I’ll get to the following article when time allows. It’s in a June, 2012, issue of Diabetes Care. (Didn’t they publish management principles just six months ago? Jeez.)
-Steve
I’ll get to the following article when time allows. It’s in a June, 2012, issue of Diabetes Care. (Didn’t they publish management principles just six months ago? Jeez.)
-Steve
Filed under Drugs for Diabetes
Dr. Parker – I am curious what your thoughts will be when you review this.
My guess is this probably creates more confusion and grief for Doctor notwithstanding great thoughts.
To me there seemed to be a sea change in attitude of ADA that was incredible.
two statements:
Any rise in glycemia is the net result of glucose influx exceeding glucose outflow from the plasma compartment. In the fasting state, hyperglycemia is directly related to increased hepatic glucose production.
In the postprandial state, further glucose excursions result from the combination of insufficient suppression of this glucose output and defective insulin stimulation of glucose disposal in target tissues, mainly
skeletal muscle. Once the renal tubular transport maximum for glucose is exceeded, glycosuria curbs, though does not
prevent, further hyperglycemia.
( Really – liver is part of problem, energy balance and low cab diets may play role.)
role of metformin:
Metformin, a biguanide, remains the most widely used first-line type 2 diabetes drug; its mechanism of action predominately
involves reducing hepatic glucose production (54,55).
( Salk and John Hopkins childrens research on metformin may be right.)
otherwise – have great day.
Hi, Jim. I can’t wait to read it…but must wait. Sounds interesting. I knew they had to revise statements about rosiglitazone since we’ll see far fewer prescriptions written for it in the U.S. Too many hoops for docs to jump through, and with good reason (cardiac toxicity!).
-Steve