing insulin resistance in other tissues (i.e. subcutaneous fat & muscle).
TNF is secreted from visceral fat. It interferes with IRS protein in cell signaling of GLUT-4 translocation. This reduces the release of adiponectin (usually secreted w/subcutaneous fat), which normally inhibits insulin resistance & inflammation.
(Adiposity - Slide 13)
What is the mechanism responsible for atherosclerosis that is similar to the one for type II DM, but has nothing to do with it?
Cytokines (adipokines) attack the coronary arteries instead of the IRS and cause atherosclerosis.
(Adiposity - Slide 14)
How is the amount of fat a person has normally determined?
Body weight (adiposity) is normally stabilized by balancing energy intake & energy expenditure (homeostasis).
(Appetite Regulation - Slide 15)
How does this homeostasis (balancing of energy intake & expenditure) occur?
Neural & endocrine afferent pathways provide feedback for regulating neural & behavioral aspects of eating.
(Appetite Regulation - Slide 15)
What is the difference between homeostatic and non-homeostatic regulation of energy uptake?
Homeostatic - result of feedback regulation from the internal milieu (adipose, intestines, pancreas, etc) on hypothalamic/brain stem actions on eating.
Non-homeostatic - involves cognition, motivation, drive, stress (i.e. limbic’s system’s processing of environment, early life events, predispositions, etc).
(Appetite Regulation - Slide 16)
How does the ileal brake work?
Ileal brake is the reduction of GI motility. It happens by a satiety peptide acting on the anorexigenic hypothalmic pathway to stimulate insulin release (parasympathetic) and inhibit glucagon release/GI motility/Secretion.
(Appetite Regulation - Slide 30)
How can the ileal brake be used clinically for weight loss?
Slower eating permits activation of these satiety signals to reduce meal size.
(Appetite Regulation - Slide 30)
What are the basic gastric cells types and what are their functions?
Mucus Cells: secrete mucus & bicarb
Parietal Cells: secrete HCl, intrinsic factor (IF)
Peptic (Chief) Cells: secrete pepsinogen, gastric lipase
Enterochromatffin-like Cell: secretes histamine
G cells: secretes gastrin
D cells: secretes somatostatin
(Salivary & Gastric Secretion - Slide 18, 19)
What stimulates the production of HCl?
Peptides stimulate gastrin release, which stimulates acid secretion. Vagus nerve stimulates acid secretion and inhibits somatostatin release
(Salivary & Gastric Secretion - Slide 22)
What inhibits HCl production?
Acid stimulates somatostatin (SS) release which inhibits gastrin release
(Salivary & Gastric Secretion - Slide 22)
Where is vitamin B12 absorbed and what are the steps required to absorb it?
Terminal ileum (from later lecture), but it depends on secretion of IF from gastric parietal cells & uptake by ileal cells. Steps Required: dissociation from R-proteins by pepsin, binding with IF, and absorption by ileal cells & transport into portal vein.
(Salivary & Gastric Secretion - Slide 23)
(Intestinal Secretion - Slide 4)
What is the function of mucus? And what is its pathway of secretion chemically?
Protection from HCl
Ach -> G cells -> Gastrin -> Parietal cells -> HCl -> Goblet cells -> mucus -> HCO3
(Salivary & Gastric Secretion - Slide 31)
Why is an acidic environment necessary to begin the digestion of proteins? What is the overall chemical pathway to stimulate protein digestion?
Because acid secreted into the stomach converts pepsinogen to pepsin (protease), which is the main enzyme that breaks down proteins.
Ach -> G cells -> Gastrin -> Parietal cells -> HCl - > Pepsinogen -> Pepsin -> Protein
(Salivary & Gastric Secretion - Slide 28, 32)
