Objective: The investigation was performed to study the effects of 200 mg oral caffeine on glucose tolerance. Design: Single-blind Latin square with active treatment (caffeine) and placebo. Setting: The University of Padova, Department of Internal Medicine. Subjects: 30 nonsmoking healthy subjects aged 26±32 years who abstained not only from coffee but also from tea, chocolate and cola for 4 weeks and who had given their informed consent. Interventions: A 75 g oral glucose tolerance test (OGTT) was performed after giving caffeine or placebo (highly decaffeinated coffee). Results: The glycaemic curve was normal in all subjects and was similar in the two groups until the second hour; in subjects taking caffeine a shift towards the right was detected at the 2nd, 3rd and 4th hours in comparison to those taking the placebo. Blood insulin levels were comparable after caffeine and after placebo along the entire OGTT. Conclusions: The data suggest that caffeine intake induces a rise in blood glucose levels that is insulin independent. Sponsor:

1. In 12 unselected outpatients with chronic obstructive pulmonary disease and six controls, arterial pH, PaO2, PaCO2 and oxygen saturation (SaO2), forced expiratory volume in 1.0 s (FEV1.0) and vital capacity were measured. Subjects were grouped into those with or without obstruction based on the Tiffenau index. The Baseline Dyspnoea Index was employed to objectify the severity of dyspnoea and the Borg index to evaluate the subjective sensation. Blood pressure was measured with a sphygmomanometer; calf arterial flow both at rest and during reactive hyperaemia with a plethysmograph. Basal and minimal resistance were calculated.2.FEV1.0 was 26% lower in patients with obstruction than in controls, and was also lower in patients with moderate-to-severe obstruction compared with those with mild or no obstruction. Arterial flow (75% greater in the patients with obstruction) progressively increased with increasing severity of obstruction, being 54% higher in those with mild obstruction than in those with no obstruction (P<0.001), and 28% higher in moderate-severe than in mild obstruction (P<0.005). In multiple regressions, F correlated inversely with FEV1.0, PaO2 and SaO2, and directly with PaCO2. Basal resistance correlated positively with FEV1.0, SaO2 and the Tiffenau index, and inversely with PaCO2 (r=-0.52, P=0.02). Minimal resistance was significantly lower in obstructed than in non-obstructed subjects. Both basal and minimal resistance progressively decreased, although insignificantly, with worsening bronchial obstruction. PaCO2 did not correlate with any haemodynamic parameter. Borg index correlated indirectly with FEV1.0 and basal resistance directly with arterial flow.3. Patients with chronic obstructive pulmonary disease therefore tend to show chronic vasodilatation depending on hypoxia rather than PaCO2. Other mechanisms could be involved in this phenomenon. The Borg index is a good indicator of oxygen desaturation and vasodilatation.

The circadian rhythm is controlled by adrenergic fibres transmitted via the spinal cord.

1. In 12 unselected outpatients with chronic obstructive pulmonary disease and six controls, arterial pH, PaO2, PaCO2 and oxygen saturation (SaO2), forced expiratory volume in 1.0 s (FEV1.0) and vital capacity were measured. Subjects were grouped into those with or without obstruction based on the Tiffenau index. The Baseline Dyspnoea Index was employed to objectify the severity of dyspnoea and the Borg index to evaluate the subjective sensation. Blood pressure was measured with a sphygmomanometer; calf arterial flow both at rest and during reactive hyperaemia with a plethysmograph. Basal and minimal resistance were calculated.2.FEV1.0 was 26% lower in patients with obstruction than in controls, and was also lower in patients with moderate-to-severe obstruction compared with those with mild or no obstruction. Arterial flow (75% greater in the patients with obstruction) progressively increased with increasing severity of obstruction, being 54% higher in those with mild obstruction than in those with no obstruction (P<0.001), and 28% higher in moderate-severe than in mild obstruction (P<0.005). In multiple regressions, F correlated inversely with FEV1.0, PaO2 and SaO2, and directly with PaCO2. Basal resistance correlated positively with FEV1.0, SaO2 and the Tiffenau index, and inversely with PaCO2 (r=-0.52, P=0.02). Minimal resistance was significantly lower in obstructed than in non-obstructed subjects. Both basal and minimal resistance progressively decreased, although insignificantly, with worsening bronchial obstruction. PaCO2 did not correlate with any haemodynamic parameter. Borg index correlated indirectly with FEV1.0 and basal resistance directly with arterial flow.3. Patients with chronic obstructive pulmonary disease therefore tend to show chronic vasodilatation depending on hypoxia rather than PaCO2. Other mechanisms could be involved in this phenomenon. The Borg index is a good indicator of oxygen desaturation and vasodilatation.

No abstract