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- Understanding Cystic Fibrosis by Karen Hopkin
- Understanding Cystic Fibrosis (Understanding Health And Sickness Series) 1998
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Understanding Cystic Fibrosis by Karen Hopkin
Healthy age-, sex-, and weight-matched control subjects were also studied using a glucose-potentiated arginine test, a mixed meal, and h continuous glucose monitoring. All participants met criteria for normal glucose tolerance prior to study. Conversely, when potentiated by hyperglycemia, arginine-stimulated insulin secretion was lower in PI-CF.
C-peptide—based measures of insulin secretion produced similar results, implying that between-group differences were not explained by differences in hepatic insulin extraction. Glucagon responses were also impaired in the PI-CF group. In response to a mixed meal, glucose was higher and insulin secretion was lower in the PI-CF group.
Understanding Cystic Fibrosis (Understanding Health And Sickness Series) 1998
However, it remains to be ascertained whether insulin secretion in this group was indeed appropriate for the prevailing insulin action via calculation of a disposition index. Unfortunately, the time course of insulin secretion reconstructed by deconvolution in this experiment is dependent on the concentration and time course of plasma glucose. Another interesting finding noted during the mixed meal was the impaired active glucagon-like peptide 1 GLP-1 and total gastric inhibitory polypeptide response to meal ingestion in the PI-CF group.
Ultimately, the processes driving the temporal decline in secretory function that lead to diabetes in patients with and without cystic fibrosis are poorly understood. However, there are some important observations arising from the study of islet function that provide context to this series of experiments. Insulin release in response to hyperglycemia is a composite of de novo synthesis, docking, and release of preformed insulin granules assembled and stored during fasting Isolated islets, isolated perfused pancreata, and the in vivo response to intravenous glucose is characterized by a biphasic pattern First-phase insulin secretion is thought to represent the release of preformed, stored insulin granules, whereas the second phase represents secretion of newly synthesized insulin Multiple studies demonstrate absent first-phase secretion in people with type 2 diabetes Does this explain the decreased and delayed response to an oral challenge?
What is its significance? Is insulin granule storage truly defective in type 2 diabetes or is it representative of a global synthetic defect? How do these compare with those obtained using arginine with or without glucose potentiation? Intravenous arginine depletes preformed insulin granules 15 , Subsequent insulin secretion in response to hyperglycemia if measured at frequent intervals would be likely to represent the provision of new insulin by de novo synthesis and might provide additional insight into the mechanisms leading to defective insulin secretion in people with type 2 diabetes or cystic fibrosis.
The significance of this is unknown, and at present, there is little data as to how the GLP-1 response to intravenous arginine changes across glucose tolerance states. GLP-1 secretion is affected by luminal nutrient concentrations and gastrointestinal motility The significance of the decreased incretin hormone concentrations observed in PI-CF remains unclear at present but may represent enteroendocrine dysfunction unique to cystic fibrosis. One might speculate that in the presence of pancreatic insufficiency, despite pancreatic enzyme replacement, a decrease in the products of intraluminal digestion impairs incretin hormone secretion, which seems to primarily affect postprandial de novo insulin synthesis Insulin concentrations reflect the net sum of two processes—insulin secretion and hepatic insulin clearance—which may change independently with worsening glucose tolerance Therefore, measurement of insulin secretion is best accomplished from deconvolution of C-peptide concentrations, as was the case in the study by Sheikh et al.
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This is necessary because the half-life of C-peptide is longer than that of insulin and accumulates in the circulation. Knowledge of its clearance is necessary to calculate insulin secretion However, estimating proinsulin secretion from proinsulin concentrations is problematic as proinsulin has a long half-life in the circulation and the kinetics of its clearance in individuals is not well characterized. A proinsulin—to—C-peptide ratio does not solve this problem, as the half-life of C-peptide differs from that of proinsulin, limiting the usefulness of this parameter 4.
Given this background, we hope that the study by Sheikh et al. This may help develop novel insights into the processes that drive postprandial insulin secretion in health, in cystic fibrosis, and in type 2 diabetes.
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In that context, the current study is an important first step in this direction. No potential conflicts of interest relevant to this article were reported. Readers may use this article as long as the work is properly cited, the use is educational and not for profit, and the work is not altered.
More information is available at http: We only request your email address so that the person you are recommending the page to knows that you wanted them to see it, and that it is not junk mail. We do not capture any email address. Skip to main content. Diabetes Jan; 66 1: Figure 1 Multiple gastrointestinal factors could influence the insulin secretory response to a meal challenge.
Footnotes See accompanying article, p. Diabetes Care ; The oral minimal model method.
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