A low-glycemic index diet combined with exercise reduces insulin resistance, postprandial hyperinsulinemia, and glucose-dependent insulinotropic polypeptide responses in obese, prediabetic humans.
BACKGROUND
The optimal lifestyle intervention that reverses diabetes risk factors is not known.


OBJECTIVE
We examined the effect of a low-glycemic index (GI) diet and exercise intervention on glucose metabolism and insulin secretion in obese, prediabetic individuals.


METHODS
Twenty-two participants [mean ± SEM age: 66 ± 1 y; body mass index (in kg/m(2)): 34.4 ± 0.8] underwent a 12-wk exercise-training intervention (1 h/d for 5 d/wk at ≈ 85% of maximum heart rate) while randomly assigned to receive either a low-GI diet (LoGIX; 40 ± 0.3 units) or a high-GI diet (HiGIX; 80 ± 0.6 units). Body composition (measured by using dual-energy X-ray absorptiometry and computed tomography), insulin sensitivity (measured with a hyperinsulinemic euglycemic clamp with [6,6-(2)H(2)]-glucose), and oral glucose-induced insulin and incretin hormone secretion were examined.


RESULTS
Both groups lost equal amounts of body weight (-8.8 ± 0.9%) and adiposity and showed similar improvements in peripheral tissue (+76.2 ± 14.9%) and hepatic insulin sensitivity (+27.1 ± 7.1%) (all P < 0.05). However, oral glucose-induced insulin secretion was reduced only in the LoGIX group (6.59 ± 0.86 nmol in the prestudy compared with 4.70 ± 0.67 nmol in the poststudy, P < 0.05), which was a change related to the suppressed postprandial response of glucose-dependent insulinotropic polypeptide. When corrected for changes in β cell glucose exposure, changes in insulin secretion were attenuated in the LoGIX group but became significantly elevated in the HiGIX group.


CONCLUSIONS
Although lifestyle-induced weight loss improves insulin resistance in prediabetic individuals, postprandial hyperinsulinemia is reduced only when a low-GI diet is consumed. In contrast, a high-GI diet impairs pancreatic β cell and intestinal K cell function despite significant weight loss. These findings highlight the important role of the gut in mediating the effects of a low-GI diet on type 2 diabetes risk reduction.
Solomon
Thomas Pj
TP
Department of Pathobiology, Lerner Research Institute and Nutrition, Case Western Reserve University, Cleveland, OH, USA. kirwanj@ccf.org
Haus
Jacob M
JM
Kelly
Karen R
KR
Cook
Marc D
MD
Filion
Julianne
J
Rocco
Michael
M
Kashyap
Sangeeta R
SR
Watanabe
Richard M
RM
Barkoukis
Hope
H
Kirwan
John P
JP
D050154:Adiposity / Q000502:physiology; D000368:Aged; D003131:Combined Modality Therapy; D015444:Exercise / Q000502:physiology*; D005260:Female; D005749:Gastric Inhibitory Polypeptide / Q000097:blood; D005951:Glucose Tolerance Test; D038321:Glycemic Index; D006801:Humans; D006946:Hyperinsulinism / Q000097:blood / Q000628:therapy*; D007328:Insulin / Q000097:blood* / Q000378:metabolism; D007333:Insulin Resistance / Q000502:physiology*; D000078790:Insulin Secretion; D008099:Liver / Q000503:physiopathology; D008297:Male; D009765:Obesity / Q000097:blood / Q000178:diet therapy / Q000628:therapy*; D019518:Postprandial Period; D015431:Weight Loss / Q000502:physiology*
D007328:Insulin; D005749:Gastric Inhibitory Polypeptide