[Isolation of the islands of Langerhans of the rat pancreas and evaluation of islet function in vitro].
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Hyperinsulinemia
Amylin
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Thyroxine treatment induced experimental hyperthyroidism in ob/ob mice, inhibited glucose-induced insulin secretion from the isolated perfused ob/ob mouse pancreas, and reduced total pancreas insulin content. In contrast, glucose-induced insulin release from incubated pancreatic islets and insulin content of pancreatic islets from ob/ob mice isolated by freehand microdissection were not reduced after thyroxine treatment when expressed per microgram dry islet. Histological examination of the ob/ob mouse pancreas revealed islets without degenerative lesions of islet cells. Granularity of beta cells was well preserved. The average number of pancreatic islets was unchanged. However, the beta cell area was significantly decreased in relation to the total pancreatic parenchyma after thyroxine treatment. This implies that insulin release and content per pancreatic islet was half of that of the controls. ATP content of islets was slightly reduced. Glucose oxidation and glucose utilization by islets from treated mice were slightly increased. Thyroxine treatment of the animals did not abolish the stimulation of 45Ca2+ uptake by glucose, but it did suppress the potentiating effect of fasting on the stimulatory effect of glucose on 45Ca2+ uptake. The metabolic characteristics of islets from experimentally hyperthyroid mice are those of all hyperthyroid tissues. The results provide no evidence for the view that the effects of thyroxine treatment may be due to disturbed metabolic function or energy deprivation of pancreatic islets. Inhibition of insulin secretion from the pancreas after thyroxine administration is apparently due to a reduction in pancreas insulin content and a diminished pancreatic islet volume. Reduced pancreatic islet volume represents most probably a reduction of individual islet cell volume.
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Changes in Somatostatin Concentration in Pancreas and Other Tissues of Streptozotocin Diabetic Rats*
Changes in immunoreactive somatostatin were examined in islets, whole pancreas, stomach, and hypothalamus of streptozotocin-diabetic rats. There was no change in islet somatostatin content at 2 days after the administration of streptozotocin, but thereafter, somatostatin progressively increased in the diabetic animals by 45% at 2 weeks, 230% at 6 weeks, and 500% by 6 months. By contrast, islet glucagon rose acutely and maintained a constant 2-fold elevation irrespective of the duration of the diabetes. Morphometric analysis of the somatostatin- and glucagon-producing cells in the islets revealed an apparent augmentation of both cell types. The concentration of somatostatin per total pancreas was also increased in the diabetic animals, suggesting that the islet increase was part of a true increase in pancreatic somatostatin. Pancreatic glucagon was unchanged despite the islet increase. The increase in pancreatic somatostatin was paralleled by an elevation in gastric somatostatin concentration, implying a common mechanism in response to streptozotocin for the somatostatin cells in these two sites. There was no change in hypothalamic somatostatin concentration. Islet somatostatin was also increased in alloxan-diabetic rats. suggesting that streptozotocin does not stimulate the D cells directly.
Delta cell
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Release of somatostatin and insulin from perifused islets of fasted and control rats was compared. After a fasting period of 48 h glucose-induced insulin release but not somatostatin release was diminished. Islets from fasted rats released significantly more somatostatin in the presence of 3.3 mM glucose than islets from controls. Simultaneously, the somatostatin content of isolated islets from fasting rats was significantly decreased. The results indicate that the low secretory activity of islet B cells in the fasting state is associated with a high secretory activity of islet D cells.
Insulin oscillation
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Immunoreactive neurotensin (IR-NT) content in 2 N acetic acid extracts of pancreas was measured in genetically diabetic (C57BL/KsJ db/db and ob/ob) and obese (C57BL/6J ob/ob and db/db) mice and normal littermate controls from 5 to 24 wk of age to determine the relationship of any changes to the development of metabolic abnormalities. Pancreatic IR-NT in obese mice showed no consistent change compared with lean littermate controls. In contrast, diabetic mice demonstrated an increase in pancreatic IR-NT that occurred at 6–8 wk of age, and maximal about the time of islet B-cell failure (8–10 wk), and persisted over the study period. Pancreatic IR-NT eluted in two peaks on reverse phase high-pressure liquid chromatography, one of which exhibited a retention time similar to that of synthetic NT. These findings suggest that pancreatic IR-NT concentration is regulated by insulin, with elevated levels occurring in association with insulin deficiency and its metabolic consequences but not with insulin resistance. Taken together with the previous demonstration that NT influences pancreatic islet hormone secretion, the present findings support a possible role of endogenous NT in islet hormone regulation.
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Abstract Although galanin has been shown to be present in pancreatic islet cells, there is no literature available on the pattern of distribution and the effect of galanin in the pancreas of diabetic animals or human models. The aim of this study was to examine whether galanin immunoreactivity changes after the onset of diabetes mellitus in the rat model. The present study used immunohistochemical techniques to examine the pattern of distribution of galanin–like immunoreactive cells in the pancreas of rats with streptozotocin‐induced diabetes. The effect of galanin on insulin secretion from intact rat pancreatic tissue fragments was also investigated using a radioimmunoassay technique. Numerous galanin–like immunoreactive cells were observed in both the peripheral and central regions of the islet of Langerhans of normal rat pancreas. By contrast, the islets of diabetic rat pancreas contained significantly (P < 0.0001) fewer galanin–like immunoreactive cells than nondiabetic rats. Galanin was colocalized with insulin in the islets of normal and diabetic rats. Galanin had an inhibitory effect on insulin secretion from the isolated pancreatic tissue fragments of normal and diabetic rats at all concentrations (10 −12 to 10 −6 M) employed. Galanin at 10 −9 M caused a significant (P < 0.02) decrease in insulin secretion from normal rat pancreatic tissue fragments compared to basal. These observations indicate that galanin may play a significant role in the regulation of insulin secretion.
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Obesity in the Zucker rat is accompanied by hyperlipemia, hyperinsulinism, insulin resistance, pancreatic hyperplasia, and islet hypertrophy. This study correlates the morphologic heterogeneity of isolated pancreatic islets with secretion of insulin and glucagon in a perifusion system. Islet size was arbitrarily defined as large (>0.45 mm) or small (<0.12 mm). Protein content and volume (V = 4/3πr3) were calculated for groups and individual islets, respectively. Islets from obese rats secreted more insulin in response to glucose and aminophylline than islets from lean rats (peak 7.8 ± 2.4 vs. 1.5 ± 0.37 μU/islet/min, P < 0.005). Insulin release was related directly to islet size and protein content. Small islets from lean and obese animals produced less insulin per islet than large islets (P < 0.005). In terms of islet volume, however, large islets were inefficient insulin releasers as compared to small islets (P < 0.005). Stimulation with Br-cAMP released glucagon from islets of lean but not from large islets of obese animals (peak 11 ±3.3 vs. 4.1 ± 0.3 pg/μg protein per minute, P < 0.05). Arginine produced the same effect on glucagon release (P < 0.05) as stimulation with Br-cAMP. The observed increased insulin release rates and the blunted glucagon response are related to islet size in the pancreas of the Zucker rat.
Insulin oscillation
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Hyperinsulinemic and hypoglycemic rats with islet cell tumors induced by streptozotocin were shown to have significantly decreased immunoreactive insulin and somatostatin concentration (expressed as per g wet weight (w. wt)) and content (expressed as per whole pancreas) in the pancreas surrounding the tumor as compared to those of age and weight adjusted controls. The pancreatic glucagon concentration of the former was significantly lower than that of the latter but no significant difference between glucagon content in the two groups was observed. Thus, inverse relationships were demonstrated between circulating insulin and somatostatin as well as insulin in the pancreas. It is suggested that a large amount of insulin in plasma results in a decrease in pancreatic insulin and somatostatin.
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To investigate the possible role of islet amyloid polypeptide (IAPP) in the development of type 2 diabetes mellitus, we examined the IAPP content and secretion in pancreatic islets isolated from ventromedial hypothalamic (VMH)-lesioned rats and genetically obese Zucker rats, using a specific RIA for IAPP. Obesity and hyperinsulinemia were observed in rats 21 days after VMH lesioning. IAPP content was increased in the islets of VMH-lesioned rats compared with findings in the shamoperated controls (100.9 ± 6.6 vs. 72.8 ± 3.85 fmol/islet; P < 0.01). Isolated islets of VMH-lesioned rats secreted larger amounts of IAPP in the presence of 2.8 mM and 16.7 mM glucose (2.99 ± 0.98 and 11.2 ± 1.29 fmol · islet-1 · 3 h-1) than was noted in sham-operated rats (ND and 6.65 ± 0.78 fmol islet-1 · 3 h-1). In the obese Zucker rats, aged 14 weeks, IAPP concentrations in the islets were elevated compared with lean rats (133.3 ± 10.6 vs. 84.4 ± 8.5 fmol/islet; P < 0.01). The isolated islets secreted larger amounts of IAPP in response to 2.8 mM and 16.7 mM glucose (2.83 ± 0.88 and 15.81 ± 1.35 fmol · islet-1 · 3 h-1) than did those from lean control rats (0.36 ± 0.19 and 12.49 ± 1.20 fmol · islet-1 · 3 h-1). These results strongly suggest that overproduction and hypersecretion of IAPP occur in animals with obesity and hyperinsulinemia. (Endocrinology128: 2739–2744, 1991)
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The β-cell function, total islet volume, and number were studied in 1- to 18-month-old mice, together with the extractable pancreatic insulin and glucagon. The β-cell function, determined as the total amount of insulin released in response to glucose from the in vitro perfused pancreas showed an agerelated increase, without any differences in the kinetics of insulin secretion between young and old mice. The total islet number and area in each individual pancreas was determined planimetrically after selective staining of the islets by perfusing the pancreas with dithizone. The islet area increased from 5.4 ± 1.7 mm2 at 1 month to 16.3 ± 2.1 mm2 at 18 months, whereas the number of islets remained virtually unchanged (1072 ± 51). Pancreatic insulin increased with age by nearly 500%, in contrast to a 35% reduction in pancretic glucagon. There was a strong relationship between body weight and total pancreatic DNA (P = 4.7 ×10-8), islet area (P = 3.2 × 10-7), insulin secretory capacity (P = 7 × 10-4), and total pancreatic insulin (P = 1.9 × 10-5), but no relationship between body weight and islet number. The insulin secretory capacity increased proportionally to the increase in islet area (P = 9.9 Times; 10-3). The islet area and total pancreatic insulin were closely related (P = 2.8 × 10-12), as were pancreatic insulin and the insulin secretory capacity (P = 3.3 × 10-11). There was a negative relationship between pancreatic glucagon and islet area (P = 0.005) and between pancreatic glucagon and insulin (P = 0.01). The close relationship between pancreatic insulin and islet area, shown to be an expression of islet volume, makes it possible to estimate the volume of the endocrine pancreas after standard RIA of pancreatic insulin. The combined morphometric and physiological analysis is unique in studying islet cell function relative to the volume of the endocrine pancreas.
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