Hypoglycemia owing to inappropriate glucagon secretion treated with a continuous subcutaneous glucagon infusion system

1990 ◽  
Vol 122 (3) ◽  
pp. 319-322 ◽  
Author(s):  
Roger Abs ◽  
Louis Verbist ◽  
Marleen Moeremans ◽  
Pierre Blockx ◽  
Ivo De Leeuw ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Case Report ◽  
Female Patient ◽  
Glucose Level ◽  
Glucagon Secretion ◽  
Glucagon Release ◽  
Plasma Glucagon ◽  
Arginine Test ◽  
Fasting Plasma ◽  
Infusion System

Abstract A selective glucagon deficiency was documented in a 36-year-old female patient suffering from severe hypoglycemic attacks. The extremely low fasting plasma glucagon levels could not be stimulated by hypoglycemia. The increase in plasma glucagon during stimulation with arginine did not prevent hypoglycemia provoked by the simultaneous insulin secretion. Treatment consisting of a continuous sc glucagon infusion system resulted in correction of both postabsorptive and postprandial hypoglycemia. Further lowering of the glucose level during an arginine test could be the hallmark of this hypoglycemic syndrome characterized by an inappropriate glucagon secretion. This case report would indicate that epinephrine cannot prevent hypoglycemia when glucagon release is completely deficient.

Cell type-specific activation of metabolism reveals that β-cell secretion suppresses glucagon release from α-cells in rat pancreatic islets

2006 ◽  
Vol 290 (2) ◽  
pp. E308-E316 ◽  
Author(s):  
Rui Takahashi ◽  
Hisamitsu Ishihara ◽  
Akira Tamura ◽  
Suguru Yamaguchi ◽  
Takahiro Yamada ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Cell Activation ◽  
Tricarboxylic Acid Cycle ◽  
Expression System ◽  
Hormone Secretion ◽  
Glucagon Secretion ◽  
Glucagon Release ◽  
Β Cells ◽  
Β Cell

Abnormal glucagon secretion is often associated with diabetes mellitus. However, the mechanisms by which nutrients modulate glucagon secretion remain poorly understood. Paracrine modulation by β- or δ-cells is among the postulated mechanisms. Herein we present further evidence of the paracrine mechanism. First, to activate cellular metabolism and thus hormone secretion in response to specific secretagogues, we engineered insulinoma INS-1E cells using an adenovirus-mediated expression system. Expression of the Na+-dependent dicarboxylate transporter (NaDC)-1 resulted in 2.5- to 4.6-fold ( P < 0.01) increases in insulin secretion in response to various tricarboxylic acid cycle intermediates. Similarly, expression of glycerol kinase (GlyK) increased insulin secretion 3.8- or 4.2-fold ( P < 0.01) in response to glycerol or dihydroxyacetone, respectively. This cell engineering method was then modified, using the Cre- loxP switching system, to activate β-cells and non-β-cells separately in rat islets. NaDC-1 expression only in non-β-cells, among which α-cells are predominant, caused an increase (by 1.8-fold, P < 0.05) in glucagon secretion in response to malate or succinate. However, the increase in glucagon release was prevented when NaDC-1 was expressed in whole islets, i.e., both β-cells and non-β-cells. Similarly, an increase in glucagon release with glycerol was observed when GlyK was expressed only in non-β-cells but not when it was expressed in whole islets. Furthermore, dicarboxylates suppressed basal glucagon secretion by 30% ( P < 0.05) when NaDC-1 was expressed only in β-cells. These data demonstrate that glucagon secretion from rat α-cells depends on β-cell activation and provide insights into the coordinated mechanisms underlying hormone secretion from pancreatic islets.

Adrenergic modulation of pancreatic glucagon and insulin secretion in sheep

1988 ◽  
Vol 254 (3) ◽  
pp. R518-R523 ◽  
Author(s):  
S. Oda ◽  
A. Hagino ◽  
A. Ohneda ◽  
Y. Sasaki ◽  
T. Tsuda
Keyword(s):  
Insulin Secretion ◽  
Intravenous Infusion ◽  
Glucagon Secretion ◽  
Receptor Activation ◽  
Plasma Glucagon ◽  
Epinephrine Infusion ◽  
Plasma Insulin Concentration ◽  
Pancreatic Glucagon ◽  
Adrenergic Modulation ◽  
Glucagon And Insulin

The effect of intravenous infusion of epinephrine, either alone or together with various doses of phentolamine or propranolol, on the secretion of both glucagon and insulin was determined in six sheep. Intravenous infusion of epinephrine alone caused increases in plasma glucagon and glucose concentrations and produced a slight but significant decrease in plasma insulin concentration. The concomitant infusion of propranolol and epinephrine augmented glucagon release and inhibited insulin secretion. Combined propranolol plus epinephrine infusion also caused a marked hyperglycemia. The concomitant infusion of phentolamine and epinephrine produced slight inhibition of glucagon secretion and markedly promoted insulin secretion. Epinephrine-induced hyperglycemia was eliminated by phentolamine infusion. The effects of isoproterenol infusion on plasma glucagon, insulin, and glucose concentrations were similar to that caused by the concomitant infusion of phentolamine and epinephrine. The effects of isoproterenol were abolished by the infusion of propranolol. It is concluded that an alpha-receptor mechanism is the most important component of adrenergic modulation of pancreatic glucagon secretion, whereas beta-receptor activation stimulates and alpha-receptor activation inhibits insulin secretion in sheep.

scholarly journals Somatostatin Inhibits Insulin and Glucagon Secretion via Two Receptor Subtypes: An in Vitro Study of Pancreatic Islets from Somatostatin Receptor 2 Knockout Mice*

Endocrinology ◽  
2000 ◽  
Vol 141 (1) ◽  
pp. 111-117 ◽  
Author(s):  
M. Z. Strowski ◽  
R. M. Parmar ◽  
A. D. Blake ◽  
J. M. Schaeffer
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Insulin Release ◽  
Somatostatin Receptor ◽  
Glucagon Secretion ◽  
Endocrine Function ◽  
Receptor Subtype ◽  
Glucagon Release ◽  
Glucagon And Insulin

Abstract Somatostatin (SST) potently inhibits insulin and glucagon release from pancreatic islets. Five distinct membrane receptors (SSTR1–5) for SST are known, and at least two (SSTR2 and SSTR5) have been proposed to regulate pancreatic endocrine function. Our current understanding of SST physiology is limited by the receptor subtype selectivity of peptidyl SST analogs, making it difficult to assign a physiological function to an identified SST receptor subtype. To better understand the physiology of SSTRs we studied the in vitro effects of potent subtype-selective nonpeptidyl SST analogs on the regulation of pancreatic glucagon and insulin secretion in wild-type (WT) and in somatostatin receptor 2 knockout (SSTR2KO) mice. There was no difference in basal glucagon and insulin secretion between islets isolated from SSTR2KO and WT mice; however, potassium/arginine-stimulated glucagon secretion was approximately 2-fold higher in islets isolated from SSTR2KO mice. Neither SST nor any SSTR-selective agonist inhibited basal glucagon or insulin release. SST-14 potently inhibited stimulated glucagon secretion in islets from WT mice and much less effectively in islets from SSTR2KO mice. The SSTR2 selective analog L-779,976 inhibited glucagon secretion in islets from WT, but was inactive in islets from SSTR2KO mice. L-817,818, an SSTR5 selective analog, slightly reduced glucagon release in both animal groups, whereas SSTR1, -3, and -4 selective analogs were inactive. SST and L-817,818 inhibited glucose stimulated insulin release in islets from WT and SSTR2KO mice. L-779,976 much less potently reduced insulin secretion from WT islets. In conclusion, our data demonstrate that SST inhibition of glucagon release in mouse islets is primarily mediated via SSTR2, whereas insulin secretion is regulated primarily via SSTR5.

Secretory effects of secretin on isolated perfused porcine pancreas.

1978 ◽  
Vol 235 (4) ◽  
pp. E381 ◽  
Author(s):  
S L Jensen ◽  
J Fahrenkrug ◽  
J J Holst ◽  
C Kühl ◽  
O V Nielsen ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Secretion ◽  
Insulin Response ◽  
Glucagon Secretion ◽  
Oral Glucose ◽  
Glucagon Release ◽  
Exocrine Pancreatic Secretion ◽  
Constant Concentration ◽  
Porcine Pancreas

The effect of pure natural porcine secretin on endocrine and exocrine pancreatic secretion was studied in the totally isolated perfused porcine pancreas. The exocrine pancreatic responses to secretin correspond well with those obtained in the anesthetized pig. The lowest concentration of secretin observed to increase pancreatic secretion was 2.8 pmol/liter, whereas the maximum pancreatic responses were obtained at a secretin concentration of 92 pmol/liter. The infusion of secretin in concentrations ranging from 2.8 to 278 pmol/liter in the presence of a constant concentration of glucose (7.5, 5.0, or 3.5 mmol/liter) was without effect on the insulin and glucagon release. Infusion of secretin at a concentration of 834 pmol/liter in the presence of glucose at 7.5 mmol/liter provoked a significant (P less than 0.01) short-lived increase in insulin secretion. However, there was no effect on the glucagon secretion. The results of this study indicate that neither the augmented insulin response nor the suppression of glucagon elicited by oral glucose depend on secretin.

scholarly journals Failure of chronic hyperinsulinemia to suppress pancreatic glucagon in vivo in the rat

1991 ◽  
Vol 69 (3) ◽  
pp. 437-443 ◽  
Author(s):  
Patricia L. Brubaker ◽  
Tsutomu Kazumi ◽  
Tsutomu Hirano ◽  
Mladen Vranic ◽  
George Steiner
Keyword(s):  
Drinking Water ◽  
Low Density Lipoprotein ◽  
Density Lipoprotein ◽  
Glucagon Secretion ◽  
Glucagon Release ◽  
Plasma Glucagon ◽  
Pancreatic Glucagon ◽  
Glucose Levels ◽  
Endogenous Release

To determine the effects of chronic hyperinsulinemia on glucagon release, rats were made hyperinsulinemic for 14 days by supplementation of drinking water with sucrose (10%; sucrose-fed) to increase endogenous release or by implantation of osmotic minipumps (subcutaneous, s.c; or intraperitoneal, i.p.) to deliver exogenous insulin (6 U/day). Both s.c. and i.p. rats also had sucrose in the drinking water to prevent hypoglycemia. Plasma insulin levels were significantly elevated in sucrose-fed, s.c, and i.p. rats. However, glucose levels were significantly elevated in sucrose-fed rats only. Surprisingly, plasma glucagon concentrations were elevated in i.p. and s.c. rats and were not suppressed in sucrose-fed rats. Inverse relationships were found between the plasma levels of insulin and glucose (n = 65; r = −0.42, p < 0.0001) and between glucose and glucagon (n = 73; r = −0.46, p < 0.0001). However, unexpectedly, a positive correlation between insulin and glucagon (n = 65; r = 0.47, p < 0.0001) was established. As suppression of plasma glucagon levels below basal was not observed in any of the hyperinsulinemic or hyperglycemic rats, we wished to establish further whether pancreatic glucagon release could be suppressed below basal levels in the rat by another means. Thus, high doses of somatostatin (50–100 μg∙kg−1∙min−1) were infused for 45 min into normal rats without or with a concomitant hyperinsulinemic, hyperglycemic glucose clamp. Somatostatin fully suppressed insulin, but although plasma glucagon levels were decreasd by somatostatin infusion relative to saline-infused animals, there was still no suppression below basal levels. Thus, the rat A cells are less sensitive to somatostatin than are those of other species. The results of this study demonstrate that chronic endogenous or exogenous hyperinsulinemia does not inhibit glucagon secretion, even in the presence of hyperglycemia. Factors other than insulin may therefore play an important role in the regulation of the pancreatic A cell in the chronic hyperinsulinemic rat.Key words: glycemia, insulin, glucagon, somatostatin, very low density lipoprotein.

scholarly journals Temporal Patterns of Glucagon and Its Relationships with Glucose and Insulin following Ingestion of Different Classes of Macronutrients

Nutrients ◽  
2022 ◽  
Vol 14 (2) ◽  
pp. 376
Author(s):  
Christian Göbl ◽  
Micaela Morettini ◽  
Benedetta Salvatori ◽  
Wathik Alsalim ◽  
Hana Kahleova ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Area Under The Curve ◽  
Glucagon Secretion ◽  
Plasma Glucagon ◽  
Food Ingestion ◽  
Mixed Meal ◽  
C Peptide ◽  
Significant Relationships ◽  
Basal Insulin Secretion ◽  
Secretion Inhibition

Background: glucagon secretion and inhibition should be mainly determined by glucose and insulin levels, but the relative relevance of each factor is not clarified, especially following ingestion of different macronutrients. We aimed to investigate the associations between plasma glucagon, glucose, and insulin after ingestion of single macronutrients or mixed-meal. Methods: thirty-six participants underwent four metabolic tests, based on administration of glucose, protein, fat, or mixed-meal. Glucagon, glucose, insulin, and C-peptide were measured at fasting and for 300 min following food ingestion. We analyzed relationships between time samples of glucagon, glucose, and insulin in each individual, as well as between suprabasal area-under-the-curve of the same variables (ΔAUCGLUCA, ΔAUCGLU, ΔAUCINS) over the whole participants’ cohort. Results: in individuals, time samples of glucagon and glucose were related in only 26 cases (18 direct, 8 inverse relationships), whereas relationship with insulin was more frequent (60 and 5, p < 0.0001). The frequency of significant relationships was different among tests, especially for direct relationships (p ≤ 0.006). In the whole cohort, ΔAUCGLUCA was weakly related to ΔAUCGLU (p ≤ 0.02), but not to ΔAUCINS, though basal insulin secretion emerged as possible covariate. Conclusions: glucose and insulin are not general and exclusive determinants of glucagon secretion/inhibition after mixed-meal or macronutrients ingestion.

Pancreastatin inhibits insulin secretion and stimulates glucagon secretion in mice

Diabetes ◽  
1988 ◽  
Vol 37 (3) ◽  
pp. 281-285 ◽  
Author(s):  
B. Ahren ◽  
S. Lindskog ◽  
K. Tatemoto ◽  
S. Efendic
Keyword(s):  
Insulin Secretion ◽  
Glucagon Secretion

Healing Of A Large Osteolytic Mandibular Lesion – A Case Report

2018 ◽  
Author(s):  
Ingrid Różyło-Kalinowskav ◽  
Karolina Sidor
Keyword(s):  
Case Report ◽  
Female Patient ◽  
Surgical Approach ◽  
Orthodontic Treatment ◽  
Incidental Finding ◽  
Osteolytic Lesion ◽  
Panoramic Radiograph ◽  
Endodontic Treatment ◽  
Osteolytic Lesions

The purpose of this article was to present a case report of 11–year old female patient with a large osteolytic mandibular lesion which healed after endodontic treatment. The patient was referred for radio diagnostics due to an incidental finding of a large osteolytic lesion of the area of the left lower first and second premolars in the panoramic radiograph taken before orthodontic treatment. CBCT was performed and the patient asked to have teeth 33-35 treated by endodontics before surgery. The patient missed the surgical appointment and when she reappeared several months later, the lesion showed signs of healing thus surgery were aborted. The presented case testifies to the observation that even large osteolytic lesions can heal after endodontic treatment without surgical approach.

Study of Possible Relation between Fasting Plasma Glucagon, Gestational Diabetes and Development of Type 2 DM

2020 ◽  
Vol 16 (2) ◽  
pp. 148-155 ◽  
Author(s):  
Ashraf Okba ◽  
Salwa Seddik Hosny ◽  
Alyaa Elsherbeny ◽  
Manal Mohsin Kamal
Keyword(s):  
Gestational Diabetes ◽  
Pregnant Women ◽  
Post Partum ◽  
Plasma Glucagon ◽  
Type 2 Dm ◽  
Fasting Plasma ◽  
Before And After ◽  
Two Phases

Background and Aims: Women who develop GDM (gestational diabetes mellitus) have a relative insulin secretion deficiency, the severity of which may be predictive for later development of diabetes. This study aimed to investigate the role of fasting plasma glucagon in the prediction of later development of diabetes in pregnant women with GDM. Materials and Methods: The study was conducted on 150 pregnant women with GDM after giving informed oral and written consents and being approved by the research ethical committee according to the declaration of Helsinki. The study was conducted in two phases, first phase during pregnancy and the second one was 6 months post-partum, as we measured fasting plasma glucagon before and after delivery together with fasting and 2 hour post-prandial plasma sugar. Results: Our findings suggested that glucagon levels significantly increased after delivery in the majority 14/25 (56%) of GDM women who developed type 2 DM within 6 months after delivery compared to 6/20 (30%) patients with impaired fasting plasma glucose (IFG) and only 22/105 (20%) non DM women, as the median glucagon levels were 80,76, 55, respectively. Also, there was a high statistical difference between fasting plasma glucagon post-delivery among diabetic and non-diabetic women (p ≤ 0.001). These results indicated the useful role of assessing fasting plasma glucagon before and after delivery in patients with GDM to predict the possibility of type 2 DM. Conclusion: There is a relatively high glucagon level in GDM patients, which is a significant pathogenic factor in the incidence of subsequent diabetes in women with a history of GDM. This could be important in the design of follow-up programs for women with previous GDM.

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