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The release of immunoreactive gastric inhibitory polypeptide (IR-GIP) in response to a standard meal was examined in 10 normal subjects and 15 type I (insulin-dependent) diabetics 7 days (test I), 14 days (test II), and 3 months (test III) after time of diagnosis. During all three tests, the diabetics had significantly lower plasma IR-GIP concentrations than the controls from 15-90 min after the standard meal. The IR-GIP response in the diabetics measured as the integrated area under the response curve corresponded to 70% of that of normal subjects. beta-cell function evaluated from the C-peptide response to the meal increased significantly from test I to test III whereas the IR-GIP response was similar during all three tests. As GIP is known to potentiate glucose-induced insulin secretion and possibly the biosynthesis of insulin, the low IR-GIP responses in subjects with type I diabetes may significantly influence insulin levels and hyperglycemia.

Most studies agree that specific regions of the hippocampus and specific subcortical regions show neuronal loss in Alzheimer’s disease (AD). The aim of the study was to use design-based stereological methods to obtain an estimate of the total glial cell population in 14 AD cases and 20 controls to determine whether brains from AD patients have a different number of neocortical glial cells than controls. The mean total number of neocortical glial cells was 25.9 × 10⁹ for the AD group and 29.1 × 10⁹ for the control group, 2p = 0.18. The mean total number of neocortical neurons was 18.9 × 10⁹ for the AD group and 21.2 × 10⁹ for the control group, 2p = 0.059. Estimates of the sum of all glial cells and neurons in the neocortex were in the order of 50 billion cells with a glia to neuron ratio of 1.37 in both groups.