The ultrastructure of the islets of Langerhans in normal and obese-hyperglycemic mice

Björkman, Nils; Hellerström, Claes; Hellman, Bo

doi:10.1007/bf00320321

Cited by 120 publications

(14 citation statements)

References 20 publications

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“…Our surface area measurements were gathered from 20 cell membranes, 20 nuclei, and 12 mitochondrial networks, once again evenly split between alpha and beta cells. All cell-type differentiation was performed by visual inspection, using such well-documented cues as secretory granule appearance (Björkman et al, 1963; Mikami and Mutoh, 1971; Orci, 1974) and cytoplasmic lucency (Lacy, 1957; Lazarus and Volk, 1964; Winborn, 1963). …”

Section: Methodsmentioning

confidence: 99%

Quantitative analysis of mouse pancreatic islet architecture by serial block-face SEM

Pfeifer

Shomorony

Aronova

et al. 2015

Journal of Structural Biology

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We have applied serial block-face scanning electron microscopy (SBF-SEM) to measure parameters that describe the architecture of pancreatic islets of Langerhans, microscopic endocrine organs that secrete insulin and glucagon for control of blood glucose. By analyzing entire mouse islets, we show that it is possible to determine (1) the distributions of alpha and beta cells, (2) the organization of blood vessels and pericapillary spaces, and (3) the ultrastructure of the individual secretory cells. Our results show that the average volume of a beta cell is nearly twice that of an alpha cell, and the total mitochondrial volume is about four times larger. In contrast, nuclear volumes in the two cell types are found to be approximately equal. Although the cores of alpha and beta secretory granules have similar diameters, the beta granules have prominent halos resulting in overall diameters that are twice those of alpha granules. Visualization of the blood vessels revealed that every secretory cell in the islet is in contact with the pericapillary space, with an average contact area of 9 ± 5% of the cell surface area. Our data show that consistent results can be obtained by analyzing small numbers of islets. Due to the complicated architecture of pancreatic islets, such precision cannot easily be achieved by using TEM of thin sections.

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Section: Methodsmentioning

confidence: 99%

Quantitative analysis of mouse pancreatic islet architecture by serial block-face SEM

Pfeifer

Shomorony

Aronova

et al. 2015

Journal of Structural Biology

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“…Light microscopic examinations of pancreatic islets revealed hypoplasia of B-cells before the onset of diabetes, and after the onset of diabetes, hydropic and vacuolar degeneration as well as atrophy and pyknosis was observed in them. In hereditary diabetic animals such as obese mice (Bleisch et al, 1952), NZO mice (Bielschowsky and Bielschowsky, 1956), yellow obese mice and KK mice (Nakamura, 1965), the hypertrophy of pancreatic islets are observed. On the other hand, Chinese hamsters (Carpenter et al, 1967) and sand rats (Hackel et al, 1965) show a reduced number of pancreatic islets and various degenerative lesions which are similar to those of the experimental congenital diabetic rat.…”

Section: S Y N Osismentioning

confidence: 99%

“…After the onset of diabetes, marked degranulation, irregularly sac-shaped dilatation of granular endoplasmic reticulum as well as swelling and vacuolation of mitochondria were observed. Degranulation and an increased number of ribosomes have been observed in the pancratic B-cells of alloxan diabetic rabbits, cats which had received intraperitoneal administration of glucose (Williamson, 1960), glucagon treated rats which were fed high carbohydrate diets , and spontaneous diabetic rodents, namely, obese mice (Bjorkman et al 1963), KK mice (Nakamura and Yamada, 1969), diabetic hybrid mice (Like et al 1965) and sand rats (Like and Miki, 1967). These secretion of insulin.…”

Section: S Y N Osismentioning

confidence: 99%

Electron Microscopic Studies of the Pancreatic Islets and Some Other Organs in Experimental Congenital Diabetic Rats

Yamamoto

1971

Endocrinol Japon

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Nineteen rats were obtained by the mating of two spontaneous diabetic males, that had diabetes for over one month, with three nondiabetic females, all of which were born from alloxan diabetic rats in the same successive generations. General observations on these animals and light and electron microscopic studies on their pancreatic islets as well as some other organs were performed. Among 19 rats, 11 developed diabetes spontaneously without any treatment, 5 of which showed long persistent diabetes.(a) Before the onset of diabetes, the pancreatic B-cells showed hypoplasia (reduced in number and size). Electron microscopically, some B-cells in the granular stage showed degranulation and an increased number of ribosomes, some B-cells in the predominantly agranular stage irregular dilatation of granular endoplasmic reticulum. (b) After the onset of diabetes, some pancreatic B-cells showed hydropic degeneration and vacuolar formation, other B-cells pyknosis and atrophy. Under electron microscopy, marked degranulation, swelling and vacuolation of mitochondria, and a decreased number of ribosomes were observed in all pancreatic B-cells, and in addition, marked irregular dilatation of granular endoplasmic reticulum in the predominantly agranular stage. The adrenal gland showed slight hypertrophy and in the cells of the fascicular zone an increased number of ribosomes and abundant dilated agranular endoplasmic reticula both before and after the onset of diabetes were observed.In the kidney, the glomerulus showed no obvious changes, but the renal tubules demonstrated deposition of glycogen particles in the diabetic stage and they did not show any degenerative lesions in their organelles. In short, in experimental congenital diabetic rats, the pancreatic B-cells work excessively to maintain the animals free of diabetes, during the early prediabetic stage; however, with the aging process their growth disturbance becomes severe, they are exhausted and show degeneration and finally spontaneous diabetes occurs. The presumed hyperfunction of their adrenal cortex accelerates the onset of diabetes.Since Okamoto (1952) found hypoplasia of the pancreatic B-cells in the descendants of alloxan diabetic rabbits, many investigations on these animals have been made, with many interesting results. That is, the diabetic animals (rabbits, rats and guinea pigs) in which diabetes was induced by the administration of alloxan or other diabetogenic substances, were mated after being kept diabetic for more than one month, to obtain F1 offspring and this process was repeated to obtain F2 and several subsequent genrations. On examination it was revealed that these descendants had hypoplasia of the pancreatic B-cells (reduced in number and in size), increased percentage of acidophiles in the adenohypophysis and hypertrophy of the adrenal cortex (especially zona fasciculata). These changes gradually

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“…There are signs of β-cell degranulations in islets from obese mice with increased nuclear and nucleolar size. 1,[37][38][39] The islets of the obese mice are remarkably hyperemic; 30,39,40 pseudocysts, dilated ducts and dilated capillaries are also common findings in ob-mouse islets. 32 The obese hyperglycemic syndrome is characterized by an increase in the extractable insulin of pancreas in both young (2 months old) and mature (4 months old) ob/ob mice than their lean littermates.…”

Section: Islet Morphology and Biochemistrymentioning

confidence: 99%

Obesity, Diabetes and Leptin: Lessons Learned from Obese Hyperclycemic Mice

Ahmed

1970

Ibrahim Med. Coll. J.

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The recent epidemic nature of obesity and association of obesity with the development of type 2 diabetes demands dissection of the pathophysiology of this morbid disorder which is essential for better understanding of the process of evolution of insulin resistance. Different animal models have been used to explore the mechanism linking obesity to insulin resistance and type 2 diabetes. The discovery of ob gene and its product, leptin, has revealed the signaling system regulating energy balance in rodents. The mice lacking this ob gene, ob/ob mice, display obesity, hyperglycemia and hyperinsulinemia and has been extensively used for the study of type 2 diabetes and for potential drug development. In this review, the features and development of obese hyperglycemic syndrome, the role of leptin in the pathogenesis of the syndrome and finally the applicability of the findings in rodents to body weight regulation and pathogenesis of insulin resistance in humans have been summarized.

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The ultrastructure of the islets of Langerhans in normal and obese-hyperglycemic mice

Cited by 120 publications

References 20 publications

Quantitative analysis of mouse pancreatic islet architecture by serial block-face SEM

Quantitative analysis of mouse pancreatic islet architecture by serial block-face SEM

Electron Microscopic Studies of the Pancreatic Islets and Some Other Organs in Experimental Congenital Diabetic Rats

Obesity, Diabetes and Leptin: Lessons Learned from Obese Hyperclycemic Mice

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