Increased plasma pancreatic polypeptide (PP) in diabetic ketoacidosis; normalization following treatment

1980 ◽  
Vol 93 (4) ◽  
pp. 466-469 ◽  
Author(s):  
S. Skare ◽  
K. F. Hanssen ◽  
G. Lundqvist

Abstract. As both hypoglycaemia and hyperglycaemia may modify plasma levels pancreatic polypeptide (PP), we measured plasma PP by a homologous radioimmunoassay in seven diabetics who were admitted to the hospital in overt diabetic ketoacidosis (initial blood glucose 27.1–55.0 mmol/l). None had circulating PP-antibodies. All were treated with continuous infusion of insulin and fluids. Before starting treatment, plasma PP ranged from 2585–136 pmol/l (mean 629 pmol/l). Following treatment plasma PP decreased gradually in all patients. The following morning mean plasma PP was 242 pmol/l, 67 pmol/l when one uraemic patient was excluded. The normal value is less than 100 pmol/l. This study shows that plasma PP is clearly elevated in diabetic ketoacidosis and decreases following treatment.

1998 ◽  
Vol 274 (2) ◽  
pp. E317-E320 ◽  
Author(s):  
Bernard Coulie ◽  
Jan Tack ◽  
Roger Bouillon ◽  
Theo Peeters ◽  
Jozef Janssens

The selective 5-hydroxytryptamine-1 receptor agonist sumatriptan inhibits exocrine pancreatic function in humans. No data are available on the effect of sumatriptan on fasting and postprandial endocrine pancreatic function in humans. To elucidate the influence of 5-hydroxytryptamine-1 receptor activation by sumatriptan on endocrine pancreatic function and blood glucose homeostasis, we determined plasma levels of somatostatin, glucagon, pancreatic polypeptide, insulin, and C-peptide before and after subcutaneous administration of sumatriptan (6 mg) in seven healthy volunteers, and we measured blood glucose and insulin plasma levels during an oral glucose tolerance test after placebo and after subcutaneous administration of sumatriptan (6 mg) in seven healthy volunteers. Sumatriptan significantly decreased the mean plasma levels of somatostatin, glucagon, pancreatic polypeptide, insulin and C-peptide ( P < 0.001) and also significantly decreased mean and peak plasma levels of insulin after an oral glucose challenge ( P < 0.02 and P = 0.04, respectively) without affecting glucose homeostasis. From our study, we speculate that activation of the 5-hydroxytryptamine-1 receptor inhibits endocrine pancreatic secretion.


Author(s):  
Dario Pitocco ◽  
Mauro Di Leo ◽  
Linda Tartaglione ◽  
Emanuele Gaetano Rizzo ◽  
Salvatore Caputo ◽  
...  

Background: Diabetic Ketoacidosis (DKA) is one of the most commonly encountered diabetic complication emergencies. It typically affects people with type 1 diabetes at the onset of the disease. It can also affect people with type 2 diabetes, although this is uncommon. Methods: Research and online content related to diabetes online activity is reviewed. DKA is caused by a relative or absolute deficiency of insulin and elevated levels of counter regulatory hormones. Results: Goals of therapy are to correct dehydration, acidosis and to reverse ketosis, gradually restoring blood glucose concentration to near normal. Conclusion: Furthermore it is essential to monitor potential complications of DKA and if necessary, to treat them and any precipitating events.


2021 ◽  
Vol 69 (1) ◽  
Author(s):  
Nora El Said Badawi ◽  
Mona Hafez ◽  
Heba Sharaf Eldin ◽  
Hend Mehawed Abdelatif ◽  
Shimaa Atef ◽  
...  

Abstract Background The debate for the optimum sodium concentration in the rehydration solution in diabetic ketoacidosis (DKA) persists till the moment. The aim was to compare the outcome of 0.9% saline versus 0.45% saline in children with moderate and severe (DKA) regarding the effect on serum electrolytes, duration of DKA resolution and the incidence of hyperchloremia. Results A retrospective analysis of 121 children with moderate or severe DKA was done. After the initial 4 h in which both groups received normal saline, patients were divided into two groups continuing on 0.9% (N=72) or switched to 0.45% saline (N=49). Serum chloride and Cl/Na ratios were significantly higher in 0.9% saline group at 4 and 8 h. The 0.9% saline group had significantly higher proportion of hyperchloremia at 4 and 8 h (P value: 0.002, 0.02). The median duration of correction of DKA (14 h among 0.9% saline versus 10 h among 0.45% saline) without significant difference (P value= 0.43). The change in plasma glucose, effective osmolarity, corrected Na levels were comparable between groups. Conclusion There is an unavoidable iatrogenically induced rise in serum chloride with higher incidence of hyperchloremia with the use of normal saline in rehydration of children presenting in DKA and shock. The use of 0.45% saline as post-bolus rehydration fluid is not associated with a decline in the corrected serum sodium concentration and does not affect the rate of correction of acidosis or rate of drop in blood glucose or duration of DKA resolution when compared to normal saline.


2021 ◽  
Author(s):  
Peter M. Wolfgram ◽  
Mogen Frenkel ◽  
Pamela Gage ◽  
Rebecca Sprague ◽  
Ashley Servi ◽  
...  

2006 ◽  
Vol 291 (4) ◽  
pp. G611-G620 ◽  
Author(s):  
Lixin Wang ◽  
Nicole R. Basa ◽  
Almaas Shaikh ◽  
Andrew Luckey ◽  
David Heber ◽  
...  

LPS injected intraperitoneally decreases fasted plasma levels of ghrelin at 3 h postinjection in rats. We characterized the inhibitory action of LPS on plasma ghrelin and whether exogenous ghrelin restores LPS-induced suppression of food intake and gastric emptying in fasted rats. Plasma ghrelin and insulin and blood glucose were measured after intraperitoneal injection of LPS, intravenous injection of IL-1β and urocortin 1, and in response to LPS under conditions of blockade of IL-1 or CRF receptors by subcutaneous injection of IL-1 receptor antagonist (IL-1Ra) or astressin B, respectively, and prostaglandin (PG) synthesis by intraperitoneal indomethacin. Food intake and gastric emptying were measured after intravenous injection of ghrelin at 5 h postintraperitoneal LPS injection. LPS inhibited the elevated fasted plasma ghrelin levels by 47.6 ± 4.9%, 58.9 ± 3.3%, 74.4 ± 2.7%, and 48.9 ± 8.7% at 2, 3, 5, and 7 h postinjection, respectively, and values returned to preinjection levels at 24 h. Insulin levels were negatively correlated to those of ghrelin, whereas there was no significant correlation between glucose and ghrelin. IL-1Ra and indomethacin prevented the first 3-h decline in ghrelin levels induced by LPS, whereas astressin B did not. IL-1β inhibited plasma ghrelin levels, whereas urocortin 1 had no influence. Ghrelin injected intravenously prevented an LPS-induced 87% reduction of gastric emptying and 61% reduction of food intake. These data showed that IL-1 and PG pathways are part of the early mechanisms by which LPS suppresses fasted plasma ghrelin and that exogenous ghrelin can normalize LPS-induced-altered digestive functions.


Author(s):  
Mogen Frenkel ◽  
Shannon H. Baumer-Mouradian ◽  
Ashley Servi ◽  
Pamela Gage ◽  
Rebecca Sprague ◽  
...  

PEDIATRICS ◽  
1963 ◽  
Vol 32 (6) ◽  
pp. 1002-1006
Author(s):  
Donnell D. Etzwiler

Glucagon or a placebo preparation was administered to 65 juvenile diabetics on 74 separate occasions. When the initial blood glucose of these children showed them to be in reasonably good control, glucagon produced a hyperglycemic effect. However, when the blood glucose levels were markedly elevated, the effect of glucagon was less predictable. The depletion of liver glycogen stores and the possible effect of contaminating insulin in glucagon preparations are discussed.


2019 ◽  
Vol 10 ◽  
pp. 204201881987540 ◽  
Author(s):  
Ming-Shun Hsieh ◽  
Sung-Yuan Hu ◽  
Chorng-Kuang How ◽  
Chen-June Seak ◽  
Vivian Chia-Rong Hsieh ◽  
...  

Background: The association between type 2 diabetes and hospital outcomes of sepsis remains controversial when severity of diabetes is not taken into consideration. We examined this association using nationwide and hospital-based databases. Methods: The first part of this study was mainly conducted using a nationwide database, which included 1.6 million type 2 diabetic patients. The diabetic complication burden was evaluated using the adapted Diabetes Complications Severity Index score (aDCSI score). In the second part, we used laboratory data from a distinct hospital-based database to make comparisons using regression analyses. Results: The nationwide study included 19,719 type 2 diabetic sepsis patients and an equal number of nondiabetic sepsis patients. The diabetic sepsis patients had an increased odds ratio (OR) of 1.14 (95% confidence interval 1.1–1.19) for hospital mortality. The OR for mortality increased as the complication burden increased [aDCSI scores of 0, 1, 2, 3, 4, and ⩾5 with ORs of 0.91, 0.87, 1.14, 1.25, 1.56, and 1.77 for mortality, respectively (all p < 0.001)]. The hospital-based database included 1054 diabetic sepsis patients. Initial blood glucose levels did not differ significantly between the surviving and deceased diabetic sepsis patients: 273.9 ± 180.3 versus 266.1 ± 200.2 mg/dl ( p = 0.095). Moreover, the surviving diabetic sepsis patients did not have lower glycated hemoglobin (HbA1c; %) values than the deceased patients: 8.4 ± 2.6 versus 8.0 ± 2.5 ( p = 0.078). Conclusions: For type 2 diabetic sepsis patients, the diabetes-related complication burden was the major determinant of hospital mortality rather than diabetes per se, HbA1c level, or initial blood glucose level.


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