Exocrine pancreatic function in juvenile diabetics

Domschke, Wolfram; Tympner, F; Domschke, S; Demling, L

doi:10.1007/bf01237787

Cited by 70 publications

(40 citation statements)

References 12 publications

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“…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: 93%

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

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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.

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Section: Discussionsupporting

confidence: 93%

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

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“…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].…”

Section: Discussionmentioning

confidence: 91%

“…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. Our results are more in keeping with the latter observations, since we failed to demonstrate clear relationships between the extent of exocrine atrophy and residual insulin positivity, the age at onset or duration of diabetes.…”

Section: Discussionmentioning

confidence: 98%

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

1987

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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...

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“…In addition, early observations of tissues of diabetic patients further supported the concept that islet hormones influence the exocrine pancreas. Pancreas from diabetic patients frequently displays signs of exocrine insufficiency, with reduction of bicarbonate and amylase output in response to secretin/CCK (Vacca et al 1964;Balk et al 1975;Domschke et al 1975;Frier et al 1976Frier et al ,1978Sato et al 1984;el Newihi et al 1988). On the other hand, pancreatic exocrine deficiency caused by chronic pancreatitis is frequently associated with impaired glucose tolerance (Bank et al 1975;) or overt diabetes (Nyboe Andersen et al 1982;Kalthoff et al 1984;Domschke et al 1985;Cavallini et al 1992).…”

Section: Functional Implication Of Endocrine-duct Associationsmentioning

confidence: 99%

Association between Endocrine Pancreas and Ductal System. More than an Epiphenomenon of Endocrine Differentiation and Development?

Bertelli

Bendayan

2005

J Histochem Cytochem.

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S U M M A R YTraditional histological descriptions of the pancreas distinguish between the exocrine and the endocrine pancreas, as if they were two functionally distinct glands. This view has been proven incorrect and can be considered obsolete. Interactions between acinar and islet tissues have been well established through numerous studies that reveal the existence of anatomical and functional relationships between these compartments of the gland. Less attention, however, has traditionally been paid to the relationships occurring between the endocrine pancreas and the ductal system. Associations between islet tissue and ducts are considered by most researchers as only a transient epiphenomenon of endocrine development. This article reviews the evidence that has emerged in the last 10 years demonstrating the existence of stable, close, and systematic relationships between these two pancreatic compartments. Functional and pathophysiological implications are considered, and the existence of an "acinar-duct-islet" axis is put forward. The pancreas appears at present to be an integrated organ composed of three functionally related components of well-orchestrated endocrine and exocrine physiological responses.

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Exocrine pancreatic function in juvenile diabetics

Cited by 70 publications

References 12 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

Association between Endocrine Pancreas and Ductal System. More than an Epiphenomenon of Endocrine Differentiation and Development?

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