Changes in pancreatic islets in aging Wistar and Zucker rats: a histochemical and ultrastructural morphometric study

Ogneva, V.; Nikolov, B.

doi:10.1016/0047-6374(94)90096-5

Cited by 12 publications

(6 citation statements)

References 22 publications

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“…These features of islet adaptation such as decreased stimulation index might be multifactorial and could be ascribed to the reduced threshold of the b-cells, 27,28 defect in insulin secretion, 27,28 hypertriglyceridemia, 29 inflammation, 30 hyperleptinemia, 31 oxidative stress 32 and IR 33 reported in different animal models/human studies of obesity. TEM data also showed less dense insulin granules in b-cells of mutants 12 suggestive of impaired secretory function.…”

Section: E998099-6mentioning

confidence: 96%

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Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Singh¹,

Ganneru²,

Malakapalli³

et al. 2014

Islets

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WNIN/GR-Ob mutant rat is a novel animal model to study metabolic syndrome (obesity, insulin resistance, hyperinsulinemia, impaired glucose tolerance and cardiovascular diseases). We have investigated the islet characteristics of obese mutants at different age groups (1, 6 and 12 months) to assess the islet changes in response to early and chronic metabolic stress. Our data demonstrates altered islet cell morphology and function (hypertrophy, fibrotic lesions, vacuolation, decreased stimulation index, increased TNFa, ROS and TBARS levels) in mutants as compared to controls. Furthermore, network analysis (gene-gene interaction) studied in pancreas demonstrated increased inflammation as a key factor underlying obesity/metabolic syndrome in mutants. These observations pave way to explore this model to understand islet adaptation in response to metabolic syndrome.

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Section: E998099-6mentioning

confidence: 96%

“…Increased proportion of light granules in b-cells of obese rats signify immediate insulin secretion, whereas the dense and dark insulin granules in controls (lean/ parental controls) signify stored insulin. 12 …”

Section: Development Of Mild Fibrosismentioning

confidence: 99%

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Singh¹,

Ganneru²,

Malakapalli³

et al. 2014

Islets

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“…Correct islet architecture facilitates the mature pattern of hormone release, directionality of intra-islet paracrine signaling, and connection with the microvasculature 6 , 7 . The typical islet architecture is disrupted in obesity, insulin resistance, and diabetes in both humans and rodents 8 – 14 . Structural islet integrity and architecture are also disrupted in cadaver islets during isolation and culture prior to islet transplantation, as well as after infusion into the portal vein 15 – 18 .…”

Section: Introductionmentioning

confidence: 99%

Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells

Adams

Gilbert

Paiz

et al. 2018

Sci Rep

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Pancreatic islets of Langerhans display characteristic spatial architecture of their endocrine cell types. This architecture is critical for cell-cell communication and coordinated hormone secretion. Islet architecture is disrupted in type-2 diabetes. Moreover, the generation of architecturally correct islets in vitro remains a challenge in regenerative approaches to type-1 diabetes. Although the characteristic islet architecture is well documented, the mechanisms controlling its formation remain obscure. Here, we report that correct endocrine cell type sorting and the formation of mature islet architecture require the expression of Roundabout (Robo) receptors in β cells. Mice with whole-body deletion of Robo1 and conditional deletion of Robo2 either in all endocrine cells or selectively in β cells show complete loss of endocrine cell type sorting, highlighting the importance of β cells as the primary organizer of islet architecture. Conditional deletion of Robo in mature β cells subsequent to islet formation results in a similar phenotype. Finally, we provide evidence to suggest that the loss of islet architecture in Robo KO mice is not due to β cell transdifferentiation, cell death or loss of β cell differentiation or maturation.

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“…The leptin receptor fatty gene (Lepr fa ) is a recessive mutation that leads to leptin receptor deficiency, and homozygous animals (fa/fa) show obesity, hyperphagia, insulin resistance, hyperinsulinemia, and glucose intolerance [5,15,23,27,28,31]. Zucker diabetic fatty rats are homozygous for the fa allele of the leptin receptor gene and develop type 2 diabetes with obesity.…”

Section: Introductionmentioning

confidence: 99%

The Influence of Dietary Restriction on the Development of Diabetes and Pancreatitis in Female WBN/Kob-Fatty Rats

et al. 2010

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Abstract:Original WBN/Kob male rats commonly develop chronic pancreatitis by the age of 3 months, while diabetes mellitus occurs at 9 months. In contrast, female rats of this strain do not show pancreatitis or diabetes. The WBN/Kob-fatty rat is a homozygous (fa/fa) congenic strain for the fa allele of the leptin receptor gene (Lepr). In WBN/Kob-fatty rats, both females and males provide a model of non-insulin-dependent diabetes with obesity. The leptin receptor fatty gene (Lepr fa ) induces obesity and hyperphagia. In the present study, we examined the effect of dietary restriction on pancreatitis and diabetes in female WBN/Kob-fatty rats. Five female fatty rats comprised a restricted feeding group with paired-feeding from 3 to 13 weeks of age, and five female lean rats comprised a control group with paired-feeding. At 13 weeks of age, two of the five female fatty rats of the control group developed diabetes mellitus, while no female fatty rats of the restricted feeding group developed diabetes mellitus. At this stage, pathological changes of the pancreas were observed in female fatty rats. All female fatty rats showed severe interlobular, intra-lobular and intra-islet fibrosis. In female fatty rats of the restricted feeding group, pathological changes of the pancreas were milder those of the free-feeding fatty group. Although dietary restriction could not completely prevent pancreatitis in female fatty rats, the development of diabetes was inhibited by its reduction of the severity of pancreatitis.

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Changes in pancreatic islets in aging Wistar and Zucker rats: a histochemical and ultrastructural morphometric study

Cited by 12 publications

References 22 publications

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Islet adaptation to obesity and insulin resistance in WNIN/GR-Ob rats

Endocrine cell type sorting and mature architecture in the islets of Langerhans require expression of Roundabout receptors in β cells

The Influence of Dietary Restriction on the Development of Diabetes and Pancreatitis in Female WBN/Kob-Fatty Rats

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