scholarly journals Lack of compensatory increase in islet blood flow and islet mass in GK rats following 60% partial pancreatectomy

2005 ◽  
Vol 184 (2) ◽  
pp. 319-327 ◽  
Author(s):  
Annika M Svensson ◽  
Claes-Göran Östenson ◽  
Birgitta Bodin ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Glucose Tolerance ◽  
Wistar Rats ◽  
Pancreatic Blood Flow ◽  
Partial Pancreatectomy ◽  
Islet Mass ◽  
Gk Rats ◽  
Islet Blood Flow ◽  
Islet Volume ◽  
Female Wistar Rats

The effects of a 60% partial pancreatectomy were studied in hyperglycemic GK (Goto–Kakizaki) rats. Partial pancreatectomy or a sham operation was performed on 12-week-old female Wistar rats, GK rats or hybrids between male GK rats and female Wistar rats. Measurements of pancreatic blood flow and islet blood flow were performed by a microsphere technique 2 weeks after surgery. Glucose tolerance was decreased in hybrid compared with Wistar rats, and in GK rats compared with both hybrid and Wistar rats before surgery. Partial pancreatectomy induced minor changes in glucose tolerance. Wistar rats had a decreased islet mass following partial pancreatectomy. Both hybrid and GK rats showed a significant decrease in relative islet volume, but only GK rats in total islet mass, compared with Wistar rats 2 weeks after surgery. Pancreatic blood flow and islet blood flow did not significantly differ between sham-operated Wistar, hybrid or GK rats. After partial pancreatectomy, islet blood flow in relation to islet mass increased 3-fold in Wistar rats and 2-fold in hybrid rats. In contrast, GK rats showed no increase in islet blood flow following partial pancreatectomy. It is concluded that compensatory mechanisms after partial pancreatectomy are operating less effciently in hybrid and GK rats.

Diet-induced obesity and pancreatic islet blood flow in the rat: a preferential increase in islet blood perfusion persists after withdrawal of the diet and normalization of body weight

1996 ◽  
Vol 151 (3) ◽  
pp. 507-511 ◽  
Author(s):  
A M Svensson ◽  
C Hellerström ◽  
L Jansson
Keyword(s):  
Blood Flow ◽  
Body Weight ◽  
Glucose Tolerance ◽  
Pancreatic Islet ◽  
Wistar Rats ◽  
Blood Perfusion ◽  
Cafeteria Diet ◽  
Standard Diet ◽  
Diet Induced Obesity ◽  
Islet Blood Flow

Abstract The aim of the present study was to evaluate the effects of diet-induced obesity on pancreatic islet blood perfusion in normal Wistar rats. Furthermore, we investigated to what extent any obesity-associated changes in islet blood flow could be reversed after reversion to a normal diet with normalization of body weight. Young adult female Wistar rats were offered a palatable mixed high-caloric diet (cafeteria diet) in addition to standard pelleted chow. Age-matched control rats received standard pelleted chow only. After 4 weeks the diet-treated rats had a body weight of approximately 15% more than that of the controls. All diet-treated rats had decreased glucose tolerance and increased serum insulin concentrations, but basal blood glucose concentrations were similar in anesthetized diet-treated and control rats. Whole pancreatic and islet blood flow rates were measured with a microsphere technique. The islet blood flow as well as fractional islet blood flow were increased (P<0·01) in rats fed the cafeteria diet, while blood perfusion of the whole pancreas was similar to that of the control rats. In a second experiment, rats received the cafeteria diet for 4 weeks and were then fed standard pelleted food alone for another 3 weeks, while controls received standard diet for 7 weeks. After this period total body weight, retroperitoneal fat pad weight and glucose tolerance were similar to those of the controls. Whole pancreatic blood flow was unchanged as compared with that of control rats. However, both islet blood flow (P<0·01) and fractional blood flow (P<0·01) were increased. We conclude that diet-induced obesity in rats is associated with decreased glucose tolerance, hyperinsulinemia and a specific increase in absolute and fractional islet blood perfusion. This increase persists for at least 3 weeks after the diet is withdrawn despite normalization of body weight and glucose tolerance. Journal of Endocrinology (1996) 151, 507–511

Effects of glucagon-like peptide-1-(7–36)-amide on pancreatic islet and intestinal blood perfusion in Wistar rats and diabetic GK rats

2007 ◽  
Vol 112 (6) ◽  
pp. 345-351 ◽  
Author(s):  
Annika M. Svensson ◽  
Claes-Göran Östenson ◽  
Suad Efendic ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Wistar Rats ◽  
Blood Perfusion ◽  
Glucose Administration ◽  
Gk Rats ◽  
Islet Blood Flow ◽  
Glucagon Like Peptide ◽  
Glucagon Like Peptide 1 ◽  
Pre Treatment

The aim of the present study was to evaluate the effects of GLP-1 [glucagon-like peptide-1-(7–36)-amide] on total pancreatic, islet and intestinal blood perfusion in spontaneously hyperglycaemic GK rats and normal Wistar rats using a microsphere technique. GK rats had hyperglycaemia and increased pancreatic and islet blood flow. Blood glucose concentrations were not affected when measured shortly (8 min) after GLP-1 administration in either GK or Wistar rats. GLP-1 had no effects on baseline pancreatic or islet blood flow in Wistar rats, but did prevent the blood flow increase normally seen following glucose administration to these animals. In GK rats, administration of GLP-1 decreased both pancreatic and islet blood flow. Glucose administration to the GK rats decreased pancreatic and islet blood flow. This decrease was not affected by pre-treatment with GLP-1. We conclude that administration of GLP-1 leads to a decrease in the augmented blood flow seen in islets of diabetic GK rats. The GLP-1-induced action on islet blood perfusion may modulate output of islet hormones and contribute to the antidiabetogenic effects of the drug in Type 2 diabetes (non-insulin-dependent diabetes).

Pancreatic islet blood flow in normal and obese-hyperglycemic (ob/ob) mice

1996 ◽  
Vol 271 (6) ◽  
pp. E990-E995 ◽  
Author(s):  
P. O. Carlsson ◽  
A. Andersson ◽  
L. Jansson
Keyword(s):  
Blood Flow ◽  
Blood Perfusion ◽  
Pancreatic Tissue ◽  
Pancreatic Blood Flow ◽  
Flow Measurements ◽  
Islet Mass ◽  
Arterial Blood ◽  
Islet Blood Flow ◽  
Different Strains ◽  
Blood Flow Measurements

The present study evaluated whether a microsphere technique could be used for islet blood flow measurements in anesthetized mice. When this was confirmed, we applied the technique in different strains of mice. Approximately 9 x 10(4) microspheres could be given without interfering with mean arterial blood pressure. Mixing of the microspheres with arterial blood was adequate, and the extraction of microspheres in capillary beds was nearly 100%. In NMRI mice whole pancreatic blood flow was estimated to be 0.54 +/- 0.11 ml.min-1.g pancreatic tissue-1 and islet blood flow to be 18 +/- 4 microliters.min-1.g pancreas-1 (n = 12 animals per experiment), whereas corresponding values in lean C57Bl/6 mice were twice as high. In C57Bl/6 mice glucose (3 g/kg iv) doubled islet blood flow without affecting whole pancreatic blood flow, whereas no effect was seen after an equimolar dose of 3-O-methylglucose. In obese-hyperglycemic C57Bl/6 mice, islet blood flow was more than five times higher than in the lean C57Bl/6 mice when expressed as blood flow per gram pancreas. However, when islet blood perfusion was corrected for islet weight, it was lower in the obese than in the lean mice, suggesting an impaired ability in obese mice to increase blood flow in concert with the increased islet mass. This may contribute to the insufficient insulin secretion and resulting hyperglycemia seen in these animals.

Pancreatic and islet blood flow in F1-hybrids of the non-insulin-dependent diabetic GK-Wistar rat

1994 ◽  
Vol 130 (6) ◽  
pp. 612-616 ◽  
Author(s):  
Annika M Svensson ◽  
Samy M Abdel-Halim ◽  
Suad Efendic ◽  
Leif Jansson ◽  
Claes-Göran Östenson
Keyword(s):  
Blood Flow ◽  
Glucose Tolerance ◽  
Pancreatic Islets ◽  
Blood Perfusion ◽  
Wistar Rat ◽  
F1 Hybrids ◽  
Partial Pancreatectomy ◽  
Islet Blood Flow ◽  
Insulin Dependent ◽  
Insulin Dependent Diabetic

Svensson AM, Abdel-Halim SM, Efendic S, Jansson L, Östenson C-G. Pancreatic and islet blood flow in F1 -hybrids of the non-insulin-dependent diabetic GK-Wistar rat. Eur J Endocrinol 1994:130:612–16. ISSN 0804–4643 Previous studies have indicated that various conditions under which an increased functional load is posed on the pancreatic islets, e.g. partial pancreatectomy and continuous glucose infusions, may influence the microcirculation of the pancreas. To investigate further the effects of elevated functional demand on the islets, the blood perfusion of the whole pancreas and the pancreatic islets was measured with a microsphere technique in an animal model presenting impaired glucose tolerance and mild hyperglycemia, namely F 1-hybrids of the spontaneously non-insulin-dependent diabetic GK-Wistar rat. Normal Wistar rats served as controls. All hybrids had a pathological intraperitoneal glucose tolerance test 1 week before the blood flow measurements, which were performed in 10–12-week-old rats. Both the whole pancreatic and the islet blood flows were increased in the hybrids compared to controls. The fractional islet blood flow, i.e. the fraction of whole pancreatic blood flow diverted through the islets, also was increased in the hybrid rats (12.6 ±0.6% vs 9.8 ±0.5% in controls, p <0.01). A bilateral abdominal vagotomy performed 30 min before the blood flow measurement markedly decreased the blood flow values of the islets and the whole pancreas in both groups of rats. After vagotomy, the islet blood flow in the hybrid rats was similar to that of the vagotomized control animals (8.2 ± 0.8 and 7.5 ± 1.4%, respectively). It is concluded that the increased pancreatic and islet blood perfusion observed in F 1-hybrids of the GK-Wistar rat depends on a mechanism mediated by the vagus nerve. Annika M Svensson, Department of Medical Cell Biology, Biomedical Centre, PO Box 571, S-75123 Uppsala, Sweden

Duodenal-jejunal bypass protects GK rats from β-cell loss and aggravation of hyperglycemia and increases enteroendocrine cells coexpressing GIP and GLP-1

2011 ◽  
Vol 300 (5) ◽  
pp. E923-E932 ◽  
Author(s):  
Madeleine Speck ◽  
Young Min Cho ◽  
Ali Asadi ◽  
Francesco Rubino ◽  
Timothy J. Kieffer
Keyword(s):  
Glucose Tolerance ◽  
Glucose Homeostasis ◽  
Wistar Rats ◽  
Enteroendocrine Cells ◽  
Cell Populations ◽  
Cell Area ◽  
Β Cell ◽  
Enteroendocrine Cell ◽  
Gk Rats ◽  
Jejunal Bypass

Dramatic improvement of type 2 diabetes is commonly observed after bariatric surgery. However, the mechanisms behind the alterations in glucose homeostasis are still elusive. We examined the effect of duodenal-jejunal bypass (DJB), which maintains the gastric volume intact while bypassing the entire duodenum and the proximal jejunum, on glycemic control, β-cell mass, islet morphology, and changes in enteroendocrine cell populations in nonobese diabetic Goto-Kakizaki (GK) rats and nondiabetic control Wistar rats. We performed DJB or sham surgery in GK and Wistar rats. Blood glucose levels and glucose tolerance were monitored, and the plasma insulin, glucagon-like peptide-1 (GLP-1), and glucose-dependent insulinotropic polypeptide (GIP) levels were measured. β-Cell area, islet fibrosis, intestinal morphology, and the density of enteroendocrine cells expressing GLP-1 and/or GIP were quantified. Improved postprandial glycemia was observed from 3 mo after DJB in diabetic GK rats, persisting until 12 mo after surgery. Compared with the sham-GK rats, the DJB-GK rats had an increased β-cell area and a decreased islet fibrosis, increased insulin secretion with increased GLP-1 secretion in response to a mixed meal, and an increased population of cells coexpressing GIP and GLP-1 in the jejunum anastomosed to the stomach. In contrast, DJB impaired glucose tolerance in nondiabetic Wistar rats. In conclusion, although DJB worsens glucose homeostasis in normal nondiabetic Wistar rats, it can prevent long-term aggravation of glucose homeostasis in diabetic GK rats in association with changes in intestinal enteroendocrine cell populations, increased GLP-1 production, and reduced β-cell deterioration.

scholarly journals Duct ligation and pancreatic islet blood flow in rats: physiological growth of islets does not affect islet blood perfusion

2005 ◽  
Vol 153 (2) ◽  
pp. 345-351 ◽  
Author(s):  
Leif Jansson ◽  
Birgitta Bodin ◽  
Örjan Källskog ◽  
Arne Andersson
Keyword(s):  
Blood Flow ◽  
Pancreatic Islet ◽  
Serum Insulin ◽  
Blood Perfusion ◽  
Islet Function ◽  
Sprague Dawley ◽  
Islet Mass ◽  
Islet Blood Flow ◽  
Sprague Dawley Rats ◽  
Duct Ligation

Objectives: The aim of this study was to evaluate islet blood-flow changes during stimulated growth of the islet organ without any associated functional impairment of islet function. Design: A duct ligation encompassing the distal two-thirds of the pancreas was performed in adult, male Sprague–Dawley rats. Methods: Pancreatic islet blood flow was measured in duct-ligated and sham-operated rats 1, 2 or 4 weeks after surgery. In some animals studied 4 weeks after surgery, islet blood flow was also measured also during hyperglycaemic conditions. Results: A marked atrophy of the exocrine pancreas was seen in all duct-ligated rats. Blood glucose and serum insulin concentrations were normal. An increased islet mass was only seen 4 weeks after surgery. No differences in islet blood perfusion were noted at any time point after duct ligation. In both sham-operated and duct-ligated rats islet blood flow was increased during hyperglycaemia; the response was, however, slightly more pronounced in the duct-ligated part of the gland. Conclusions: Normal, physiological islet growth does not cause any major changes in the islet blood perfusion or its regulation. This is in contrast to findings during increased functional demands on the islets or during deteriorated islet function, when increased islet blood flow is consistently seen.

Relation between blood flow and morphology in islet organ of rat pancreas

1985 ◽  
Vol 249 (1) ◽  
pp. E43-E48 ◽  
Author(s):  
N. Lifson ◽  
C. V. Lassa ◽  
P. K. Dixit
Keyword(s):  
Blood Flow ◽  
Rat Pancreas ◽  
Islet Blood Flow ◽  
Islet Volume ◽  
Islet Tissue ◽  
Islet Size

By intra-arterial postmortem staining of the pancreas with hematoxylin after the administration of nonradioactive microspheres to anesthetized unfasted rats, the following values (+/-SE) were obtained: mean single islet volume, 1.00 +/- 0.12 nl (median 0.32 +/- 0.04 nl, n = 14); pancreatic intensity of perfusion, 1.18 +/- 0.14 ml X min-1 X g-1 (n = 10); percentage of pancreatic flow to islets, 6 +/- 1% (n = 10); single islet blood flow, 20 +/- 3 ml X min-1 (n = 10); and islet perfusion, 19 +/- 3 ml X min-1 X g-1 (n = 10). Perfusion of islet tissue was calculated to be above average for very small islets and to decrease with increasing islet size to become below average for very large ones. Details of the distribution of the total islet flow to subpopulations of islets grouped according to single islet size are shown pictorially.

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