Diploid, Tetraploid and Octaploid Beta Cells in the Islets of Langerhans of the Normal Human Pancreas

Ehrie, Michael G; Swartz, Frank J.

doi:10.2337/diab.23.7.583

Cited by 44 publications

(26 citation statements)

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“…The occurrence of polyploid B cells in adult human endocrine pancreas has previously been well documented [37] and the presence of giant B cell nuclei in the pancreas of cases with persistent neonatal hypoglycaemia with hyperinsulinism have been reported [3,13,18,[38][39][40]. The present study is, however, the first quantitative analysis of these phenomena in the islet parenchyma in cases with persistent neonatal hypoglycaemia with hyperinsulinism and in the age-matched normoglycaemic infants.…”

Section: Discussionmentioning

confidence: 66%

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Rahier¹,

et al. 1984

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Summary.Pancreatic tissue obtained at subtotal pancreatectomy from 15 infants with persistent hypoglycaemia with hyperinsulinism, and autopsy specimens from 23 age-matched normoglycaemic controls, were studied with morphometric methods after immunocytochemical staining of the four main islet cell types (A, B, D and pancreatic polypeptide cells). In three cases, a focal lesion was detected by gross examination. Macroscopic or microscopic examination did not distinguish the 12 other cases from controls. As found previously, nesidioblastosis was not a specific feature of the pancreas in infantile hypoglycaemia, being observed in age-matched controls as well. In cases with hypoglycaemia the volume density of B cells was not significantly increased; that of the A cells was within normal range. The volume density of pancreatic polypeptide cells was markedly augmented and that of somatostatin cells was significantly decreased. The mean nuclear volume of the B cells was increased by 40% in cases with diffuse changes, but in cases with a focal lesion this increase was restricted to the abnormal area. This finding is of decisive importance for diagnosis and has therapeutic implications. The increase in B-cell nuclear size is thought to reflect an enhanced functional activity of these cells. On the other hand, the figures obtained for the volume density of B and D cells must be viewed with some reservation because degranulation may interfere with accurate detection of these cells.Key words: Persistent hypoglycaemia, nesidioblastosis, islet cells, islet adenoma, immunocytochemistry. Thirty years after its initial description by McQuarrie[1], the syndrome of persistent neonatal hypoglycaemia with hyperinsulinism still remains poorly understood. Nesidioblastosis [2], i.e. diffuse and disseminated proliferation of islet cells budding off from ducts, has been repeatedly proposed as the underlying pathological lesion in the pancreas [3][4][5][6][7][8][9][10][11]. As a consequence of this proliferation, an increase in the mass of insulin cells was proposed to be the morphological antecedent of the hyperinsulinism [12]. Recent observations based on quantitative immunohistochemical investigations have shown, however, that nesidioblastosis is a common feature of the pancreas in normal neonates and infants [13-181.The concept of nesidioblastosis as the structural lesion underlying persistent neonatal hypoglycaemia with hyperinsulinism has thus been questioned and other aetiologies have been proposed. Thus, a decrease of somatostatin-containing cells was detected in several cases by quantitative histological/histochemical [18] and immunohistochemical [19][20][21][22] analyses of the endocrine pancreas and was corroborated by radioimmunoassay measurements of a low concentration of somatostatin in extracts of whole pancreas [20]. Other reported abnormalities are the loss of centrilobular aggregation of the endocrine cells, and the existence of small clusters of endocrine parenchymal cells throughout the exocrine tissue associated with a...

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Section: Discussionmentioning

confidence: 66%

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Rahier¹,

et al. 1984

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“…Most of these studies by Swartz and associates have used nuclear volume as an index of polyploid class which they found correlated well with Feulgen DNA content as measured by microdensitometry [2,[9][10][11]. In their studies with mice, tetraploidy was detected in beta cells of both normal and diabetic (C57B1/K.S) mice, but none of the other en docrine cells of the islets of Langerhans were polyploid.…”

Section: Discussionmentioning

confidence: 90%

Cell Cycle Analysis of the Postnatal Mouse Pancreas

Webb¹,

Dore²,

Grogan³

1982

Neonatology

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DNA flow cytometry was used to quantitate changes in distribution of cells in each phase of the cell cycle during postnatal development of the mouse pancreas. From birth through day 20 the cells in each phase remained relatively constant, after which there occurred increases in G₂-M and S phase cells and a decrease in G₀-G₁ phase cells. Polyploidy first became evident at 20 days and increased to 9% by the adult stage at 90 days. The importance of polyploidy is discussed as it may represent a parameter that can be exploited to detect and evaluate the progression of changes in the pancreas of diabetics.

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“…The naturally high frequency of tetraploid hepatocytes might therefore support the successful fusion of some bone marrowϪderived cells with liver cells. Most pancreatic ␤-cells in vivo are diploid, but ␤-cells with more than two sets of chromosomes are present in human and rodent islets (30,31). Thus it seems possible that a low rate of fusion between bone marrowϪ derived cells and ␤-cells occurs in vivo.…”

Section: Discussionmentioning

confidence: 99%

No Evidence for Significant Transdifferentiation of Bone Marrow Into Pancreatic β-Cells In Vivo

et al. 2004

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Several recent studies have suggested that the adult bone marrow harbors cells that can differentiate into tissues from all three germ layers. Other reports have contradicted these findings or attributed them to cell fusion. In this study, we investigated whether bone marrow؊derived cells contribute to the renewal of adult pancreatic endocrine cells, in particular insulinproducing ␤-cells, in vivo. To address this issue, we studied mice transplanted with green fluorescent protein (GFP)؊positive, sex-mismatched bone marrow. We also extended our studies to pancreatic injury models (partial pancreatectomy and streptozotocin administration). All animals showed stable full donor chimerism in the peripheral blood and microscopic analysis at 4 -6 weeks and 3 months after transplantation, indicating that the GFP ؉ and Y chromosome؊positive donor bone marrow contributed substantially to blood, lymphatic, and interstitial cells in the pancreas. However, after examining >100,000 ␤-cells, we found only 2 ␤-cells positive for GFP, both of which were in control animals without pancreatic injury. Thus our study results did not support the concept that bone marrow contributes significantly to adult pancreatic ␤-cell renewal.

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Diploid, Tetraploid and Octaploid Beta Cells in the Islets of Langerhans of the Normal Human Pancreas

Cited by 44 publications

References 0 publications

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

The basic structural lesion of persistent neonatal hypoglycaemia with hyperinsulinism: deficiency of pancreatic D cells or hyperactivity of B cells?

Cell Cycle Analysis of the Postnatal Mouse Pancreas

No Evidence for Significant Transdifferentiation of Bone Marrow Into Pancreatic β-Cells In Vivo

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