The hypothesis that propionate is a short-term feed intake-regulating agent was studied. Mature wether sheep were infused over 20 min with Na propionate into the mesenteric vein, while feed intake and feeding pattern were monitored over 1.5 h. Feed intake was reduced by infusions at 2 mmol/min, which were associated with marked increases in jugular as well as portal concentrations of insulin, glucose, and propionate. In a second experiment, animals were infused with 2 mmol/min Na propionate into the portal vein. No decrease in feed intake was observed, although there were similar increases in insulin, glucose, and propionate as found in mesenteric vein-infused animals. It is concluded that mesenteric propionate in high doses acts as a satiety factor. Possible explanations for the difference between site of infusion may be a different distribution of the infusate over the liver and/or the presence of propionate-sensitive receptors in the mesenteric/portal vein region. It seems unlikely that insulin concentrations are involved in inducing satiety in propionate-infused animals.

Purpose of Review Beta-cell replacement is the best therapeutic option for patients with type 1 diabetes. Because of donor scarcity, more extended criteria donors are used for transplantation. Donation after circulatory death donors (DCD) are not commonly used for pancreas transplantation, because of the supposed higher risk of complications. This review gives an overview on the pathophysiology, risk factors, and outcome in DCD transplantation and discusses different preservation methods. Recent Findings Studies on outcomes of DCD pancreata show similar results compared with those of donation after brain death (DBD), when accumulation of other risk factors is avoided. Hypothermic machine perfusion is shown to be a safe method to improve graft viability in experimental settings. Summary DCD should not be the sole reason to decline a pancreas for transplantation. Adequate donor selection and improved preservation techniques can lead to enhanced pancreas utilization and outcome.

No abstract

Summary Brain death (BD) leads to a systemic inflammation associated with the activation of coagulation, which could be related to decreased microcirculatory perfusion. Evidence shows that females exhibit higher platelet aggregability than males. Thus, we investigated sex differences in platelets, coagulation and microcirculatory compromise after BD. BD was induced in male and female (proestrus) Wistar rats. After 3 h, we evaluated: (i) intravital microscopy to evaluate mesenteric perfusion and leucocyte infiltration; (ii) platelet aggregation assay; (iii) rotational thromboelastometry; and (iv) Serum NOx‐. Female rats maintained the mesenteric perfusion, whereas male reduced percentage of perfused vessels. Male BD presented higher platelet aggregation than the controls. In contrast, female BD had lower platelet aggregation than the control. Thromboelastometry indicated a reduction in clot firmness with increased clotting time in the female group compared with the male group. Serum NOx‐ level in female BD was higher than that in the male BD and female control. There is sex dimorphism in platelet function and clotting process, which are altered in different ways by BD. Thus, it is possible to connect the reduction in microcirculatory perfusion in males to intravascular microthrombi formation and the maintenance of perfusion in females to a higher inflammatory response and NO synthesis.