Dietary carbohydrate modification enhances insulin secretion in persons with the metabolic syndrome.
BACKGROUND
The metabolic syndrome markedly increases the risk of type 2 diabetes and cardiovascular disease, but the influence of dietary modification on insulin and glucose metabolism independent of weight loss is still poorly understood.


OBJECTIVE
Our aim was to test whether carbohydrate dietary modifications improve insulin sensitivity and secretion and glucose tolerance in overweight or obese persons with the metabolic syndrome, even in the absence of weight loss.


METHODS
We assessed the effect of carbohydrate modification on insulin and glucose metabolism in 72 overweight or obese men and women with the metabolic syndrome, as determined according to the National Cholesterol Education Program criteria. The subjects were randomly assigned to 12-wk diets in which either rye bread and pasta or oat and wheat bread and potato were the main carbohydrate sources (34% and 37% of energy intake, respectively).


RESULTS
Body weight did not significantly change in either group during the trial. No significant difference was observed in the changes in fasting glucose and insulin concentrations or in glucose and insulin areas under the curve between the groups during a 2-h oral-glucose-tolerance test. The insulinogenic index (an index of early insulin secretion) increased more in the rye bread and pasta group than in the oat and wheat bread and potato group (33.2% compared with 5.5%; P = 0.026). In the combined groups, an enhanced insulinogenic index was associated with improved glucose tolerance, whereas weight gain worsened glucose tolerance. Moreover, even modest weight gains abolished the relative improvement in the insulinogenic index in the rye bread and pasta group compared with the oat and wheat bread and potato group (P for the interaction between weight change and group = 0.019).


CONCLUSIONS
Rye bread and pasta-based carbohydrate modification enhances early insulin secretion in persons with the metabolic syndrome, which may lower the risk of deteriorating glucose tolerance and development of type 2 diabetes.
Laaksonen
David E
DE
Department of Medicine, University of Kuopio, Kuopio, Finland. david.laaksonen@uku.fi
Toppinen
Leena K
LK
Juntunen
Katri S
KS
Autio
Karin
K
Liukkonen
Kirsi-Helena
KH
Poutanen
Kaisa S
KS
Niskanen
Leo
L
Mykkänen
Hannu M
HM
D000328:Adult; D000368:Aged; D019540:Area Under Curve; D001786:Blood Glucose / Q000187:drug effects / Q000378:metabolism*; D001835:Body Weight / Q000502:physiology; D001939:Bread; D003924:Diabetes Mellitus, Type 2 / Q000517:prevention & control; D004040:Dietary Carbohydrates / Q000008:administration & dosage* / Q000627:therapeutic use; D005215:Fasting; D005260:Female; D005951:Glucose Tolerance Test; D038321:Glycemic Index; D006801:Humans; D007328:Insulin / Q000378:metabolism*; D000078790:Insulin Secretion; D008297:Male; D024821:Metabolic Syndrome / Q000178:diet therapy* / Q000378:metabolism*; D008875:Middle Aged; D009765:Obesity / Q000378:metabolism*; D012434:Secale
D001786:Blood Glucose; D004040:Dietary Carbohydrates; D007328:Insulin