Studies of diabetic instability. II. Tests of insulinogenic reserve with infusions of arginine, glucagon, epinephrine, and saline

Cremer, G; Molnar, George D.; Taylor, William F.; Moxness, Karen E.; Gatewood, Laël C.; Ackerman, Eugene; Rosevear, John W.

doi:10.1016/0026-0495(71)90033-3

Cited by 33 publications

(21 citation statements)

References 32 publications

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“…It has been hypothesized that those patients with preexisting type 2 diabetes may be at decreased risk, because the constant hyperinsulinemic state depletes pancreatic stores and prevents the rebound hyperinsulinemia that occurs after pheochromocytoma resection. 22 In our study and in the review by Plouin et al, 6 a preoperative diagnosis of diabetes was not identified as a risk factor for postoperative hypoglycemia. There was no difference in preoperative fasting glucose levels between those who did and did not develop hypoglycemia.…”

Section: Discussionmentioning

confidence: 75%

Hypoglycemia after resection of pheochromocytoma

Chen

Hodin

Pandolfi

et al. 2014

Surgery

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Section: Discussionmentioning

confidence: 75%

Hypoglycemia after resection of pheochromocytoma

Chen

Hodin

Pandolfi

et al. 2014

Surgery

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“…The small insulinogenic reserve may be sufficient to maintain a certain degree of glucose homoeostasis even though insulin secretion is impaired. Glucagon is a potent stimulus to insulin release (Cremer et al 1971;Oakley et al 1976;Samols et al 1965). In insulin treated adult diabetics with short duration as well as in non-diabetic adults the C-peptide response to glucagon injection is closely correlated to the response to a standardized breakfast ).…”

Section: Discussionmentioning

confidence: 98%

C-Peptide in Diabetic Children After Stimulatoin With Clucagon Compared With Fasting C-Peptide Levels in Non-Diabetic Children

Ludvigsson

Hedïng

1977

Acta Endocrinologica

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Fasting serum C-peptide and total immunoreactive insulin (IRI) were determined in 38 non-diabetic children and adolescents 6\p=n-\22 years old. C-peptide varied between 0.22\p=n-\0.73 pmol/ml (mean \m=+-\ sd, 0.45 \ m=+-\ 0.11). There was a tendency to higher values during puberty. No difference was found between subjects with or without a family history for diabetes. IRI varied between 0\p=n-\31 \g=m\U/ml(mean \ m=+-\ sd, 11.3 \ m=+-\ 6.5). The C-peptide response to glucagon was studied in 10 insulin dependent juvenile diabetics 11\p=n-\19 years old, who had had measurable amounts of fasting C-peptide on some occasions during the previous years. Duration of diabetes varied between 4\p=n-\12years. A slight but significant rise in C-peptide level occurred in 3 patients. Their metabolic control estimated on the basis of daily urinalysis was "excellent" or "good". The results support the hypothesis that even trace remnants of the beta cell function may be of importance for the metabolic control in juvenile diabetes.In a previous study we found that some juvenile diabetics with onset of dia¬ betes at the age of 1-16 years have signs of persisting beta cell function beyond the post-initial remission period as evident from measurable amounts of fasting serum C-peptide (Ludvigsson 8c Heding 1976). This residual beta cell func¬ tion seems to be of importance for the diabetic control Ludvigsson, to be publ.; Ludvigsson et al. 1977). However, comparisons between the C-peptide levels in diabetic and non-diabetic children could not 364

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“…Studies on stable and unstable groups of insulin-treated diabetic patients indicated that residual beta cell function was present in the former patients. 33 The continuing ability to secrete insulin in insulin treated adult onset diabetics has also been documented by Karem et al 34 using acidethanol extracts of total serum insulin. Insulin therapy was successfully discontinued in these patients.…”

Section: Fraction Number Figure 10mentioning

confidence: 89%

Circulating C-peptide Immunoreactivity: Studies in Normals and Diabetic Patients

et al. 1972

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The discovery of proinsulin and recognition of its intracellular conversion to insulin and C-peptide, which are stored and subsequently secreted together, have provided a simple method for monitoring β-cell function in insulinrequiring diabetics in whom insulin antibodies hinder measurement of immunoreactive insulin. Using an antiserum which reacts with antigenic determinants in human Cpeptide and this region in proinsulin and its intermediates we have measured C-peptide immunoreactivity (CPR) in unextracted serum and characterized its components. During oral glucose tolerance tests (OGTT) in nine healthy subjects, fasting serum CPR was 1.3 ± 0.3 ng./ml. and peaked at 4.4 ± 0.8 ng./ml. (60 min.). These values were positively correlated with immunoreactive insulin levels (IRI). CPR was undetectable in five newly diagnosd, untreated diabetics with fasting blood sugars above 200 mg./100 ml. and unmeasurable IRI. Similarly, serum CPR could not be measured in five ketosis-prone juvenile diabetics who had received insulin for longer than five years.' In contrast, fasting CPR was 2.7 ± 0.7 ng./ml. in twelve insulin-treated adult onset diabetics and rose to 5.0 ± 1.1 ng./ml. two hours after glucose. Several of these sera were extracted in acid-ethanol, gel-filtered. and measured against human proinsulin and C-peptide standards. Fasting proinsulin levels were markedly elevated, while C-peptide levels were comparatively low. Both components increased after glucose administration. As these diabetics had circulating insulin antibodies it was postulated that the elevated proinsulin levels represented circulating proinsulininsulin antibody complexes. Evidence favoring this possibility was derived from in vitro experiments in which human I-125-proinsulin was incubated with diabetic sera and the samples analyzed by gel filtration, paper electrophoresis and immune precipitation. Similar experiments with 1-125-C-peptide showed no evidence for preferential binding to plasma proteins in diabetic sera. Residual β-cell secretory capacity is thus present in many insulin-treated adult onset diabetics. The C-peptide immunoassay should facilitate the prospective study of β-cell function in these patients.

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Studies of diabetic instability. II. Tests of insulinogenic reserve with infusions of arginine, glucagon, epinephrine, and saline

Cited by 33 publications

References 32 publications

Hypoglycemia after resection of pheochromocytoma

Hypoglycemia after resection of pheochromocytoma

C-Peptide in Diabetic Children After Stimulatoin With Clucagon Compared With Fasting C-Peptide Levels in Non-Diabetic Children

Circulating C-peptide Immunoreactivity: Studies in Normals and Diabetic Patients

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