Relationship between insulin secretion, insulin content and dry weight of single rat pancreatic islets

1980 ◽  
Vol 94 (3) ◽  
pp. 365-370
Author(s):  
G. H. J. Wolters ◽  
W. Konijnendijk
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Outer Surface ◽  
Basal Insulin ◽  
Dry Weight ◽  
Insulin Content ◽  
Curvilinear Relationship ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

Abstract. Single islets were incubated at glucose 5 mm for 60 min and subsequently at glucose 15 mm for 30 min. The insulin content of the incubated islets was proportional to the dry weight of the islets. The insulin secretion (Y) demonstrated a curvilinear relationship with the dry weight (X) of the islets, which could be described by the function Y = aX⅔ (a being a constant). On basis of this function it can be calculated that the insulin secretion of a particular islet is proportional to its outer surface. The consequence of this is that small sized islets secrete relatively much more insulin than large islets. Islets isolated with either purified or crude collagenase gave the same results except that a higher basal insulin secretion was observed with crude collagenase.

scholarly journals Pancreatic Thyrotropin Releasing Hormone and Mechanism of Insulin Secretion

2018 ◽  
Vol 50 (1) ◽  
pp. 378-384 ◽  
Author(s):  
Vladimír  Štrbák
Keyword(s):  
Insulin Resistance ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Basal Insulin ◽  
Thyrotropin Releasing Hormone ◽  
Insulin Content ◽  
Β Cells ◽  
Releasing Hormone ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

Thyrotropin releasing hormone (TRH; pGlu-His-ProNH2) is expressed also in pancreatic β cells where it is colocalized in secretory granules with insulin. High perinatal changes of the TRH gene expression and TRH concentrations in rat pancreatic islets coincide with the perinatal maturation of the adequate insulin secretory responsiveness to glucose and other nutrient secretagogues. TRH secretion from pancreatic islets is stimulated by glucose and inhibited by insulin. Disruption of the TRH gene in knockout mice results in hyperglycemia accompanied by impaired insulin secretory response to glucose. Progress in understanding TRH - insulin relations may be substantial for improving knowledge of pathophysiological mechanisms included in changes of insulin secretion with possible clinical impact. Block of the last step of biosynthesis of α-amidated peptides, including TRH by disulfiram (DS) treatment of adult male rats subcutaneously with 200 mg/kg for five days in our experiments resulted in barely detectable levels of peptidyl-glycine α-amidating monooxygenase (PAM) in their pancreatic islets. TRH in physiological concentration (1 nM) does not affect basal insulin secretion from intact rat pancreatic islets. In contrast, basal insulin secretion from islets of DS-treated rats is four times higher compared to controls and could not be further stimulated by high-glucose. The addition of 1 nM TRH into medium decreased immediately basal insulin secretion in DS (TRH lacking) islets to control level and normalized also their response to glucose. Interestingly, absence of the secretory response to glucose in islets from TRH depleted rats was connected with their increase of insulin content during stimulation. Glucose stimulation together with 1 nM TRH normalized also insulin content in DS islets. Apparently, high insulin content in islets from TRH depleted animals is a result of block of regulatory secretion pathway redirected to constitutional secretion which was corrected by the addition of TRH. Type 2 diabetes mellitus is a disease characterized by various range from predominant insulin resistance with relative insulin deficiency to a predominant secretory defect with insulin resistance. These symptoms suggest a possible role of TRH dysregulation. In conclusion, presence of TRH in β cells ensures appropriate low basal (constitutive) insulin secretion. Release of TRH induced by glucose and possibly by other secretagogues has autocrine effect resulting in directing insulin secretion to regulatory pathway reacting to stimulation. If some defects of insulin secretion could be treated by TRH, various ways of applications (also oral and nasal) could be utilized. Moreover, positive side effects shown in animal experiments may accompany the treatment: TRH has the potential to prevent apoptosis and promotes insulin-producing cell proliferation and has also aging-reversing properties.

Leptin suppresses basal insulin secretion from rat pancreatic islets

1997 ◽  
Vol 70 (2-3) ◽  
pp. 179-182 ◽  
Author(s):  
Kaori Ishida ◽  
Takashi Murakami ◽  
Akira Mizuno ◽  
Mitsuru Iida ◽  
Masamichi Kuwajima ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Basal Insulin ◽  
Rat Pancreatic Islets ◽  
Basal Insulin Secretion

scholarly journals Insulin Secretion Is Increased in Pancreatic Islets of Neuropeptide Y-Deficient Mice

Endocrinology ◽  
2007 ◽  
Vol 148 (12) ◽  
pp. 5716-5723 ◽  
Author(s):  
Yumi Imai ◽  
Hiral R. Patel ◽  
Evan J. Hawkins ◽  
Nicolai M. Doliba ◽  
Franz M. Matschinsky ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Neuropeptide Y ◽  
Pancreatic Islets ◽  
High Fat Diet ◽  
Basal Insulin ◽  
High Fat ◽  
Y1 Receptor ◽  
Basal Insulin Secretion ◽  
Glucose Stimulated Insulin Secretion ◽  
Deficient Mice

Neuropeptide Y (NPY), whose role in appetite regulation is well known, is also expressed in pancreatic islets. Although previous studies indicated that application of NPY to pancreatic islets inhibits insulin secretion, its physiological role in the regulation of insulin secretion is not fully understood. We hypothesized that NPY in islets tonically suppresses insulin secretion and the reduction of islet NPY increases insulin secretion. To address the hypothesis, islet function of NPY-deficient mice was analyzed. Although there was little change in glucose homeostasis in vivo, pancreatic islets from NPY-deficient mice had higher basal insulin secretion (1.5 times), glucose-stimulated insulin secretion (1.5 times), and islet mass (1.7 times), compared with wild-type mouse. Next we sought to determine whether the expression of NPY and Y1 receptor in islets was altered in hyperinsulinemia associated with obesity. Islets from C57BL/6J mice on a high-fat diet had 1.9 times higher basal insulin secretion and 2.4 times higher glucose-stimulated insulin secretion than control mice, indicating islet adaptation to obesity. Expression of NPY and Y1 receptor mRNA levels was decreased by 70 and 64%, respectively, in high-fat diet islets, compared with controls. NPY and Y1 receptor in islets were also reduced by 91 and 80%, respectively, in leptin-deficient ob/ob mice that showed marked hyperinsulinemia. Together these results suggest that endogenous NPY tonically inhibits insulin secretion from islets and a reduction of islet NPY may serve as one of the mechanisms to increase insulin secretion when islets compensate for insulin resistance associated with obesity.

scholarly journals Decreased basal insulin secretion from pancreatic islets of pups in a rat model of maternal obesity

2016 ◽  
Vol 231 (1) ◽  
pp. 49-57 ◽  
Author(s):  
Elena Zambrano ◽  
Tonantzin Sosa-Larios ◽  
Lizbeth Calzada ◽  
Carlos A Ibáñez ◽  
Carmen A Mendoza-Rodríguez ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Basal Insulin ◽  
Pancreatic Beta Cells ◽  
Maternal Obesity ◽  
Metabolic Diseases ◽  
Model Assessment ◽  
Male And Female ◽  
Basal Insulin Secretion

Maternal obesity (MO) is a deleterious condition that enhances susceptibility of adult offspring to metabolic diseases such as type 2 diabetes. The objective is to study the effect of MO on in vitro insulin secretion and pancreatic cellular population in offspring. We hypothesize that a harmful antenatal metabolic environment due to MO diminishes the basal glucose-responsive secretory function of pancreatic beta cells in offspring. Mothers were fed a control (C) or high-fat diet from weaning through pregnancy (120 days) and lactation. At postnatal days (PNDs) 36 and 110, pups were killed, peripheral blood was collected and pancreatic islets were isolated. Basal insulin secretion was measured in vitro in islets for 60 min. It was found that blood insulin, glucose and homeostasis model assessment (HOMA) index were unaffected by maternal diet and age in females. However, male MO offspring at PND 110 showed hyperinsulinemia and insulin resistance compared with C. Body weight was not modified by MO, but fat content was higher in MO pups compared with C pups. Triglycerides and leptin concentrations were higher in MO than in C offspring in all groups except in females at PND 36. Pancreatic islet cytoarchitecture was unaffected by MO. At PND 36, islets of male and female C and MO offspring responded similarly to glucose, but at PND 110, male and female MO offspring islets showed a 50% decrease in insulin secretion. It was concluded that MO impairs basal insulin secretion of offspring with a greater impact on males than females, and this effect mainly manifests in adulthood.

cAMP enhances insulin secretion by an action on the ATP-sensitive K+ channel-independent pathway of glucose signaling in rat pancreatic islets

Diabetes ◽  
1999 ◽  
Vol 48 (5) ◽  
pp. 1006-1012 ◽  
Author(s):  
H. Yajima ◽  
M. Komatsu ◽  
T. Schermerhorn ◽  
T. Aizawa ◽  
T. Kaneko ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
K Channel ◽  
Glucose Signaling ◽  
Rat Pancreatic Islets

Human and rat amylin have no effects on insulin secretion in isolated rat pancreatic islets

1991 ◽  
Vol 177 (3) ◽  
pp. 932-938 ◽  
Author(s):  
Carol L. Broderick ◽  
Gerald S. Brooke ◽  
Richard D. DiMarchi ◽  
Gerald Gold
Keyword(s):  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Rat Pancreatic Islets ◽  
Isolated Rat

Abstract 63: ACE2 Deficiency Reduces Insulin Content of Isolated Pancreatic Islets and Plasma Insulin Concentrations Post-Glucose Challenge in Obese C57BL/6 Mice

Hypertension ◽  
2013 ◽  
Vol 62 (suppl_1) ◽  
Author(s):  
Robin C Shoemaker ◽  
Lisa A Cassis
Keyword(s):  
Gene Expression ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Plasma Insulin ◽  
Insulin Content ◽  
Isolated Pancreatic Islets ◽  
Diet Induced Obesity ◽  
Glucose Challenge ◽  
Ace2 Gene ◽  
Deficient Mice

Objective: Diet-induced obesity promotes type 2 diabetes (T2D). Drugs that inhibit the renin-angiotensin system (RAS) have been demonstrated in clinical trials to decrease the onset of T2D. Angiotensin converting enzyme 2 (ACE2) negatively regulates the RAS by catabolizing angiotensin II (AngII). Preliminary data indicate that ACE2 deficient mice display impairments in glucose homeostasis at 8 weeks of age. We tested the hypothesis that ACE2 deficiency promotes the development of glucose intolerance and β-cell dysfunction in mice with diet-induced obesity. Methods and Results: Male Ace2 +/y or -/y mice were fed a low fat (LF, 10% kcal as fat) or high fat (HF, 60% kcal as fat) diet for 5 or 17 weeks. After 5 weeks, plasma insulin concentrations (0, 30 min) following a glucose challenge were significantly greater in HF versus ( vs) LF-fed mice. However, glucose-stimulated increases in plasma insulin concentrations were decreased in HF-fed ACE2 deficient mice compared to controls (2.96 ± 0.18 vs 4.44 ± 0.40 ng/ul, respectively; P<0.01). Surprisingly, isolated pancreatic islets from HF-fed mice of either genotype released similar concentrations of insulin in response to glucose. However, mRNA abundance of insulin was significantly reduced in islets from HF-fed Ace2 -/y compared to +/y mice (1.76 ± 0.17 vs 2.54 ± 0.18 insulin/18S ratio; P<0.05). After 17 weeks, the plasma insulin response to glucose was further reduced in the HF-fed ACE2 deficient mice compared to controls (8.07 ± 0.98 vs 13.90 ± 1.10 ng/ul; P<0.01). Further, LF-fed ACE2 deficient mice also displayed reductions in plasma glucose-stimulated insulin concentrations (1.92 ± 0.98 vs 3.09 ± 0.98 ng/ul; P<0.01). Islets from HF-fed wild type mice displayed reduced ACE2 gene expression compared to LF (0.069 ± 0.009 vs 0.169 ± 0.01, ACE2/18S ratio; P<0.001) and AngII totally suppressed islet glucose-stimulated insulin secretion compared to vehicle (-0.16 ± 0.18 vs 0.9 ± 0.26, fold change over basal; P<0.05). Conclusions: These results demonstrate that ACE2 deficiency promotes the development of T2D by regulating islet insulin content. Moreover, diet-induced obesity reduces islet ACE2 gene expression with augmented AngII-induced impairment of insulin secretion.

scholarly journals Reactive Oxygen Species Stimulate Insulin Secretion in Rat Pancreatic Islets: Studies Using Mono-Oleoyl-Glycerol

PLoS ONE ◽  
2012 ◽  
Vol 7 (1) ◽  
pp. e30200 ◽  
Author(s):  
Marylana Saadeh ◽  
Thomas C. Ferrante ◽  
Ada Kane ◽  
Orian Shirihai ◽  
Barbara E. Corkey ◽  
...  
Keyword(s):  
Reactive Oxygen Species ◽  
Insulin Secretion ◽  
Pancreatic Islets ◽  
Reactive Oxygen ◽  
Oxygen Species ◽  
Stimulate Insulin Secretion ◽  
Rat Pancreatic Islets
Sign in / Sign up

Export Citation Format

Share Document