Pancreatic Glucagon-Like Immunoreactivity in a Pancreatectomized Patient

Botha, J. L.; Vinik, A; P, Child; Paul, Mahinder; Jackson, W. P. U.

doi:10.1055/s-0028-1093536

Cited by 18 publications

(3 citation statements)

References 4 publications

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“…The normalization and stabilization of blood glucose by a closed-loop system before our test may help to explain the difference in the effect of somatostatin. Nevertheless, the observations of Gerich et al 16 and Botha et al 24 failed to show a suppressive effect of somatostatin on blood glucose levels. However, in the first study, 16 the infusion of somatostatin, although it did not lower plasma glucose levels, induced an antihyperglycemic effect similar to our observations, since blood glucose remained stable during 2 h even though the last subcutaneous insulin injection had been administered 24 h previously, and control without SRIFwas not shown.…”

Section: Minutes Figure 3 Insulin Withdrawal In Four Pancreatectomizmentioning

confidence: 93%

“…Barnes and Bloom, 13 Villanueva et al, 19 and Muller et al 25 found that duodeno-pancreatectomized humans possess no circulating 3500-dalton glucagon, although Botha et al 24 claimed to have detected some. Tiengo et al 62 found the glucagon immunoreactivity was precipitated by ethanol, suggesting that it was essentially related to big plasma glucagon.…”

Section: Minutes Figure 3 Insulin Withdrawal In Four Pancreatectomizmentioning

confidence: 96%

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Glucagon Immunoreactivity and Antidiabetic Action of Somatostatin in the Totally Duodeno-Pancreatectomized and Gastrectomized Human

Bringer¹,

Mirouze²,

Marchal³

et al. 1981

Diabetes

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Ten patients who had been totally duodeno-pancreatectomized and totally (N = 1) or partially gastrectomized (N = 9) for chronic pancreatitis (N = 9) or pancreatic carcinoma (N = 1) were investigated. None had a measurable basal level of either plasma C-peptide or a C-peptide response to i.v. glucagon. Immunoreactive glucagon (IRG) was present in all patients, and the mean level (69 +/- 8 pg/ml) was not significantly different from the mean observed in normal subjects (81 +/- 16 pg/ml). Plasma IRG was unequivocally stimulated by arginine in 2 of the 10 subjects. The effect of somatostatin on plasma glucose and IRG during an oral glucose tolerance test was studied in 5 of the 10 patients. The effects of somatostatin on spontaneous hyperglycemia, plasma growth hormone, and IRG after withdrawal of insulin treatment was studied in 4 patients. Somatostatin blunted both the hyperglycemic and paradoxical IRG responses to the glucose challenge, and reduced the spontaneous rise of blood glucose that occurred after insulin withdrawal. This latter effect was not related to clear-cut changes in plasma growth hormone or in IRG. These data confirm the existence of circulating IRG in pancreatectomized patients and demonstrate the presence of circulating IRG in a completely gastrectomized and pancreatectomized patient. The somatostatin-induced improvement in glucose tolerance in the oral glucose tolerance test seems to be related to a reduction of the paradoxical IRG response. In contrast, the inhibition by somatostatin of the rise in blood glucose which occurs after insulin withdrawal does not seem to be mediated through IRG or growth hormone.

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Section: Minutes Figure 3 Insulin Withdrawal In Four Pancreatectomizmentioning

confidence: 93%

Section: Minutes Figure 3 Insulin Withdrawal In Four Pancreatectomizmentioning

confidence: 96%

Glucagon Immunoreactivity and Antidiabetic Action of Somatostatin in the Totally Duodeno-Pancreatectomized and Gastrectomized Human

Bringer¹,

Mirouze²,

Marchal³

et al. 1981

Diabetes

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“…These metabolic features may repre- sent a pattern diametrically opposite to that described in the glucagonoma syndrome [39]. Six other studies, however, have documented the presence of IRG or glucagon-like immunoreactivity in plasma from pancreatectomized patients (a total of 13 subjects) and from some groups of patients with chronic pancreatitis [31,40,44]; the 30 K antiserum was used in most of these reports and plasma samples were submitted to various extraction procedures in three studies [31,42,43]. However plasma IRG was not increased by arginine [42, 431, adrenaline [42] or cessation of insulin therapy [43]; it was paradoxically increased by oral glucose or meals [43].…”

Section: Discussionmentioning

confidence: 99%

Absence of islet Alpha cell function in pancreatectomized patients

et al. 1982

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Plasma immunoreactive glucagon, C-peptide and substrates (glucose, lactate, and alanine) were measured in 21 pancreatectomized patients and 28 patients with chronic calcifying pancreatitis during arginine infusion. Results were compared with those obtained in control and in insulin-dependent diabetic subjects, and in pancreatectomized subjects receiving a combined infusion of glucagon and arginine or somatostatin and arginine. Plasma immunoreactive glucagon in the pancreatectomized patients was 230 +/- 26 pg/ml (control subjects 100 +/- 13 pg/ml, p less than 0.001), but was unchanged following arginine or somatostatin. Following ethanol extraction of plasma it became undetectable. Similar results were obtained in patients with chronic pancreatitis. In contrast to the insulin-dependent diabetic subjects, no changes in blood glucose, lactate, and alanine concentrations were found during arginine infusion in the pancreatectomized or pancreatitis patients. Addition of glucagon restored the metabolic response to arginine in the pancreatectomized patients. Our results confirm previous smaller studies that in pancreatectomized patients, A cell function is absent or insignificant.

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Diabetes Secondary to Acquired Disease to the Pancreas

Prato¹,

Coppelli²,

Tiengo³

2004

International Textbook of Diabetes Mellitus

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Secondary diabetes is a condition of hyperglycemia which develops after the destruction of the pancreatic tissue by an acquired disease with subsequent impairment of exocrine and endocrine pancreatic functions. In general, any pathologic process of the pancreatic acinar tissue may results in an insult to its endocrine component, leading to some degree of hormone insufficiency. This condition was first described in 1788 by Sir Thomas Cawley, but it was soon appreciated that hyperglycemia can ensues acute and chronic pancreatitis, partial and total pancreatectomy, neoplasia as well as systemic processes involving the pancreas, such as hemochromatosis and cystic fibrosis. The Expert Committee on the Diagnosis and Classification of Diabetes Mellitus of the American Diabetes Association has identified these forms of diabetes as “diabetes secondary to diseases of the exocrine pancreas.” The new diagnostic criteria for diabetes introduced by the ADA and WHO Expert Committees are likely to influence the prevalence of diabetes in patients with diseases of the exocrine pancreas, but direct assessment using the new criteria is still too scanty. When the 1979 NDDG and 1985 WHO criteria are used, it can be calculated that diabetes secondary to disease of the exocrine pancreas represents, approximately, 0.5% of all cases of diabetes mellitus. Its frequency is likely to be twice as high in populations with heavy alcohol consumption. In the tropics, the prevalence of diabetes secondary to fibrocalculous pancreatitis can be as high as 10–20%. At variance with the selective B‐cell destruction occurring in type 1 diabetes, pancreatic diabetes is characterized by concomitant destruction of all endocrine cells of the islet of Langherans. The dual insulin–glucagon deficit is responsible for many of the metabolic and clinical manifestation of this form of diabetes, including lower risk for ketoacidosis and more frequent and severe hypoglycemic episodes. Since the late 1950s, the general idea has been that secondary diabetes was not associated with vascular complications. However, with the improved life expectancy of these patients during the past few years, a similar prevalence of retinopathy and microalbuminuria has been described in pancreatic and type 1 diabetes mellitus. The knowledge of the hormonal, metabolic, and clinical features of these forms of diabetes is essential in defining the most appropriate therapeutic strategies.

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Pancreatic Glucagon-Like Immunoreactivity in a Pancreatectomized Patient

Cited by 18 publications

References 4 publications

Glucagon Immunoreactivity and Antidiabetic Action of Somatostatin in the Totally Duodeno-Pancreatectomized and Gastrectomized Human

Glucagon Immunoreactivity and Antidiabetic Action of Somatostatin in the Totally Duodeno-Pancreatectomized and Gastrectomized Human

Absence of islet Alpha cell function in pancreatectomized patients

Diabetes Secondary to Acquired Disease to the Pancreas

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