Insulin and glucagon in rats with Islet cell tumors Induced by small doses of streptozofoclii

1981 ◽  
Vol 59 (8) ◽  
pp. 818-823 ◽  
Author(s):  
Gen Yoshino ◽  
Tsutomu Kazumi ◽  
Soichiro Morita ◽  
Shighaki Baba
Keyword(s):  
Plasma Glucose ◽  
Islet Cell ◽  
Insulin Response ◽  
Oral Glucose ◽  
Islet Cell Tumors ◽  
Glucose Levels ◽  
Tumor Bearing ◽  
Small Doses ◽  
Wet Weight ◽  
Glucose Plasma

Plasma insulin and glucagon responses to oral glucose loading were examined in rats with islet cell tumors induced by a single intravenous injection of streptozotocin (30 or 40 mg/kg body weight). Twenty-four macroscopic and six microscopic tumors occurred in 21 rats. In 15 of 21 tumor-bearing rats, there was exaggerated insulin release in response to oral glucose. Plasma glucose levels did not rise with the oral glucose load and were comparable to those seen in normal animals. Hence these rats are described as having "responsive tumors." In six rats with "nonresponsive tumors" there was no insulin response and the plasma glucose levels rose. No significant differences in plasma glucagon levels were observed between the two groups. Nonresponsive tumors as well as responsive tumors contained a significant amount of extractable insulin (17.68 ± 8.60 and 35.07 ± 10.05 mg/g wet weight, respectively) and detectable amounts of immunoreactive glucagon (1.47 ± 0.61 and 2.24 ± 0.67 μg/g wet weight, respectively).These results suggest that a small dose of streptozotocin produces two types of islet cell tumors. One is insulin producing and insulin secreting whereas the other is insulin producing but not insulin secreting.

Insulin modulates glucose-dependent insulinotropic polypeptide (GIP) secretion from enteroendocrine K cells in rats

2011 ◽  
Vol 392 (10) ◽  
pp. 909-918 ◽  
Author(s):  
Nigel Irwin ◽  
Jacqueline M.E. Francis ◽  
Peter R. Flatt
Keyword(s):  
Plasma Glucose ◽  
Oral Glucose ◽  
Glucose Lowering ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Elevated Glucose ◽  
Plasma Insulin Levels ◽  
Glucose Plasma ◽  
And Control ◽  
Intestinal Weight

Abstract Effects of insulin excess and deficiency on glucose-dependent insulinotropic polypeptide (GIP) was examined in rats following insulinoma transplantation or streptozotocin (STZ) administration. Over 14 days, food intake was increased (p<0.001) in both groups of rats, with decreased body weight (p<0.01) in STZ rats. Non-fasting plasma glucose levels were decreased (p<0.01) and plasma insulin levels increased (p<0.001) in insulinoma-bearing rats, whereas STZ treatment elevated glucose (p<0.001) and decreased insulin (p<0.01). Circulating GIP concentrations were elevated (p<0.01) in both animal models. At 14 days, oral glucose resulted in a decreased glycaemic excursion (p<0.05) with concomitant elevations in insulin release (p<0.001) in insulinoma-bearing rats, whereas STZ-treated rats displayed similar glucose-lowering effects but reduced insulin levels (p<0.01). GIP concentrations were augmented in STZ rats (p<0.05) following oral glucose. Plasma glucose and insulin concentrations were not affected by oral fat, but fat-induced GIP secretion was particularly (p<0.05) increased in insulinoma-bearing rats. Exogenous GIP enhanced (p<0.05) glucose-lowering in all groups of rats accompanied by insulin releasing (p<0.001) effects in insulinoma-bearing and control rats. Both rat models exhibited increased (p<0.001) intestinal weight but decreased intestinal GIP concentrations. These data suggest that circulating insulin has direct and indirect effects on the synthesis and secretion of GIP.

scholarly journals Plasma Glucose Levels of Asthma Patients Using Inhaled Fluticasone

2020 ◽  
Author(s):  
Md. Atikur Rahman ◽  
Md. Nazmul Hasan ◽  
Md. Abdur Rahim ◽  
Shamim Ahmed ◽  
Salina Parvin Munni ◽  
...  
Keyword(s):  
Plasma Glucose ◽  
Study Groups ◽  
Cross Sectional Study ◽  
Oral Glucose ◽  
Cross Sectional ◽  
Glucose Levels ◽  
Long Duration ◽  
Asthma Patients ◽  
Comparative Group ◽  
Glucose Plasma

Abstract Objective: Inhaled fluticasone is used in asthma for a long duration. However, It’s an adverse effect on glycaemia is debatable. This study explored the effect of inhaled fluticasone in long term asthma patients. A comparative cross-sectional study was conducted among the adult normoglycaemic asthma patients in Bangladesh between June 2017 to May 2018. The study groups were getting inhaled fluticasone for a minimum of three months whereas comparative group were not on any steroids. Each group had 35 eligible participants. Results: In study group, mean plasma glucose at fasting was 5.27 ± 0.48 mmol/L, 2-hour after 75gm oral glucose was 6.04 ± 1.21 mmol/L and mean of HbA1c was 5.57 ± 0.41 % whereas in comparative group these were 5.17 ± 0.59 mmol/L, 5.69 ± 1.09 mmol/L, 5.47 ± 0.40 % respectively (p= 0.25, 0.20, 0.75 respectively). Duration of inhaled fluticasone use had no specific co-relation with fasting plasma glucose, plasma glucose 2-hour after 75gm oral glucose and HbA1c% (r= 0.016, p= 0.46; r= 0.015, p= 0.47; r= 0.019, p= 0.42 respectively).

scholarly journals Prevention of Postprandial Hyperglycemia by Ophthalmic Nanoparticles Based on Protamine Zinc Insulin in the Rabbit

Pharmaceutics ◽  
2021 ◽  
Vol 13 (3) ◽  
pp. 375
Author(s):  
Saori Deguchi ◽  
Fumihiko Ogata ◽  
Takumi Isaka ◽  
Hiroko Otake ◽  
Yosuke Nakazawa ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Plasma Glucose ◽  
Polyacrylic Acid ◽  
Rabbit Model ◽  
Postprandial Hyperglycemia ◽  
Postprandial Blood Glucose ◽  
Oral Glucose ◽  
Glucose Levels ◽  
Protamine Zinc Insulin ◽  
Bead Mill

Postprandial hyperglycemia, a so-called blood glucose spike, is associated with enhanced risks of diabetes mellitus (DM) and its complications. In this study, we attempted to design nanoparticles (NPs) of protamine zinc insulin (PZI) by the bead mill method, and prepare ophthalmic formulations based on the PZI-NPs with (nPZI/P) or without polyacrylic acid (nPZI). In addition, we investigated whether the instillation of the newly developed nPZI and nPZI/P can prevent postprandial hyperglycemia in a rabbit model involving the oral glucose tolerance test (OGTT). The particle size of PZI was decreased by the bead mill to a range for both nPZI and nPZI/P of 80–550 nm with no observable aggregation for 6 d. Neither nPZI nor nPZI/P caused any noticeable corneal toxicity. The plasma INS levels in rabbits instilled with nPZI were significantly higher than in rabbits instilled with INS suspensions (commercially available formulations, CA-INS), and the plasma INS levels were further enhanced with the amount of polyacrylic acid in the nPZI/P. In addition, the rapid rise in plasma glucose levels in OGTT-treated rabbits was prevented by a single instillation of nPZI/P, which was significantly more effective at attenuating postprandial hyperglycemia (blood glucose spike) in comparison with nPZI. In conclusion, we designed nPZI/P, and show that a single instillation before OGTT attenuates the rapid enhancement of plasma glucose levels. These findings suggest a better management strategy for the postprandial blood glucose spike, which is an important target of DM therapy.

scholarly journals Oral Glucose Augments the Counterregulatory Hormone Response during Insulin-Induced Hypoglycemia in Humans1

2001 ◽  
Vol 86 (2) ◽  
pp. 645-648
Author(s):  
Rubina A. Heptulla ◽  
William V. Tamborlane ◽  
Tony Y.-Z. Ma ◽  
Fran Rife ◽  
Robert S. Sherwin.
Keyword(s):  
Plasma Glucose ◽  
Animal Studies ◽  
Healthy Adult ◽  
Systemic Circulation ◽  
Glucose Sensors ◽  
Oral Glucose ◽  
Adult Males ◽  
Hormone Response ◽  
Glucose Levels ◽  
Acute Hypoglycemia

It has been suggested that the counterregulatory hormone (CRH) response to acute hypoglycemia is triggered via glucose sensors situated in either the hypothalamus or the portohepatic area. If the latter were critical during hypoglycemia, one would anticipate that ingestion of glucose, by raising glucose levels in the portal circulation, should attenuate CRH responses previously described in animal studies. To evaluate the effect of raising portal, but not peripheral, glucose levels during insulin-induced hypoglycemia, we performed hypoglycemic clamp studies in five healthy adult males on two occasions. On one occasion, subjects received oral glucose (OG) (25 g) during hypoglycemia; and on one occasion, noncarbohydrate-containing drink of equal volume, while maintaining plasma glucose at 55 ± 2 mg/dL (3.08 mmol/L). As a result, there were no significant differences in systemic plasma glucose levels between the two hypoglycemic clamp studies, and basal CRH concentrations were also similar. As expected, there was a brisk rise in all CRH during the control (hypoglycemia+noncarbohydrate drink) study. In the experimental study, administration of OG (hypoglycemia+OG), to raise intraportal glucose levels during systemic hypoglycemia, did not attenuate CRH responses. Indeed, OG enhanced the rise in epinephrine, glucagon, and GH. Increases in cortisol and norepinephrine did not differ between the two studies. Therefore, our data suggest that increasing the level of glucose in the portal vein above that in the systemic circulation, during hypoglycemia, enhances (rather than suppresses) CRH responses. Thus, ingestion of glucose may reverse hypoglycemia directly by provision of substrate, as well as indirectly by stimulating counteregulatory mechanisms.

scholarly journals Acute plasma glucose increase, but not early insulin response, regulates plasma ghrelin

2003 ◽  
pp. 403-406 ◽  
Author(s):  
L Briatore ◽  
G Andraghetti ◽  
R Cordera
Keyword(s):  
Plasma Glucose ◽  
Healthy Subjects ◽  
Insulin Response ◽  
Glucose Levels ◽  
Healthy Control ◽  
Early Insulin Response ◽  
Effect Of Glucose ◽  
Type 2 Diabetic

OBJECTIVE: The independent role of glucose and insulin in ghrelin regulation is still controversial; this is also because in healthy subjects it is difficult to isolate the increase of glucose from that of insulin. The aim of this study was to discriminate the effect of glucose increase alone and early insulin response on plasma ghrelin, comparing ghrelin variation after i.v. glucose between healthy subjects and type 2 diabetic (T2DM) subjects, in whom the early insulin response to i.v. glucose is abolished. METHODS: Plasma glucose, insulin and ghrelin levels were measured 0, 3, 5, 10, 30, 45 and 60 min after a 5 g glucose i.v. bolus in seven healthy control subjects and eight T2DM subjects. RESULTS: There were no significant differences in body mass index, basal insulin and basal ghrelin between T2DM and healthy subjects. Basal glucose levels were higher in T2DM subjects than in controls. After i.v. glucose administration, plasma glucose increased significantly in both groups and the glucose peak was higher in T2DM subjects than in controls (9.67+/-1.25 (s.d.) vs 6.88+/-1.00 mmol/l, P<0.01). Insulin increased rapidly in controls, while in T2DM subjects, plasma insulin did not rise in the first 10 min. After the glucose bolus, plasma ghrelin showed a significant reduction both in controls and in T2DM subjects after 5 min. CONCLUSION: These findings indicate that a low-dose i.v. glucose bolus reduces ghrelin both in controls and in T2DM subjects and therefore that early insulin response does not affect plasma ghrelin.

Hypothalamic obesity in female rats in absence of vagally mediated hyperinsulinemia

1980 ◽  
Vol 239 (6) ◽  
pp. E437-E441 ◽  
Author(s):  
B. M. King ◽  
G. R. Phelps ◽  
L. A. Frohman
Keyword(s):  
Fasting Glucose ◽  
Insulin Response ◽  
Female Rats ◽  
Oral Glucose ◽  
Fasting Insulin ◽  
Hypothalamic Obesity ◽  
Glucose Levels ◽  
Rapid Absorption ◽  
Intact Rats

In order to assess the role of vagally mediated hyperinsulinemia in hypothalamic obesity, plasma insulin and glucose levels were assayed in vagotomized and sham-vagotomized female rats after a 6-h fast and after a measured glucose meal both before and 10–14 days after ventromedial hypothalamic (VMH) lesions. Both groups displayed similar gains in body weight in the first 10 days after VMH lesions, but only the sham-vagotomized VMH-lesioned animals displayed elevated fasting insulin levels. Fasting glucose levels did not differ either before or after the lesion. The insulin response to oral glucose was increased in VMH rats, both in vagotomized and sham-vagotomized animals, and it is concluded that the hyperresponsiveness to oral glucose is independent of vagal mediation. Vagotomy markedly exaggerated the glucose and insulin response to oral glucose loading in both intact rats and rats with VMH lesions, probably as a result of more rapid absorption of glucose from the intestine. It is concluded that the fasting hyperinsulinemia that is characteristic of VMH animals is under vagal control and that its elimination does not prevent the development of obesity.

Glucose intolerance in thyrotoxicosis roles of insulin, glucagon and somatostatin

1987 ◽  
Vol 114 (2) ◽  
pp. 228-234 ◽  
Author(s):  
Karen S. L. Lam ◽  
Rose T. T. Yeung ◽  
Patricia W. M. Ho ◽  
S. K. Lam
Keyword(s):  
B Cell ◽  
Glucose Intolerance ◽  
Plasma Glucose ◽  
Insulin Response ◽  
Oral Glucose ◽  
Insulinogenic Index ◽  
C Peptide ◽  
Pancreatic B Cell ◽  
Significant Difference ◽  
Glucose Ingestion

Abstract. The responses in plasma glucose, insulin, C-peptide, glucagon and somatostatin to an oral glucose load were studied in 10 thyrotoxic patients and 10 matched euthyroid controls. The thyrotoxic patients had higher mean fasting plasma glucose (P < 0.05) and responded to oral glucose with an earlier peak at 30 min which was higher than the corresponding glucose level in the controls (P < 0.05). Impaired glucose tolerance was found in 3 patients. Fasting insulin and C-peptide levels were normal in the thyrotoxic patients when corrected for the higher glucose levels. Following glucose ingestion, there was no significant difference between the areas under the insulin or C-peptide curves in patients and controls, but Seltzer's insulinogenic index was reduced in the patients (P < 0.01) suggesting an impaired pancreatic B-cell response to oral glucose. Mean basal glucagon was normal in the thyrotoxic patients. However, while in the controls plasma glucagon became suppressed following glucose ingestion (P < 0.0001), no significant suppression was found in the patients. In the thyrotoxic patients, mean basal somatostatin was normal, but the area under the somatostatin curve following glucose ingestion was significantly increased (P < 0.02). Our findings suggest that décreased glucagon suppression and impaired insulin response after glucose ingestion are involved in glucose intolerance in thyrotoxicosis. Enhanced somatostatin responses to oral glucose in thyrotoxicosis may have contributed to the observed impairment in pancreatic B-cell responsiveness.

Sign in / Sign up

Export Citation Format

Share Document