Glycemic load effect on fasting and post-prandial serum glucose, insulin, IGF-1 and IGFBP-3 in a randomized, controlled feeding study.
OBJECTIVE
The effect of a low glycemic load (GL) diet on insulin-like growth factor-1 (IGF-1) concentration is still unknown but may contribute to lower chronic disease risk. We aimed to assess the impact of GL on concentrations of IGF-1 and IGF-binding protein-3 (IGFBP-3).


METHODS
We conducted a randomized, controlled crossover feeding trial in 84 overweight obese and normal weight healthy individuals using two 28-day weight-maintaining high- and low-GL diets. Measures were fasting and post-prandial concentrations of insulin, glucose, IGF-1 and IGFBP-3. In all 80 participants completed the study and 20 participants completed post-prandial testing by consuming a test breakfast at the end of each feeding period. We used paired t-tests for diet component and linear mixed models for biomarker analyses.


RESULTS
The 28-day low-GL diet led to 4% lower fasting concentrations of IGF-1 (10.6 ng/ml, P=0.04) and a 4% lower ratio of IGF-1/IGFBP-3 (0.24, P=0.01) compared with the high-GL diet. The low-GL test breakfast led to 43% and 27% lower mean post-prandial glucose and insulin responses, respectively; mean incremental areas under the curve for glucose and insulin, respectively, were 64.3±21.8 (mmol/l/240 min; P<0.01) and 2253±539 (μU/ml/240 min; P<0.01) lower following the low- compared with the high-GL test meal. There was no effect of GL on mean homeostasis model assessment for insulin resistance or on mean integrated post-prandial concentrations of glucose-adjusted insulin, IGF-1 or IGFBP-3. We did not observe modification of the dietary effect by adiposity.


CONCLUSIONS
Low-GL diets resulted in 43% and 27% lower post-prandial responses of glucose and insulin, respectively, and modestly lower fasting IGF-1 concentrations. Further intervention studies are needed to weigh the impact of dietary GL on risk for chronic disease.
Division of Endocrinology, Metabolism and Nutrition, Department of Medicine, University of Washington, Seattle, WA, USA.
S S
SS
Runchey
M N
MN
Pollak
L M
LM
Valsta
G D
GD
Coronado
Y
Y
Schwarz
K L
KL
Breymeyer
C
C
Wang
C-Y
CY
Wang
J W
JW
Lampe
M L
ML
Neuhouser
D000328:Adult; D000465:Algorithms; D015415:Biomarkers / Q000097:blood; D001786:Blood Glucose / Q000032:analysis; D015992:Body Mass Index; D018592:Cross-Over Studies; D004040:Dietary Carbohydrates / Q000009:adverse effects / Q000378:metabolism; D005260:Female; D038321:Glycemic Index; D006801:Humans; D006943:Hyperglycemia / Q000209:etiology / Q000517:prevention & control*; D006946:Hyperinsulinism / Q000209:etiology / Q000517:prevention & control*; D007328:Insulin / Q000097:blood; D007333:Insulin Resistance; D018972:Insulin-Like Growth Factor Binding Protein 3 / Q000097:blood*; D007334:Insulin-Like Growth Factor I / Q000032:analysis*; D008297:Male; D009765:Obesity / Q000097:blood / Q000178:diet therapy / Q000378:metabolism*; D050177:Overweight / Q000097:blood / Q000178:diet therapy / Q000378:metabolism*; D055815:Young Adult
D015415:Biomarkers; D001786:Blood Glucose; D004040:Dietary Carbohydrates; C515497:IGFBP3 protein, human; D007328:Insulin; D018972:Insulin-Like Growth Factor Binding Protein 3; D007334:Insulin-Like Growth Factor I