The gut hormone glucose-dependent insulinotropic polypeptide is downregulated in response to myocardial injury.

BACKGROUND: The gut incretin hormones GLP-1 (glucagon-like peptide-1) and GIP (glucose-dependent insulinotropic peptide) are secreted by enteroendocrine cells following food intake leading to insulin secretion and glucose lowering. Beyond its metabolic function GIP has been found to exhibit direct cardio- and atheroprotective effects in mice and to be associated with cardiovascular prognosis in patients with myocardial infarction. The aim of this study was to characterize endogenous GIP levels in patients with acute myocardial infarction. METHODS AND RESULTS: Serum concentrations of GIP were assessed in 731 patients who presented with clinical indication of coronary angiography. Circulating GIP levels were significantly lower in patients with STEMI (ST-elevation myocardial infarction; n=100) compared to clinically stable patients without myocardial infarction (n=631) (216.82 pg/mL [Q1-Q3: 52.37-443.07] vs. 271.54 pg/mL [Q1-Q3: 70.12-542.41], p = 0.0266). To characterize endogenous GIP levels in patients with acute myocardial injury we enrolled 18 patients scheduled for cardiac surgery with cardiopulmonary bypass and requirement of extracorporeal circulation as a reproducible condition of myocardial injury. Blood samples were drawn directly before surgery (baseline), upon arrival at the intensive care unit (ICU), 6 h post arrival to the ICU and at the morning of the first and second postoperative days. Mean circulating GIP concentrations decreased in response to surgery from 45.3 ± 22.6 pg/mL at baseline to a minimum of 31.9 ± 19.8 pg/mL at the first postoperative day (p = 0.0384) and rose again at the second postoperative day (52.1 ± 28.0 pg/mL). CONCLUSIONS: Circulating GIP levels are downregulated in patients with myocardial infarction and following cardiac surgery. These results might suggest nutrition-independent regulation of GIP secretion following myocardial injury in humans.

The pupillary light reflex (PLR) as a marker for the ability to work or drive - a feasibility study.

BACKGROUND: The PLR (pupillary light reflex) can be a marker for pathological medical conditions, such as neurodegenerative or mental health disorders and diseases as well as marker for physiological alterations, such as age, sex or iris color. PLR alterations have been described in people after alcohol consumption, as well. However, the effect of sleep deprivation on PLR parameters is still under debate. METHODS: The aim of this study was to investigate the feasibility of PLR measurements in sleep-deprived and alcohol-exposed participants. In addition, we wanted to identify PLR parameters that were altered by sleep deprivation and alcohol exposure. RESULTS: Altogether n = 50 participants have been included in this study. Differences in the PLR parameters initial diameter (dinit), latency (∆tlat), acceleration (∆ta), contraction velocity (ϑcon), quarter dilatation velocity (ϑ1/4dil), half dilatation time (∆t1/2), and the line integral (L(0.3500)) have been evaluated between baseline, sleep deprivation, as well as alcohol exposure. In a generalized linear mixed models design, we could observe statistically significant associations between the type of exposure and the PLR parameters half dilatation time and half dilatation time after the first light pulse (all p < 0.05). The participants' latency showed a significant association in dependence of the type of exposure after the second light pulse (p < 0.05). CONCLUSION: Our study delivers first promising results to further develop devices that may identify conditions that impair the ability to work or drive.