scholarly journals Ethanol Acutely Stimulates Islet Blood Flow, Amplifies Insulin Secretion, and Induces Hypoglycemia via Nitric Oxide and Vagally Mediated Mechanisms

Endocrinology ◽  
2007 ◽  
Vol 149 (1) ◽  
pp. 232-236 ◽  
Author(s):  
Zhen Huang ◽  
Åke Sjöholm
Keyword(s):  
Nitric Oxide ◽  
Blood Flow ◽  
Insulin Secretion ◽  
Islet Blood Flow

A specific β3-adrenoceptor agonist induces increased pancreatic islet blood flow and insulin secretion in rats

1996 ◽  
Vol 298 (3) ◽  
pp. 287-292 ◽  
Author(s):  
Nadia Atef ◽  
Max Lafontan ◽  
Alexandre Double ◽  
Christophe Hélary ◽  
Alain Ktorza ◽  
...  
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Islet Blood Flow ◽  
Adrenoceptor Agonist

Increased islet blood flow in obese rats: role of the autonomic nervous system

1992 ◽  
Vol 262 (5) ◽  
pp. E736-E740 ◽  
Author(s):  
N. Atef ◽  
A. Ktorza ◽  
L. Picon ◽  
L. Penicaud
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Pancreatic Islet ◽  
Ventromedial Hypothalamus ◽  
Zucker Rats ◽  
Islet Blood Flow ◽  
Obese Rats ◽  
Increased Sensitivity ◽  
Obese Zucker Rats

Hyperinsulinemia, a main feature of both human and animal obesity, has been demonstrated to be due to both an increased sensitivity to nutrient secretagogues and an impairment of the nervous regulation of insulin secretion. Recent studies have shown that pancreatic islet blood flow increases under conditions associated with an enhanced insulin secretion. The aim of this study was to determine whether or not changes in islet blood flow are present in hyperinsulinemic obese rats. Using the nonradioactive microsphere technique, we were able to show a significantly higher islet blood flow in obese rats either of the Zucker strain or Wistar rats after lesion of the ventromedial hypothalamus than in their respective lean controls. Subdiaphragmatic vagotomy had no significant effect on basal islet blood flow of lean rats, whereas it decreased significantly that of obese Zucker rats. Conversely, clonidine, an alpha 2-adrenergic agonist, induced a higher decrease of islet blood flow in obese than in lean Zucker rats. The injection of an intravenous bolus of glucose (375 mg/kg iv) increased significantly more islet blood flow in obese than in lean Zucker rats. It is concluded that obese rats present an increased pancreatic islet blood flow, which may result, at least in part, from exaggerated parasympathetic activity and lower than normal sympathetic activity. This could participate in the hyperinsulinemia observed in these rats.

Gender-specific regulation of pancreatic islet blood flow, insulin levels and glycaemia in spontaneously diabetic Goto–Kakizaki rats

2008 ◽  
Vol 115 (1) ◽  
pp. 35-42 ◽  
Author(s):  
Zhen Huang ◽  
Leif Jansson ◽  
Åke Sjöholm
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Blood Glucose ◽  
Enzyme Inhibitor ◽  
Serum Insulin ◽  
Metabolic Effects ◽  
Male Rats ◽  
Insulin Levels ◽  
Islet Blood Flow ◽  
Specific Regulation

Patients with diabetes are often treated with a statin for hyperlipidaemia and an ACE (angiotensin-converting enzyme) inhibitor or angiotensin receptor antagonist for hypertension or albuminuria. These drugs may also exert beneficial metabolic effects, causing improved glucose tolerance in patients. Gender-related differences have also been observed in the clinical responsiveness to these drugs, but the mechanism behind this is unclear. In the present study, we have investigated whether these drugs and the fatty acid palmitate influence the pancreatic microcirculation, thereby having an impact on insulin secretion and glycaemia in vivo, in spontaneously diabetic male and female Goto–Kakizaki rats. In male rats, pancreatic IBF (islet blood flow) and total PBF (pancreatic blood flow) were increased significantly by pravastatin, captopril and irbesartan. Serum insulin levels were increased by pravastatin and captopril. Palmitate suppressed pancreatic IBF and increased blood glucose. In female animals, pancreatic IBF was stimulated by captopril, candesartan and irbesartan. Total PBF was increased by captopril, candesartan and irbesartan, and by pravastatin. Palmitate suppressed pancreatic IBF and serum insulin secretion. In conclusion, the present study lends support to the view that a local pancreatic RAS (renin–angiotensin system) and pravastatin may be selectively influencing the pancreatic microcirculation and therefore affecting insulin secretion and glycaemia. NEFAs (non-esterified fatty acids) impaired pancreatic IBF, suppressed insulin secretion and increased blood glucose. Substantial gender-related differences in the vascular and metabolic responses to these drugs prevail in this animal model of diabetes.

Age-induced changes in pancreatic islet blood flow: evidence for an impaired regulation in diabetic GK rats

2000 ◽  
Vol 279 (5) ◽  
pp. E1139-E1144 ◽  
Author(s):  
Annika M. Svensson ◽  
Claes-Göran Östenson ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Glucose Metabolism ◽  
Blood Perfusion ◽  
Flow Measurements ◽  
Gk Rats ◽  
Islet Blood Flow ◽  
Longitudinal Variations ◽  
Increasing Demand ◽  
Blood Flow Measurements

The present study aimed to compare longitudinal variations in islet blood perfusion in rats with different degrees of impairment of glucose metabolism. For this purpose, mildly diabetic Goto-Kakizaki (GK) rats, glucose intolerant F1 hybrids of GK and Wistar (W) rats (H), and control W rats were examined at 5 wk, 12 wk, or 1 yr of age, using the microsphere technique for blood flow measurements. W rats showed progressively increasing islet blood flow (IBF) throughout the experiment. Both GK and H rats demonstrated increasing IBF between 5 and 12 wk. However, H rats showed no further increment in IBF at 1 yr, whereas GK rats displayed a pronounced decrease in IBF between 12 wk and 1 yr of age. The augmented IBF seen in older W rats may constitute an adaptation to the increasing demand for insulin secretion in aging rats. The inability to adapt to the increased demand for insulin secretion by upregulation of islet blood flow could contribute to the progressive deterioration of glucose metabolism seen in the aging GK rat.

Glucose intolerance and reduced islet blood flow in transgenic mice expressing the FRK tyrosine kinase under the control of the rat insulin promoter

2007 ◽  
Vol 292 (4) ◽  
pp. E1183-E1190 ◽  
Author(s):  
Cecilia Annerén ◽  
Michael Welsh ◽  
Leif Jansson
Keyword(s):  
Blood Flow ◽  
Insulin Secretion ◽  
Transgenic Mice ◽  
Tyrosine Kinase ◽  
Cell Mass ◽  
Β Cells ◽  
Β Cell ◽  
Islet Blood Flow ◽  
Insulin Promoter

The FRK tyrosine kinase has previously been shown to transduce β-cell cytotoxic signals in response to cytokines and streptozotocin and to promote β-cell proliferation and an increased β-cell mass. We therefore aimed to further evaluate the effects of overexpression of FRK tyrosine kinase in β-cells. A transgenic mouse expressing kinase-active FRK under control of the insulin promoter (RIP-FRK) was studied with regard to islet endocrine function and vascular morphology. Mild glucose intolerance develops in RIP-FRK male mice of at least 4 mo of age. This effect is accompanied by reduced glucose-stimulated insulin secretion in vivo and reduced second-phase insulin secretion in response to glucose and arginine upon pancreas perfusion. Islets isolated from the FRK transgenic mice display a glucose-induced insulin secretory response in vitro similar to that of control islets. However, islet blood flow per islet volume is decreased in the FRK transgenic mice. These mice also exhibit a reduced islet capillary lumen diameter as shown by electron microscopy. Total body weight and pancreas weight are not significantly affected, but the β-cell mass is increased. The data suggest that long-term expression of active FRK in β-cells causes an in vivo insulin-secretory defect, which may be the consequence of islet vascular abnormalities that yield a decreased islet blood flow.

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