scholarly journals Appearance of glucose-induced insulin release in fetal rat beta-cells

1998 ◽  
Vol 158 (1) ◽  
pp. 115-120 ◽  
Author(s):  
P Bergsten ◽  
K Aoyagi ◽  
E Persson ◽  
UJ Eriksson ◽  
C Hellerstrom
Keyword(s):  
Insulin Release ◽  
Glucose Concentration ◽  
Cultured Cells ◽  
Insulin Content ◽  
Isolated Cells ◽  
K Channels ◽  
Pancreatic Cells ◽  
Pancreatic Insulin ◽  
Fetal Rat ◽  
Critical Components

Fetal rat pancreatic cells were isolated from pancreatic primordia on days 12-14 of pregnancy and cultured for 48 h in the presence of 5 mmol/l glucose. Insulin accumulation in the medium over the next 24 h was measured. Cultured cells from day 12 fetuses secreted about 1 fmol insulin per pancreas in response to 5 or 15 mmol/l glucose irrespective of whether 1 mmol/l tolbutamide, 400 mumol/l diazoxide, 5 mmol/l theophylline or 10 mmol/l mannoheptulose was present. In contrast, insulin released from day 13 cultured cells increased significantly from 3.0 +/- 0.6 to 6.2 +/- 2.2 fmol per pancreas, when the glucose concentration was raised. Tolbutamide increased, diazoxide and mannoheptulose decreased and theophylline had no effect on insulin release. Even more pronounced effects were found on insulin release from day 14 cultured cells, in which theophylline also increased the release. In addition, insulin release from cells from pregnancy day 14 was 75 +/- 16 amol/min per pancreas when the cells were perifused for 15-20 min in the presence of 5 mmol/l glucose within 3 h of isolation. Increasing the glucose concentration to 15 mmol/l or adding tolbutamide increased, whereas diazoxide decreased, insulin release in the freshly isolated cells. The insulin content of rat pancreata from pregnancy day 13 was 0.06 +/- 0.01 pmol per pancreas and increased approximately 10-fold every second day up to 6.7 +/- 0.9 pmol on day 17 of pregnancy. Between day 17 and 19 the pancreatic insulin content increased about fivefold to 39 +/- 2 pmol. The present data suggest that critical components of the insulin-secretory machinery, including ATP-regulated K+ channels, glucokinase and adenylate cyclase activities, are present in the developing beta-cell earlier than hitherto thought.

Insulin release and pancreatic insulin is reduced in young prediabetic BB rats

1986 ◽  
Vol 112 (3) ◽  
pp. 367-371 ◽  
Author(s):  
Annette Svenningsen ◽  
Thomas Dyrberg ◽  
Helle Markholst ◽  
Christian Binder ◽  
Åke Lernmark
Keyword(s):  
Insulin Release ◽  
Insulin Dependent Diabetes Mellitus ◽  
Insulin Content ◽  
Dependent Diabetes Mellitus ◽  
Clinical Onset ◽  
Pancreatic Insulin ◽  
Pancreatic Insulin Content ◽  
Bb Rats ◽  
Insulin Dependent ◽  
The Mean

Abstract. The pancreases of approximately 50 days old diabetes-prone BB/Hagedorn (BB/H) and of the genetically closely related, but non-diabetic BB w-subline (control BB) rats were perfused to determine the capacity of D-glucose to release insulin before the expected development of diabetes. The BB/H rats were from a colony with 82–84% incidence of insulin-dependent diabetes mellitus (IDDM) by 140 days of age. The total amount of insulin released from the BB/H rat pancreas during stimulation with 20 mmol/l D-glucose was reduced by nearly 50% (P <0.01). The initial peak of insulin release was similar between the two groups of animals, whereas the amount of insulin released during the second peak accounted for the diminished release (P < 0.01). The extractable pancreatic insulin was 30% (P < 0.05) less in the BB/H rats. Total insulin release expressed relative to the pancreatic insulin content, was therefore not different between the two groups. It is concluded that about 20–40 days before the mean age of clinical onset of IDDM in BB/H rats, the capacity to release insulin in response to D-glucose is reduced along with a diminished pancreatic insulin content. This abnormality seems to be preceded only by islet cell surface antibodies but not by insulitis.

Insulin secretion in glucosamine-induced hyperglycemia in rats

1965 ◽  
Vol 209 (4) ◽  
pp. 797-802 ◽  
Author(s):  
Julio M. Martin ◽  
Gunta Bambers
Keyword(s):  
Insulin Secretion ◽  
Blood Glucose ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Insulin Injection ◽  
Inhibitory Effect ◽  
Base Line ◽  
Pancreatic Insulin ◽  
Hyperglycemic Effect

The hyperglycemia response produced by the injection of glucosamine in rats has been studied by comparing the effects of equal doses of glucosamine and glucose on blood glucose, circulating insulin, and pancreatic insulin content. The effect of glucosamine and glucose on insulin release from the islets has been studied in vitro by incubating slices of pancreas from normal rats and from rats injected with glucosamine. After glucosamine injection, the blood glucose rose and the circulating insulin decreased. In the glucose-injected group the hyperglycemia was lower and the circulating insulin higher. Insulin output from incubated pancreatic slices of normal rats rose when the glucose concentration in the medium was increased or when tolbutamide was added. A decrease below the base line occurred on the addition of glucosamine or when pancreas slices from glucosamine-injected rats were incubated. Insulin injection decreased the hyperglycemic effect of glucosamine whereas tolbutamide was ineffective. These results suggest that glucosamine exerts an inhibitory effect on insulin release from the pancreas.

INSULIN RELEASE, INSULIN CONTENT, AND GLUCOSE UTILIZATION IN ISOLATED MOUSE ISLETS MAINTAINED IN TISSUE CULTURE

1978 ◽  
Vol 87 (3) ◽  
pp. 535-542 ◽  
Author(s):  
Christian Eff
Keyword(s):  
Tissue Culture ◽  
Insulin Release ◽  
Glucose Concentration ◽  
Glucose Utilization ◽  
Insulin Content ◽  
Langerhans Islets ◽  
Juvenile Diabetics ◽  
Mouse Islets ◽  
High Concentrations ◽  
Remission Phase

ABSTRACT To elucidate the remission phase in juvenile diabetics the insulin release, insulin content, and glucose utilization were measured in isolated Langerhans' islets from mice maintained for 6 days in a tissue culture at a glucose concentration of 278 mmol, followed by a culture period of 4 days at 6.1 mmol glucose. These experiments revealed that the ability of the islets to store and secrete insulin during glucose stimulation decreased considerably during incubation at high concentrations of glucose. When the glucose concentration in the incubation medium was reduced, these properties could be re-established. Basal as well as glucose-stimulated glucose utilization increased greatly during incubation at high glucose concentrations. However, it was not possible to normalize the glucose utilization during 4 days' incubation at 6.1 mmol glucose. The results indicate that unphysiologically high concentrations of glucose may induce long-lasting changes in the function of Langerhans' islets.

scholarly journals A Mouse Model of Beta-Cell Dysfunction as Seen in Human Type 2 Diabetes

2018 ◽  
Vol 2018 ◽  
pp. 1-11 ◽  
Author(s):  
Jacqueline H. Parilla ◽  
Joshua R. Willard ◽  
Breanne M. Barrow ◽  
Sakeneh Zraika
Keyword(s):  
Type 2 Diabetes ◽  
Mouse Model ◽  
Insulin Release ◽  
Insulin Content ◽  
Cell Area ◽  
High Fat ◽  
Once Daily ◽  
Pancreatic Insulin ◽  
Pancreatic Insulin Content

Loss of first-phase insulin release is an early pathogenic feature of type 2 diabetes (T2D). Various mouse models exist to study T2D; however, few recapitulate the early β-cell defects seen in humans. We sought to develop a nongenetic mouse model of T2D that exhibits reduced first-phase insulin secretion without a significant deficit in pancreatic insulin content. C57BL/6J mice were fed 10% or 60% fat diet for three weeks, followed by three consecutive, once-daily intraperitoneal injections of the β-cell toxin streptozotocin (STZ; 30, 50, or 75 mg/kg) or vehicle. Four weeks after injections, the first-phase insulin response to glucose was reduced in mice when high-fat diet was combined with 30, 50, or 75 mg/kg STZ. This was accompanied by diminished second-phase insulin release and elevated fed glucose levels. Further, body weight gain, pancreatic insulin content, and β-cell area were decreased in high fat-fed mice treated with 50 and 75 mg/kg STZ, but not 30 mg/kg STZ. Low fat-fed mice were relatively resistant to STZ, with the exception of reduced pancreatic insulin content and β-cell area. Together, these data demonstrate that in high fat-fed mice, three once-daily injections of 30 mg/kg STZ produces a model of β-cell failure without insulin deficiency that may be useful in studies investigating the etiology and progression of human T2D.

scholarly journals Aminoguanidine Exerts a β-Cell Function-preserving Effect in High Glucose-cultured β-Cells (INS-1)

2000 ◽  
Vol 1 (2) ◽  
pp. 111-119 ◽  
Author(s):  
Yuji Tajiri ◽  
Valdemar Grill
Keyword(s):  
Insulin Release ◽  
High Glucose ◽  
Cell Function ◽  
Cultured Cells ◽  
Culture Media ◽  
Insulin Content ◽  
Beneficial Effects ◽  
Cell Functions ◽  
Elevated Glucose ◽  
Β Cell Function

We investigated the effects of aminoguanidine (AG) onβ-cell functions in an insulin secreting cell line (INS-1). Culture with 27 mM glucose for one week markedly decreased both insulin release and insulin content compared to culture in 0.8 mM or 3.3 mM glucose. Relative to culture at 27 mM glucose alone, the co-exposure to 1 mM AG almost doubled basal as well as glucose or 25 mM KCl-stimulated insulin release and increased insulin content by 42%. AG failed to affect release and content in cells cultured at 0.8 or 3.3 mM glucose. Preproinsulin mRNA content in 27 mM glucose-cultured cells was 52% suppressed compared to 0.8 mM glucose-cultured cells, and AG treatment partially counteracted this decline. Advanced glycosylation end product (AGE)-associated fluorescence (370 nm excitation and 440 nm emission) of cells′ extracts did not differ between 27 mM and 0.8 mM glucose-cultured cells after 1 week of culture and fluorescence was unaffected by AG. Accumulation of nitrite into culture media was markedly increased from 27 mM glucose-cultured cells, and this accumulation was 33% suppressed by AG. In conclusion, AG partially protects against glucotoxic effects in INS-1 cells. These beneficial effects may involve a decrease in early glycation products and/or nitric oxide synthase (NOS) activity. The effects which were obtained after one week of high glucose exposure may supplement AGE-associated effects seen after chronically elevated glucose.

In vitro Regulation of Insulin Release and Biosynthesis of Fetal Rat Pancreatic Cells Explanted on Pregnancy Day 16

Neonatology ◽  
1997 ◽  
Vol 71 (1) ◽  
pp. 60-68 ◽  
Author(s):  
Kazumi Aoyagi ◽  
Peter Bergsten ◽  
Ulf J. Eriksson ◽  
Ted Ebendal ◽  
Claes Hellerström
Keyword(s):  
Insulin Release ◽  
Pancreatic Cells ◽  
Fetal Rat

Electron Probe Microanalysis of Frozen Hydrated Kidneys, Isolated Cells, and Cultured Cells

1982 ◽  
Vol 40 ◽  
pp. 402-403 ◽  
Author(s):  
Claude Lechene
Keyword(s):  
Liquid Nitrogen ◽  
Electron Probe Microanalysis ◽  
Electron Probe ◽  
Cultured Cells ◽  
Liquid Nitrogen Temperature ◽  
Elemental Content ◽  
Isolated Cells ◽  
Renal Tubular Cells ◽  
Diamond Saw ◽  
Saw Blade

Electron probe microanalysis of frozen hydrated kidneysThe goal of the method is to measure on the same preparation the chemical elemental content of the renal luminal tubular fluid and of the surrounding renal tubular cells. The following method has been developed. Rat kidneys are quenched in solid nitrogen. They are trimmed under liquid nitrogen and mounted in a copper holder using a conductive medium. Under liquid nitrogen, a flat surface is exposed by sawing with a diamond saw blade at constant speed and constant pressure using a custom-built cryosaw. Transfer into the electron probe column (Cameca, MBX) is made using a simple transfer device maintaining the sample under liquid nitrogen in an interlock chamber mounted on the electron probe column. After the liquid nitrogen is evaporated by creating a vacuum, the sample is pushed into the special stage of the instrument. The sample is maintained at close to liquid nitrogen temperature by circulation of liquid nitrogen in the special stage.

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