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  #1  
Old 02-23-2012
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Embarrassed Diabetes treatment like diet and exercise!

A 57 year old man comes to the physician because of increased thirst and frequent nocturia. Following the ingestion of 75g of a glucose solution. His blood glucose is 293mg/dl. treatment with a strict diet and exercise program is begun. Which of the following has been shown to have treatment effects most similar to those seen with diet and exercise in patient whit this disease?

A- Acarbose
B- Exenatide
C- Glyburide
D- Metformin
E- Pioglitazone
F- Sitagliptin
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  #2  
Old 02-23-2012
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I'm going to go with Acarbose a alpha-glucosidase inhibitor
this will cause increase serum glucose by delaying sugar hydrolysis and glucose absorption
it also decrease postprandial hyperglycemia thus decrease demand for insulin
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  #3  
Old 02-23-2012
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A. Acarbose

Only one that we could say mimicks a good diet imo.
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  #4  
Old 02-23-2012
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hmmm......
I think its Piaglitazones........ Diet modification and weight loss increases tissue sensitivity to insulin similar action is shown by Thiazolidinediones.
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  #5  
Old 02-23-2012
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Ans D .... Metformin decreases gluconeogenesis , increases glycolysis , and improves insulin sensitivity ...... all three which happen during a excercise or fasting ......so its Metformin .....
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  #6  
Old 02-23-2012
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Metformin and Pioglitazone both have similar actions that mimic exercise.

I will go with E. Pioglitazone. It increases GLUT-4 activity very similar to exercising hence enhancing glucose uptake by muscle and adipose.
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Old 02-24-2012
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i would surely go with Metformin cos it is the considered as the the its a drug of choice for newly diagnosed type 2 DM patients..
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  #8  
Old 02-24-2012
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For now I am confused; let's go for each mechanism of action and after we gonna pick up the answer of choice guy:

(F) Sitagliptin: works to competitively inhibit the enzyme dipeptidyl peptidase 4 (DPP-4). This enzyme breaks down the incretins GLP-1 and GIP, gastrointestinal hormones released in response to a meal. By preventing GLP-1 and GIP inactivation, they are able to increase the secretion of insulin and suppress the release of glucagon by the pancreas. This drives blood glucose levels towards normal. As the blood glucose level approaches normal, the amounts of insulin released and glucagon suppressed diminishes, thus tending to prevent an "overshoot" and subsequent low blood sugar (hypoglycemia) which is seen with some other oral hypoglycemic agents.

(E) Pioglitazone: selectively stimulates the nuclear receptor peroxisome proliferator-activated receptor gamma (PPAR-γ) and to a lesser extent PPAR-α. It modulates the transcription of the insulin-sensitive genes involved in the control of glucose and lipid metabolism in the muscle, adipose tissue, and the liver. As a result, pioglitazone reduces insulin resistance in the liver and peripheral tissues; increases the expense of insulin-dependent glucose; decreases withdrawal of glucose from the liver; reduces quantity of glucose, insulin and glycated hemoglobin in the bloodstream

(D) Metformin: activates AMP-activated protein kinase (AMPK), an enzyme that plays an important role in insulin signaling, whole body energy balance, and the metabolism of glucose and fats; activation of AMPK is required for metformin's inhibitory effect on the production of glucose by liver cells. Research published in 2008 further elucidated metformin's mechanism of action, showing activation of AMPK is required for an increase in the expression of SHP, which in turn inhibits the expression of the hepatic gluconeogenic genes PEPCK and Glc-6-Pase.improves hyperglycemia primarily by suppressing glucose production by the liver (hepatic gluconeogenesis)

(C) Glyburide: works by inhibiting ATP-sensitive potassium channels in pancreatic beta cells. This inhibition causes cell membrane depolarization opening voltage-dependent calcium channel. This results in an increase in intracellular calcium in the beta cell and subsequent stimulation of insulin release.

(B) Exenatide: is an incretin mimetic. It has structural similarity and binds to the receptor for GLP-1 and displays a similar broad range of activities relevant to improving glycemic control. In the beta-cell, exenatide stimulates insulin secretion in a glucose dependent fashion and has been shown to essentially normalize the loss of first-phase insulin secretion in patients with type 2 diabetes. In the alpha-cell, it normalizes the pathologic hypersecretion of glucagon in a glucose-dependent fashion, thereby reducing hepatic glucose production in the postprandial state. The glucose dependency of both of these mechanisms have been well-documented, protecting the patient from hypoglycemia while these delicately counterbalanced hormones are normalized simultaneously

(A) Acarbose: inhibits enzymes (glycoside hydrolases) needed to digest carbohydrates, to be specific, alpha-glucosidase enzymes in the brush border of the small intestines and pancreatic alpha-amylase. Pancreatic alpha-amylase hydrolyzes complex starches to oligosaccharides in the lumen of the small intestine, whereas the membrane-bound intestinal alpha-glucosidases hydrolyze oligosaccharides, trisaccharides, and disaccharides to glucose and other monosaccharides in the small intestine. Inhibition of these enzyme systems reduces the rate of digestion of complex carbohydrates

After I was reading all this information, I think the correct answer should be E; I post all this information because a friend of mine took the examen in Decemner, they gave him 25% of question about Diabetes therapy guys, he said me. So, After reading FA & MED Essential I was not satisfied, and I decided to my own way.
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  #9  
Old 02-24-2012
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along with the above mentioned mechanism Metformin is also known to reduce insulin resistance..

The thing is exercise and dietary modification helps loose weight and thus increase insulin sensitivity.. i think metformin fits the bill perfectly..

Also as i said it is the first drug prescribed to newly diagnosed type 2 DM and other drugs r started only after suboptimal control of blood glucose levels.
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Old 02-24-2012
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Quote:
Originally Posted by manusharma1406 View Post
along with the above mentioned mechanism Metformin is also known to reduce insulin resistance..

The thing is exercise and dietary modification helps loose weight and thus increase insulin sensitivity.. i think metformin fits the bill perfectly..

Also as i said it is the first drug prescribed to newly diagnosed type 2 DM and other drugs r started only after suboptimal control of blood glucose levels.
So they never said in our case the patient is a starter diabetic
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Last edited by alfjof; 02-24-2012 at 08:31 AM.
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  #11  
Old 02-24-2012
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well pointed out... sorry.. but i still feel its metformin
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Old 02-24-2012
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whats the answer?
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  #13  
Old 02-24-2012
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Quote:
Originally Posted by Dr.NickRiviera View Post
whats the answer?
Read all mechanism of action I put and you gonna see the answer in red
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  #14  
Old 02-25-2012
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hmmm , still feel its metformin , excercise increases insulin sensitivity and increases glycolysis both are done by metformin see FA pg 304 , Glitazones only increase sensitivity ...... so metformin a better choice .

hey buddy where is this Qs from ?
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  #15  
Old 02-27-2012
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Quote:
Originally Posted by Hitman View Post
hmmm , still feel its metformin , excercise increases insulin sensitivity and increases glycolysis both are done by metformin see FA pg 304 , Glitazones only increase sensitivity ...... so metformin a better choice .

hey buddy where is this Qs from ?

I found it in Kaplan Qb 2010
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  #16  
Old 02-28-2012
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he was asking about postprandial hyperglycemia !
well of course in real life we do not diagnose DM depending on postprandial hyperglycemia , we need the fasting blood sugar readings , the HBA1C and renal status evaluation .
but i think he just focused now on high postprandial sugar readings, i will choose acarbose, it is alpha glucosidase inhibitor it decrease the carbohydrates absorption from intestinal tract so it lowers the postprandial hyperglycemia.
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  #17  
Old 08-30-2015
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I know these 2015.But i would go with metformin for the following reason.
Metformin stimulates AMPK wich basically increases cAMP/ATP ratio there for translocating GLUT4 receptors to cell member.
Much like EXCERCISING muscle where GLUT4 receptors is translocated to excercising skeletal muscle membrane INDEPENDENT of insulin in these specific scenario due to activation of the gene 5 AMP which basically increases cAMP/ATP in skeletal muscle to shunt glucose in starving muscle with having to tell the pancrease"Hey i need more insulin to translocate some GLUT4 from them working Glut-muscles" there by not compromising you to go into a hypoglycemia while excercising and not shunting glucose to the not needed energy in fat cells.

thats my 2 cent on it.Correct any one if im missing anything.
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