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 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.

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.

scholarly journals Modifications of gastric inhibitory polypeptide (GIP) secretion in man by a high-fat diet

1988 ◽  
Vol 59 (3) ◽  
pp. 373-380 ◽  
Author(s):  
L. M. Morgan ◽  
S. M. Hampton ◽  
J. A. Tredger ◽  
R. Cramb ◽  
V. Marks
Keyword(s):  
Glucose Tolerance ◽  
Energy Intake ◽  
Plasma Glucose ◽  
High Fat Diet ◽  
Gastric Inhibitory Polypeptide ◽  
Oral Glucose ◽  
Fat Intake ◽  
High Fat ◽  
C Peptide ◽  
Glucose Levels

1. Five healthy volunteers (usual fat intake 103) (SE 9) g/d and energy intake 9855 (SE 937) kJ/d were given on two separate occasions (a) 100 g oral glucose and (b) sufficient intravenous (IV) glucose to obtain similar arterialized plasma glucose levels to those after oral glucose.2. Subjects increased their fat intake by 68 (SE 9·6) % for 28 d by supplementing their diet with 146 ml double cream/d (fat intake on high-fat diet (HFD) 170 (SE 8) g/d; energy intake 12347 (SE 770)).3. The 100 g oral glucose load was repeated and IV glucose again given in quantities sufficient to obtain similar arterialized blood glucose levels. Immunoreactive plasma insulin, C-peptide and gastric inhibitory polypeptide (GIP) were measured.4. Plasma GIP levels were higher following oral glucose after the HFD (area under plasma GIP curve 0–180 min 1660 (SE 592) v. 2642 (SE 750) ng/l.h for control and HFD respectively; P < 0·05). Both insulin and C-peptide levels were significantly higher after oral than after IV glucose (P < 0·01) but neither were affected by the HFD. Glucose levels were lower following the HFD after both oral and IV glucose (area under plasma glucose curve 0–180 min, following oral glucose 6·7 (SE 0·3) mmol/l.h for control and 4·2 (SE 0·6) mmol/l.h for HFD; P < 0·01).5. Glucose-stimulated GIP secretion was thus enhanced by the HFD. Insulin secretion in response to oral glucose was unchanged, in spite of an improvement in glucose tolerance.6. The improvement in glucose tolerance post-HFD could possibly be due to a GIP-mediated inhibition of hepatic glycogenolysis, or a decreased rate of glucose uptake from the small intestine.

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.

1666-P: Metabolic Characteristic of Elevated One-Hour Plasma Glucose Levels during a 75g Oral Glucose Tolerance Test in the Nonobese Japanese Men

Diabetes ◽  
2019 ◽  
Vol 68 (Supplement 1) ◽  
pp. 1666-P
Author(s):  
MOTONORI SATO ◽  
YOSHIFUMI TAMURA ◽  
HIDEYOSHI KAGA ◽  
YUKI SOMEYA ◽  
SAORI KAKEHI ◽  
...  
Keyword(s):  
Glucose Tolerance ◽  
Oral Glucose Tolerance Test ◽  
Plasma Glucose ◽  
Glucose Tolerance Test ◽  
Tolerance Test ◽  
Oral Glucose ◽  
Oral Glucose Tolerance ◽  
Japanese Men ◽  
Glucose Levels

THE RESPONSE OF INFANTS OF DIABETIC WOMEN TO TOLBUTAMIDE AND LEUCINE AT BIRTH, AND TO GLUCOSE AND TOLBUTAMIDE AT 2 YEARS OF AGE

PEDIATRICS ◽  
1969 ◽  
Vol 43 (4) ◽  
pp. 546-557
Author(s):  
Mutya S. A. Velasco ◽  
Elsa P. Paulsen
Keyword(s):  
Glucose Tolerance ◽  
Plasma Glucose ◽  
Newborn Infants ◽  
Normal Glucose Tolerance ◽  
Diabetic Woman ◽  
Oral Glucose ◽  
Insulin Levels ◽  
Glucose Levels ◽  
Normal Glucose ◽  
Diabetic Mothers

Twelve newborn infants, 2 to 8 days old, of gestational (IGDM) and insulin-requiring (IDM) diabetic mothers responded to intravenous tolbutamide (20 mg/kg) with abnormally large decreases in plasma glucose and marked rises in plasma insulin (the latter was measured only in IGDM). Only 3 of 13 IGDM tested with leucine had significant decreases in plasma glucose. Newborn infants of normal mothers showed no changes in glucose or insulin in response to intravenous tolbutamide, and one of five had a small decrease in glucose levels after leucine. The results suggest the presence of large stores of pancreatic insulin in newborn infants of diabetic mothers which are more readily released by stimulation with tolbutamide than with leucine. The offspring of the diabetic women were restudied at 2 years of age for their response to intravenous tolbutamide and oral glucose. Seven of nine children had normal glucose and insulin levels after intravenous tolbutamide, and two had abnormally low glucose levels with high insulin levels. Three of the nine had normal glucose tolerance with normal insulin levels. The other six had abnormally elevated glucose levels which varied in duration from one-half to 2 hours. Four of the six had an accompanying hyperinsulinemia; two, who had diabetic glucose tolerance, had poor insulin responses. The findings in the 2-year-old children support a concept that the fetal environment provided by a diabetic woman has effects on carbohydrate tolerance which extend beyond the newborn period.

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