Objective: To investigate the reproducibility of the plasma glucose (PG) response to exercise in subjects with type 1 diabetes on a nonintensive insulin regimen.
Research Design And Methods: Subjects cycled for 45 min at 50% VO(2max) on two occasions (studies 1 and 2) either 1 h after lunch and usual insulin (protocol A) or after overnight fasting without morning insulin (protocol B). Identical diet, activity, and insulin (twice daily neutral and intermediate) were maintained before and during each study day. A total of 13 type 1 diabetic subjects (6 men and 7 women, BMI 24.0 +/- 0.9 kg/m(2) [means +/- SE], age 42.6 +/- 2.7 years, diabetes duration 14.1 +/- 2.8 years) completed protocol A, and 7 (3 men and 4 women, BMI 25.8 +/- 1.3 kg/m(2), age 39.7 +/- 1.3 years, diabetes duration 14 +/- 4.4 years) completed protocol B.
Results: In protocol A (fed), the fall in PG during exercise was 4.5 +/- 1.0 and 5.0 +/- 0.8 mmol/l in studies 1 and 2, respectively, whereas in protocol B (fasted), it was 0.6 +/- 0.8 and 3.4 +/- 1.6 mmol/l. Regression analysis of the change in PG in protocol A in study 1 versus study 2 showed poor reproducibility (r(2) = 0.12, P = 0.25) despite uniform conditions. In protocol B, the fall in PG was more reproducible (r(2) = 0.81, P = 0.006). In fed subjects, there was better (P = 0.01) and clinically useful reproducibility of the PG at exercise completion (r(2) = 0.77, P = 0.0001) compared with preexercise.
Conclusions: These results indicate poor reproducibility of the change in PG during exercise after feeding in type 1 diabetes on nonintensive insulin regimens but reasonable reproducibility when fasting. Exercise apparently decreases the glycemic variability after feeding, so that PG concentrations after exercise seek a reproducible "target." Thus, the absolute PG level after a typical bout of exercise in the fed state should be a good guide to carbohydrate or insulin adjustment on subsequent occasions.
Download full-text PDF |
Source |
---|---|
http://dx.doi.org/10.2337/diacare.26.2.297 | DOI Listing |
Neurology
August 2015
From Janssen Alzheimer Immunotherapy Research & Development, LLC (E.L., R.M., P.C., K.M.G., J.D., Y.L., I.C.T., S.B., E.Y., H.R.B.), South San Francisco, CA; Janssen Pharmaceutical (M.E.S.), Beerse, NV; Brigham & Women's Hospital (R.S.), Boston, MA; University of Michigan (R.K.), Ann Arbor; University of Pittsburgh (N.S.M., W.E.K., C.A.M.), PA; Butler Hospital (S.S.), Providence, RI; UCL Institute of Neurology (N.C.F.), London, UK; IXICO plc (D.L.H., A.S.L.), London, UK; Pfizer Inc. (B.T.W.), Groton, CT; Pfizer Inc. (K.B.), Collegeville, PA; Global R&D Partners, LLC (M.G.), San Diego, CA; and University of California (M.G.), San Diego.
Objective: To evaluate the effects of bapineuzumab on brain β-amyloid (Aβ) burden using (11)C-Pittsburgh compound B ((11)C-PiB)-PET.
Methods: Two phase 3 clinical trials, 1 each in apolipoprotein APOE ε4 carriers and noncarriers, were conducted in patients with mild to moderate Alzheimer disease dementia. Bapineuzumab, an anti-Aβ monoclonal antibody, or placebo, was administered by IV infusion every 13 weeks for 78 weeks.
N Engl J Med
January 2014
From Butler Hospital, Providence, RI (S.S.); Brigham and Women's Hospital, Boston (R.S.); University College London, Institute of Neurology, London (N.C.F.); University of Göteborg, Sahlgrenska University Hospital, Mölndal, Sweden (K.B.); University of Pittsburgh, Pittsburgh (W.K.); Veterans Affairs Medical Center, Seattle (M.R.); Cleo Roberts Center for Clinical Research/Sun Health Research Institute, Sun City, AZ (M.S.); Columbia University (L.S.H.) and New York University Langone Medical Center (S.F.), New York; University of Rochester School of Medicine and Dentistry, Rochester, NY (A.P.P.); Janssen Alzheimer Immunotherapy Research and Development, South San Francisco, CA (M.R., N.K., B.N., V.G., M.M., D.W., Y.L., I.C.T., E.L., E.Y., H.R.B.); Janssen Research and Development, Titusville, NJ (J.L.); Global R&D Partners and the University of California, San Diego - both in San Diego (M.G.); and Pfizer, Collegeville, PA (R.B.).
Background: Bapineuzumab, a humanized anti-amyloid-beta monoclonal antibody, is in clinical development for the treatment of Alzheimer's disease.
Methods: We conducted two double-blind, randomized, placebo-controlled, phase 3 trials involving patients with mild-to-moderate Alzheimer's disease--one involving 1121 carriers of the apolipoprotein E (APOE) ε4 allele and the other involving 1331 noncarriers. Bapineuzumab or placebo, with doses varying by study, was administered by intravenous infusion every 13 weeks for 78 weeks.
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!