Amino Acid Supplementation Nearly
Triples Insulin Secretion in Type 2 Diabetics
Diabetes Care 2003; 26:625-630.
NEW YORK (Reuters Health) Mar 18 -
The insulin response
to carbohydrate consumption in patients with type 2 diabetes is greatly
enhanced by co-ingestion of
a free amino acid/protein mixture, according to a
report in the March issue of Diabetes Care.
"Insulin secretion in response to carbohydrate intake is blunted in type
2 diabetic patients," Dr. Luc J. C. van Loon, of Maastricht
University, the Netherlands, and colleagues note. "However, it is
not clear whether the insulin response to other stimuli, such as amino acids,
is also diminished."
The researchers examined the insulinotropic capacity of a mixture containing
free leucine, phenylalanine, and a protein hydrolysate in ten patients with
type 2 diabetes of 8.9 years mean duration and in ten healthy controls.
Insulin responses were determined on two occasions--once following ingestion
of carbohydrate alone, and later in combination with the free amino
acid/protein mixture.
Compared with carbohydrate ingestion alone, co-ingestion of the amino acid/protein mixture led to a significant increase in
insulin secretory response among both type 2 diabetics and control patients
(189% and 114%, respectively; p < 0.01). Specifically, in the diabetic patients, insulin secretion went
from 2 MU/mL over a 2-hour period after
carbohydrate ingestion to 6 MU/mL per 2h after the combination test.
"Plasma glucose, glucagon, growth hormone, cortisol, insulin-like growth
factor I and insulin-like growth factor binding protein 3 responses were not
different between trials within the 2-h time frame," Dr. van Loon and
colleagues report.
They conclude that insulin secretory capacity is underestimated in type 2 diabetics, and that nutritional interventions to improve
postprandial glucose disposal warrant further study.
"Clinically, consideration of antioxidants as
adjunct therapy in type 2 diabetes is warranted because of the many reports of
elevated markers of oxidative stress in patients with this disease, which is
characterized by imperfect management of glycemia, consequent chronic
hyperglycemia, and relentless deterioration of ß-cell function." (from a
long paper) http://www.medscape.com/viewarticle/450151?mpid=11203