Exocrine pancreatic function in juvenile-onset diabetes mellitus.

Frier, B M; Saunders, Jimmy; Wormsley, K. G.; Bouchier, I. A. D.

doi:10.1136/gut.17.9.685

Cited by 167 publications

(108 citation statements)

References 17 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…These results are in agreement with previously published data (24,25). The lower trypsin levels in plasma of insulin-dependent diabetic patients have been attributed to a decrease of exocrine pancreatic secretion in this disease (26,27). Even if a ratio reg protein/trypsin was considered in this study, the highest values were observed mainly in long-standing diabetes, and not in the more active periods of diabetogenesis.…”

Section: Discussionsupporting

confidence: 82%

Serum reg protein level is not related to the beta cell destruction/regeneration process during early phases of diabetogenesis in type I diabetes

Christofilis

Carrère²,

Atlan-Gepner³

et al. 1999

European Journal of Endocrinology

View full text Add to dashboard Cite

Objective: In type I diabetes mellitus, early markers of beta cell damage are needed in order to detect the infraclinical development of the disease. The reg protein may be a good candidate, as the reg gene has been proposed to play a role in the pancreatic beta cell destruction/regeneration process during diabetogenesis in animal models of autoimmune diabetes. The aim of this study was to test the hypothesis whether serum reg protein level could be representative of either the destructive or regenerative process at the beta cell level during the early phases of type I diabetes in humans. Design and methods: We used a highly specific immunoassay to measure serum reg protein level in controls and in three groups of either diabetes prone or diabetic subjects: recently diagnosed diabetic patients, long-standing diabetic patients and islet cell antibody-positive non-diabetic subjects. Results: We found no significant difference between the values observed in these three groups in comparison with control group (90.7 Ϯ 18.1 ng/ml, 83.1 Ϯ 5.6 ng/ml, 98.7 Ϯ 24.5 ng/ml vs 85.5 Ϯ 5.6 ng/ml respectively). Moreover, when the insulin reserve was evaluated at 6 months in the recently diagnosed group, serum reg protein levels were not different between patients with or without residual insulin secretion (at onset: 103 Ϯ 42 vs 70.3 Ϯ 8.5 ng/ml respectively; at 6 months: 79.7 Ϯ 25.8 ng/ml vs 81.6 Ϯ 15 ng/ml respectively). In contrast, trypsin levels were significantly lower in every group of diabetic patients. Results were expressed as means Ϯs:e:m: and groups compared by Student's t-test (P < 0.05). Conclusions: We conclude that serum reg protein level cannot be used as a marker for the progression of the diabetogenic process in type I diabetes.

show abstract

Section: Discussionsupporting

confidence: 82%

Serum reg protein level is not related to the beta cell destruction/regeneration process during early phases of diabetogenesis in type I diabetes

Christofilis

Carrère²,

Atlan-Gepner³

et al. 1999

European Journal of Endocrinology

View full text Add to dashboard Cite

show abstract

“…This conclusion is substantiated by clinical studies on the exocrine secretory capacity of the pancreas in chronic Type I diabetes demonstrating decreased secretion of enzymes [32][33][34][35][36]. Frier et al found that the preservation of pancreatic function correlates with the duration of diabetes [32] and the persistence of B-cell secretory activity measured by C-peptide levels [33]. Domschke et al [34] and Lankisch et al [35], however, were not able to confirm these correlations.…”

Section: Discussionmentioning

confidence: 56%

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

1987

View full text Add to dashboard Cite

Summary.The relationship of residual insulin positivity in chronic Type I (insulin-dependent) diabetes and atrophy of the exocrine pancreas to duration of diabetes, age at onset and microangiopathy was studied in 26 patients (disease duration 2 to 54 years, mean 26 years). Islets containing insulin cells were found in 13/26 pancreata. In 5/13 pancreata insulin positive cells were detected in only one lobule, while in 8/13 insulin positivity was multifocal. All patients with diabetes duration less than 11 years had residual insulin cells; whereas, the rate of insulin positivity was near 40% with diabetes duration of more than 11 and 21 years, respectively. Survival of insulin cells was not clearly related to age at onset. HLA-DR expression on insulin cells was seen in one case. lnsulitis was lacking. Pancreatic volume determined in 18 patients ranged from 14-110ml (age adjusted mean 56.3 ml) and was significantly less than that of control subjects (age adjusted, mean 89.9 ml, p < 0.0001). Computerized morphometry of the exocrine pancreas revealed severe acinat atrophy due to a reduction in size of acinar cells. Acinar atrophy correlated neither with the degree of insulin positivity, disease duration nor severity of microangiopathy. The findings suggest that in about 40% of patients with Type 1 diabetes a small population of insulin cells may escape autoimmune destruction, irrespective of disease duration or age at onset. Though exocrine atrophy and insulin deficiency are associated, the variable extent of pancreatic atrophy could not to be related to such factors as amount of surviving insulin cells, duration of diabetes or microangiopathy.Key words: Chronic Type 1 (insulin-dependent) diabetes, residual insulin cells, exocrine atrophy, HLA-DR expression, diabetic microangiopathy.Loss of insulin cells characterises the islet lesions in patients with Type 1 (insulin-dependent) diabetes mellitus [1][2][3][4]. This loss, however, need not to be complete, since B cells, though severely reduced, have been demonstrated even in patients with a diabetes duration up to 37 years [1,3], The mechanisms which may protect some insulin cells from destruction by the autoimmune process underlying Type I diabetes are largely unkrlown.Another finding that characterises the pancreas in chronic Type 1 diabetes is a reduction in weight and volume [3,[5][6][7][8]. The pancreatic atrophy is attributed to the lacking trophic effect of insulin on the acinar cells [2,3,[9][10][11][12][13]. The extent of the exocrine atrophy, however, appears to vary considerably from patient to patient and has not yet been related to the remaining insulin positivity in the pancreas, to diabetes duration or to the degree of microangiopathy. * Presented in part at the 22 nd EASD meeting in Rome, 1986 ** Present address: Department of Pathology, Free University of Brussels, BelgiumThe aim of the present study was to investigate the degree and distribution of residual insulin positivity in the pancreas of patients with long-standing Type 1 diabetes by immunocyt...

show abstract

“…The secretory capacity of not only amylase (Frier et al, 1976;Lankisch et al, 1982) but also chymotrypsin (Yokoyama et al, 1982) or trypsin (Frier et al, 1980) is low. The size of the pancreas measured by computed tomography in juvenile-onset IDDs is much smaller than that in age matched non-insulin dependent diabetics (Ohno et al, 1981).…”

Section: Discussionmentioning

confidence: 99%

“…of exocrine pancreatic function has been reported in patients with juvenile-onset insulin dependent diabetes mellitus (Frier et al, 1976;Lankisch et al, 1982;Yokoyama et al, 1982). The extent to which exocrine pancreatic function is preserved correlates with the persistence of B-cell secretory activity measured by Cpeptide levels, or with the duration of the disease (Yokoyama et al, 1982;Frier et al, 1978).…”

Section: Insufficiencymentioning

confidence: 99%

Influence of B-Cell Impairment on Pancreatic Acini in NOD Mice and Streptozotocin-Induced Diabetic Rats.

et al. 1988

View full text Add to dashboard Cite

Exocrine pancreatic function insufficiency, even of short duration, has been reported in juvenile-onset insulin dependent diabetic patients. To evaluate the status of pancreatic acini under decreased B-cell function, tissue insulin, amylase, chymotrypsinogen and trypsinogen in the pancreas were measured in streptozotocin-induced diabetic rats and non-obese diabetic mice in various conditions.In streptozotocin diabetic rats, a dissociation of three enzyme contents was demonstrated in the condition with discontinuation of insulin injection, i. e., a marked decrease in amylase, a significant increase in chymotrypsinogen, but no significant change in trypsinogen.This dissociation was markedly improved in the insulin-treated condition.In non-obese diabetic mice, these enzyme contents were not significantly changed although severe insulitis together with the marked decrease in insulin content was observed. These data show that the cessation of B-cell function alone does not cause insufficiency of exocrine pancreas.

show abstract

Exocrine pancreatic function in juvenile-onset diabetes mellitus.

Cited by 167 publications

References 17 publications

Serum reg protein level is not related to the beta cell destruction/regeneration process during early phases of diabetogenesis in type I diabetes

Serum reg protein level is not related to the beta cell destruction/regeneration process during early phases of diabetogenesis in type I diabetes

Residual insulin positivity and pancreatic atrophy in relation to duration of chronic Type 1 (insulin-dependent) diabetes mellitus and microangiopathy

Influence of B-Cell Impairment on Pancreatic Acini in NOD Mice and Streptozotocin-Induced Diabetic Rats.

Contact Info

Product

Resources

About