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a Departments of Medicine, University of British Columbia, Vancouver, Canada
b Departments of Physiology, University of British Columbia, Vancouver, Canada
c Hans Kneoll Institute for Natural Product Research, Halle, Germany
d Department of Medicine, Harvard University, Boston, Massachusetts
e Linco Research Inc., St. Charles, Missouri
f Laboratory of Clinical Physiology, Gerontology Research Center, National Institute on Aging, National Institutes of Health, Baltimore, Maryland
Graydon S. Meneilly, Rm S 169, Vancouver Hospital and Health Sciences Centre, UBC Site 2211, Wesbrook Mall, Vancouver, BC V6T 2B5 E-mail: meneilly{at}interchange.ubc.ca.
Decision Editor: John E. Morley, MB, BCh
Background. The current studies were designed to examine the effect of aging and diabetes on the enteroinsular axis.
Methods. Healthy young control subjects (n = 10 young; age 23 ± 1 years; body mass index [BMI] 24 ± 1 kg/m2), healthy elderly subjects (n = 10; age 80 ± 2 years; BMI 26 ± 1 kg/m2), and elderly patients with type 2 diabetes (n = 10; age 76 ± 2 years; BMI 26 ± 2 kg/m2) underwent a 3-hour oral glucose tolerance test (glucose dose 40 gm/m2).
Results. Insulin responses were not different between young controls and elderly patients with diabetes but were significantly lower in elderly patients with diabetes and young controls than in elderly controls (young control: 178 ± 27 pM; elderly control: 355 ± 57 pM; elderly diabetes: 177 ± 30 pM; p < .05 elderly control vs young control and elderly diabetes). Total glucagon-like peptide 1 (GLP-1) responses were not significantly different between young and elderly controls and patients with diabetes (young control: 15 ± 2 pM; old control: 8 ± 2 pM; elderly diabetes: 12 ± 3 pM; p = ns). Active GLP-1 responses were also not different between young and elderly controls and patients with diabetes (young control: 5 ± 1 pM; old control: 6 ± 1 pM; elderly diabetes: 7 ± 1 pM; p = ns). However, the difference between total and active GLP levels was significantly greater in the young controls (young control: 10 ± 2 pM; old control: 2 ± 2 pM; elderly diabetes: 4 ± 2 pM; p < .05, young vs elderly). Glucose-dependent insulinotropic polypeptide responses were not different between young and elderly controls and between elderly controls and patients with diabetes but were significantly higher in elderly patients with diabetes than in young controls (young control: 97 ± 12 pM; elderly control: 121 ± 16 pM; elderly diabetes: 173 ± 27 pM; p < .05, young vs elderly diabetes). Glucagon responses were reduced in elderly controls but were similar in young controls and elderly patients with diabetes (young control: 15 ± 1 pM; elderly control: 9 ± 1 pM; elderly diabetes: 16 ± 1 pM; p < .01 elderly control vs young control and elderly diabetes). Dipeptidyl peptidase IV levels were lower in both elderly controls and patients with diabetes when compared with young controls (young control: 0.17 ± 0.01; elderly control: 0.15 ± 0.01; elderly diabetes: 0.15 ± 0.01 
OD/20 minutes; p < .05, elderly vs young).
Conclusions. We conclude that normal aging and diabetes are associated with multiple changes in the enteroinsular axis.
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