Immunohistochemical investigations of the endocrine pancreas in normoglycemic sand rats (Psammomys obesus)

Donev, S; Petkov, P; Marquié, G; Duhault, J; R, Jablenska

doi:10.1007/bf02624642

Cited by 7 publications

(4 citation statements)

References 12 publications

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“…A number of previous reports, predominantly based on rodent studies, have suggested that the majority of beta cells are located in the pancreatic tail, whereas the extent of beta cells in the pancreatic head is often held to be negligible [37,38]. This finding has often been used as a rationale for removing the pancreatic head in patients with chronic pancreatitis.…”

Section: Discussionmentioning

confidence: 99%

Metabolic consequences of a 50% partial pancreatectomy in humans

et al. 2008

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Aims/hypothesis Partial pancreatectomy is frequently performed in patients with pancreatic tumours or chronic pancreatitis, but little is known about the metabolic impact of this intervention. We examined the effects of approximately 50% partial pancreatectomy on glucose homeostasis and insulin secretion. Methods Fourteen patients with chronic pancreatitis, ten patients with pancreatic carcinoma and 13 patients with benign pancreatic tumours or extra-pancreatic masses (control group) underwent 240 min oral glucose tolerance tests before and after pancreatic tail-resection (n=12), duodenopancreatectomy (n=19) or duodenum-preserving pancreatic-head resection (n=6). Results Partial pancreatectomy led to a reduction in postchallenge insulin excursions by 49% in chronic pancreatitis patients, 52% in carcinoma patients and 55% in controls (p<0.05). Nevertheless, post-challenge glucose concentrations were transiently ameliorated after surgery (p<0.001). In the control participants, pancreatic-head resection caused a transient reduction of post-challenge glycaemia, whereas pancreatic-tail resection increased both fasting and postchallenge glycaemia (p<0.05). Insulin sensitivity was highest in chronic pancreatitis patients before surgery (p<0.01), but remained unchanged by the partial pancreatectomy. High pre-operative body weight and elevated fasting glucose levels were associated with poor glycaemic control after surgery. Conclusions/interpretation Insulin secretion is diminished after pancreatic-head and -tail resection, but post-challenge glucose concentrations can be ameliorated after pancreatichead resection. These data highlight the unequal impact of different surgical procedures on glucose control and suggest that obesity and high pre-operative glucose levels should be considered as risk factors for the development of hyperglycaemia after pancreatic surgery.

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Section: Discussionmentioning

confidence: 99%

Metabolic consequences of a 50% partial pancreatectomy in humans

et al. 2008

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“…The development of obesity is accompanied by hyperglycemia, hyperinsulinemia, decreased insulin sensitivity in adipose tissue and liver, and glucosuria, [153,154]. Comparing with normoglycemic individuals, pancreatic β-cell volume begin to decrease in the obese and diabetic sand rats, as well as GLUT 2 glucose transporter on the cellular membrane and glucokinase in the cytoplasm of β-cells [155,156]. Progressive loss of β-cells due to cell death is accompanied by hypoinsulinemia and persistent hyperglycemia, generating an irreversible diabetic state in sand rat.…”

Section: Spontaneously Hypertensive Rat/national Institute Of Health-mentioning

confidence: 99%

Development of Improved Animal Models for the Study of Diabetes

Ciobotaru¹

2013

Diabetes Mellitus - Insights and Perspectives

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“…Donev et al (1989) found that the normoglycemic P. obesus pancreas expresses all the four major pancreatic hormones, and that two types of islets could be observed. These islets were called A islets or PP islets and could be distinguished by whether glucagon or pancreatic polypeptide (PP) was the prevalent cell type in the rims of the islets.…”

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confidence: 95%

“…These islets were called A islets or PP islets and could be distinguished by whether glucagon or pancreatic polypeptide (PP) was the prevalent cell type in the rims of the islets. PP islets were found to be most prevalent in the head of the pancreas, whereas A-type islets were mostly found in the tail portion of the pancreas (Donev et al 1989). Interestingly, Pdx-1, a critical transcription factor for the formation of the pancreas and for the maintenance of β-cells, was shown to be deficient in the newborn P. obesus (Leibowitz et al 2001).…”

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confidence: 99%

Developmental Biology of the Psammomys obesus Pancreas: Cloning and Expression of the Neurogenin-3 Gene

Vedtofte¹,

Bödvarsdóttir

Karlsen

et al. 2006

J Histochem Cytochem.

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(AEK) S U M M A R Y The desert gerbil Psammomys obesus, an established model of type 2 diabetes (T2D), has previously been shown to lack pancreatic and duodenal homeobox gene 1 (Pdx-1) expression. Pdx-1 deficiency leads to pancreas agenesis in both mice and humans. We have therefore further examined the pancreas of P. obesus during embryonic development. Using Pdx-1 antisera raised against evolutionary conserved epitopes, we failed to detect Pdx-1 immunoreactivity at any time points. However, at E14.5, Nkx6.1 immunoreactivity marks the nuclei of all epithelial cells of the ventral and dorsal pancreatic buds and the only endocrine cell types found at this time point are glucagon and PYY. At E18.5 the pancreas is well branched and both glucagon-and ghrelin-positive cells are scattered or found in clusters, whereas insulin-positive cells are not found. At E22.5, the acini of the exocrine pancreas are starting to mature, and amylase and carboxypeptidase A immunoreactivity is found scattered and not in all acini. Ghrelin-, glucagon-, PYY-, gastrin-, somatostatin (SS)-, pancreatic polypeptide (PP)-, and insulin-immunoreactive cells are found scattered or in small groups within or lining the developing ductal epithelium as marked by cytokeratin 19. Using degenerate PCR, the P. obesus Neurogenin-3 (Ngn-3) gene was cloned. Nucleotide and amino acid sequences show high homology with known Ngn-3 sequences. Using specific antiserum, we can observe that Ngn-3-immunoreactive cells are rare at E14.5 but readily detectable at E18.5 and E22.5. In conclusion, despite the lack of detection of Pdx-1, the P. obesus pancreas develops similarly to Muridae species, and the Ngn-3 sequence and expression pattern is highly conserved in P. obesus. (J Histochem Cytochem 55:97-104, 2007) K E Y W O R D S Psammomys obesus neurogenin-3 type 2 diabetes developmental biology glucagon insulin pancreas sand rat THE GERBIL PSAMMOMYS OBESUS is a promising animal model for the study of type 2 diabetes (T2D) (Hackel et al. 1967;Kalman et al. 2001). The natural habitat of the P. obesus is the arid zone of the Eastern Mediterranean region and North Africa from where it was collected in the 1960s. Our animals are from the colony in Jerusalem that was established in the 1970s when it was collected from the arid shores of the Dead Sea (Shafrir and Ziv 1998). In its native habitat, the P. obesus feeds on succulent leaves of, e.g., the salt bush, which is a low-energy diet (2.98 digestible kcal/g). When transferred to laboratory rodent chow (Purina 5008, 3.31 digestible kcal/g; Charles River Laboratories, Wilmington, MA), which is high in energy to the P. obesus, z80% of our population develops diabetes. Development of diabetes begins with hyperinsulinemia, after which hyperglycemia sets in and finally overt T2D occurs. This phenotypic pattern closely resembles the pattern observed in human populations, making the P. obesus a good model for the study of T2D (Walder et al. 2000). Donev et al. (1989) found that the normoglycemic P. obesus pancreas expres...

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Immunohistochemical investigations of the endocrine pancreas in normoglycemic sand rats (Psammomys obesus)

Cited by 7 publications

References 12 publications

Metabolic consequences of a 50% partial pancreatectomy in humans

Metabolic consequences of a 50% partial pancreatectomy in humans

Development of Improved Animal Models for the Study of Diabetes

Developmental Biology of the Psammomys obesus Pancreas: Cloning and Expression of the Neurogenin-3 Gene

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