Islet Morphometry in the Diabetic Pancreas of Man

Saito, Ken; Takahashi, Tohru; Yaginuma, Nobuhisa; Iwama, Noriyuki

doi:10.1620/tjem.125.185

Cited by 37 publications

(30 citation statements)

References 21 publications

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“…Since the cases are identical to those used for islet morphometry in the foregoing study, the total islet volume Vi in each case is already known (Saito et al 1978b). The diagnosis of diabetes mellitus was made on the basis of urinalysis, fasting blood sugar level (FBS) and 50 g oral glucose tolerance test (GTT).…”

Section: Methodsmentioning

confidence: 99%

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Differential volumetry of A,B and D cells in the pancreatic islets of diabetic and nondiabetic subjects.

Saito

Yaginuma

Takahashi

1979

Tohoku J. Exp. Med.

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129

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The percentile volumes VA, VB and VD of A, B and D cells in the islets of Langerhans were histometrically estimated in the pancreases from 59 autopsy cases including maturity-and growth-onset diabetics and nondiabetics.Volumetry was performed microscopically by point counting method using a square-lattice eyepiece, then the total A, B and D cell volumes VA, VB and VD were calculated from the total islet volume V; of the pancreas estimated separately.The measurement disclosed a prominent difference in VB between the three groups. Namely, it was only 0.156 and 0.388 cm3 in the growth-and maturity-onset diabetics, much smaller values than 0.636 cm3 in nondiabetics.The simultaneous investigation on clinical records revealed a negative correlation between VB and the maximum blood sugar level during GTT, showing that VB reflects grossly the degree of glucose tolerance of the individual.The smaller VB in diabetes was attributed to the diminution of V, because VA, VB and VD were almost the same regardless of the presence or absence of diabetes.These results strongly suggested a failure of insulin produc tion in diabetes due to quantitative deficiency of B cells. pancreatic islets; A, B and D cells; volumetry; diabetes mellitus In our foregoing paper, diabetic cases were subjected to islet morphometry, in which the results were interpreted in relation to some of the important clinical data (Saito et al. 1978b). Among several morphological indices examined, the total islet volume of the pancreas revealed special functional significance, reflecting glucose tolerance in individual cases. We have further to examine whether or not the insular cell composition undergoes a considerable change in diabetes mellitus.It has been stated by many authors, on a morphometrical basis, that the numerical ratio of B to A cells was smaller in diabetes than in control, causing an absolute reduction of B cells in the former (Maclean and Ogilvie 1955;Gepts 1958). Practically, however, it seems rather awkward to count exactly the number of cells on islet sections. When one observes a group of B cell sections, for example, strict determination of the boundaries for individual cell sections appears

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Section: Methodsmentioning

confidence: 99%

“…In our foregoing paper, diabetic cases were subjected to islet morphometry, in which the results were interpreted in relation to some of the important clinical data (Saito et al 1978b). Among several morphological indices examined, the total islet volume of the pancreas revealed special functional significance, reflecting glucose tolerance in individual cases.…”

mentioning

confidence: 99%

Differential volumetry of A,B and D cells in the pancreatic islets of diabetic and nondiabetic subjects.

Saito

Yaginuma

Takahashi

1979

Tohoku J. Exp. Med.

Self Cite

129

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“…Early observations indicated that β -cell volume is significantly reduced in T2DM islets [12–14]. More recent studies with postmortem and surgical specimens of human pancreata have characterized changes in β -cell mass that occur during the evolution of T2DM [6, 15].…”

Section: Introductionmentioning

confidence: 99%

Mitochondrial Dysfunction andβ-Cell Failure in Type 2 Diabetes Mellitus

Alex

Zhao

Turk

2012

Experimental Diabetes Research

190

151

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Type 2 diabetes mellitus (T2DM) is the most common human endocrine disease and is characterized by peripheral insulin resistance and pancreatic islet β-cell failure. Accumulating evidence indicates that mitochondrial dysfunction is a central contributor to β-cell failure in the evolution of T2DM. As reviewed elsewhere, reactive oxygen species (ROS) produced by β-cell mitochondria as a result of metabolic stress activate several stress-response pathways. This paper focuses on mechanisms whereby ROS affect mitochondrial structure and function and lead to β-cell failure. ROS activate UCP2, which results in proton leak across the mitochondrial inner membrane, and this leads to reduced β-cell ATP synthesis and content, which is a critical parameter in regulating glucose-stimulated insulin secretion. In addition, ROS oxidize polyunsaturated fatty acids in mitochondrial cardiolipin and other phospholipids, and this impairs membrane integrity and leads to cytochrome c release into cytosol and apoptosis. Group VIA phospholipase A2 (iPLA2 β) appears to be a component of a mechanism for repairing mitochondrial phospholipids that contain oxidized fatty acid substituents, and genetic or acquired iPLA2 β-deficiency increases β-cell mitochondrial susceptibility to injury from ROS and predisposes to developing T2DM. Interventions that attenuate ROS effects on β-cell mitochondrial phospholipids might prevent or retard development of T2DM.

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“…Whatever the mechanisms of insulitis may be, one result is the destruction of islets. There are some reports that the number of islets is largely decreased in insulin dependent diabetes (Doniach, 1974 ;Saito et al, 1978). These findings may indicate that islets of Langerhans are destroyed acutely by viral attack or by being damaged chronically by an autoimmune mechanism in insulin dependent diabetes.…”

Section: Discussionmentioning

confidence: 96%