![]() ![]() It has been shown experimentally that in rats fasted for 72 h, β-cells had decreased intracellular insulin stores and synthesis capacity in response to glucose administration, an effect reversed within only 6 h of refeeding 16. This is further illustrated by the rapid transition from reductions in insulin secretion during acute hypoglycaemia to an increase following a return of glucose supply. In mice and rats, chronic hyperglycaemia can cause β-cell hyperplasia and hypertrophy, while chronic hypoglycaemia may lead to pronounced β-cell hypotrophy and/or β-cell death 11, 12, 13, 14, 15, indicating high plasticity of β-cell mass. the β-cell failure seen in Type 2 Diabetes and restoration of function following weight loss 10. Currently, focus is increasing on the complex functional dynamics of β-cells in response to metabolic stress, as well as the potential return to normal function when the metabolic stress has resolved, to understand e.g. These rapid changes to circulating insulin levels in response to alterations in blood glucose levels have been well characterised however, the effects of prolonged metabolic stress on β-cell dynamics are still not completely understood. Postnatally, β-cell proliferation is thought to decline significantly after infancy in humans, mice and rats 2, 3, 4, 5, 6, 7, 8 however, β-cells seem to have an extraordinary ability to rapidly adapt to food- and activity-related changes in circulating glucose levels by changing insulin secretion depending on metabolic needs 9. In conclusion, our findings indicate that prolonged hypoglycaemia inactivates β-cells, which can rapidly be reactivated when needed, demonstrating the high plasticity of β-cells even following prolonged suppression.īlood glucose is the main factor controlling pancreatic insulin secretion and β-cell function, furthermore, changes to blood glucose levels appear to influence the maintenance of β-cell mass 1. Within two days after infusion-stop, plasma glucose and c-peptide levels normalised and all remaining parameters were fully reversed after 4 weeks. Glucagon: total pancreas volume decreased during hypoglycaemia, whereas glucagon: islet volume increased. ![]() Relative β-cell nuclei: total pancreas volume decreased, while being unchanged relative to islet volume. Prolonged hypoglycaemia reduced c-peptide levels, islet volume and almost depleted islet insulin. Total volumes of pancreatic islets and β-cell nuclei, islet insulin and glucagon content, and plasma c-peptide levels were quantified. Animals were euthanized after 4 or 8 weeks of infusion, and either 2 days and 4 weeks after infusion-stop. Hypoglycaemia was induced in male and female rats by infusion of human insulin for 8 weeks, followed by a 4-week infusion-free recovery period. Here, the aim was to investigate pancreatic β-cell dynamics and function during and after prolonged hypoglycaemia. Although acute changes have been characterised, effects of prolonged metabolic stress on β-cell dynamics are still unclear. If ~isempty(find(any(stat.negclusterslabelmat(c,:)=ineg)))Ĭfg.Pancreatic β-cells have an extraordinary ability to adapt to acute fluctuations in glucose levels by rapid changing insulin production to meet metabolic needs. If ~isempty(find(any(stat.negclusterslabelmat(:,t)=ineg))) If ~isempty(find(any(stat.posclusterslabelmat(c,:)=ipos)))Ĭfg.highlightchannel = % find the channels belonging to this cluster If ~isempty(find(any(stat.posclusterslabelmat(:,t)=ipos)))Ĭfg.xlim = % find the significant time range for this cluster % load biosemi160 into q (which has sensor locations in polar coordinates
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