Antecedent Insulin Level and Pattern of Induction of Acute Hypoglycaemia do Not Affect Subsequent Counterregulatory Responses in Healthy Subjects

1993 ◽  
Vol 85 (5) ◽  
pp. 543-548 ◽  
Author(s):  
K. T. Moriarty ◽  
E. J. Simpson ◽  
R. N. Mullinger ◽  
I. A. MaCdonald ◽  
R. B. Tattersall
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Plasma Insulin ◽  
Insulin Level ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Plasma Adrenaline ◽  
Obese Subjects ◽  
Analogue Scales

1. This study was designed to determine whether the duration and pattern of prior insulin exposure modulate the symptomatic and counterregulatory responses to hypoglycaemia. 2. Ten healthy non-obese subjects (five males/five females age 25 + 1 years, mean + SEM) were made hypoglycaemic in three ways: (i) a hyperinsulinaemic (60 m-units min−1 m−2; plasma insulin concentration 95 m-units/l) clamp, with 1 h of euglycaemia, blood glucose level 4.5 mmol/l, followed by 30 min of hypoglycaemia, at a stable glucose nadir of 2.0 mmol/l (i.e. euglycaemic then hypoglycaemic clamp: E+HC); (ii) an identical hypoglycaemic clamp without preceding hyperinsulinaemic euglycaemia (i.e. a hypoglycaemic clamp: HC); (iii) insulin infusion only, discontinued at a blood glucose level of 3.0 mmol/l (II). Blood glucose level reached the same nadir as on E+HC and HC, and did not fall further. At the glucose nadir, and 15 and 30 min after, the plasma insulin concentration was 23, 7 and 4 m-units/l, respectively, on the II visit. 3. At the glucose nadir, plasma glucagon level, plasma adrenaline level, sweating rate, heart rate, blood pressure, and overall and individual symptom scores (using visual analogue scales) were the same on E+HC, HC and II. 4. There were no significant differences in neurohormonal response between E+HC and HC, but more subjects felt hypoglycaemic on E+HC on arrival at the glucose nadir (P <0.05). There was significantly more blurring of vision (1.3+0.5 versus 0.2+0.1 cm) and tingling (1.2+0.4 versus 0.2+0.1 cm) 30 min after arriving at the glucose nadir on E+HC than HC (P <0.05, analysis of variance). 5. Significant differences were only found between E+HC or HC and the II visit 15 min after arriving at the glucose nadir, when the blood glucose level had risen significantly to 2.9 mmol/l, and 30 min after arrived at the glucose nadir, by which time the blood glucose level had recovered to 3.8 mmol/l. 6. A 1 h run-in period of euglycaemic hyperinsulinaemia does not affect the hormonal or physiological response to an identical degree of hypoglycaemia, but appears to cause increased symptoms of neuroglycopenia during subsequent stable hypoglycaemia. 7. A difference in plasma insulin level within the physiological range does not affect the magnitude of symptomatic, hormonal or physiological responses to the same degree of hypoglycaemia.

Insulin-like effect of vanadyl ion on streptozotocin-induced diabetic rats

1990 ◽  
Vol 126 (3) ◽  
pp. 451-459 ◽  
Author(s):  
H. Sakurai ◽  
K. Tsuchiya ◽  
M. Nukatsuka ◽  
M. Sofue ◽  
J. Kawada
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Plasma Insulin ◽  
Active Form ◽  
Insulin Level ◽  
Plasma Insulin Level ◽  
High Concentration ◽  
Vanadyl Ion ◽  
Vanadyl Sulphate

ABSTRACT Recent studies have indicated that the blood glucose level of rats with streptozotocin (STZ)-induced diabetes (type 1) is normalized without an increase in the plasma insulin level by administration of sodium orthovanadate in the drinking water. The mechanism of this insulin-like effect of vanadate is unknown. In this study, we investigated whether vanadyl ion, which is less toxic than vanadate to rats, also has an insulin-like effect in rats with STZ-induced diabetes. When rats with STZ-induced diabetes were given a daily i.p. injection of vanadyl sulphate (9·3 and 4·6 mg vanadium/kg body weight), their blood glucose level decreased from about 22·2 to about 7·2 mmol glucose/l within 2 days and remained low for at least 12 weeks. This treatment did not affect their low plasma insulin level. Quantitative electron spin resonance (ESR) spectrometry showed that most of the vanadium (about 90%) in their tissues was present as a vanadyl form (VO2+). ESR analysis also showed that the vanadyl ion in tissues was bound endogenously with four oxygen ligands from either water or oxyamino acid residues in proteins. Vanadyl sulphate accelerated glucose incorporation into adipocytes of rats, suggesting that the action of vanadyl ion is peripheral. Interestingly, vanadyl sulphate at a high concentration (about 10 mmol/l) was more effective than insulin in enhancing glucose uptake. This study demonstrated that: (1) vanadyl sulphate (+ 4 oxidation state), like vanadate ion, normalizes the blood glucose levels of rats with STZ-induced diabetes; (2) the action of vanadyl ion is peripheral; and (3) the active form of vanadium for an insulin-like effect may be a vanadyl form, not vanadate. Journal of Endocrinology (1990) 126, 451–459

Anti-diabetic activity of diphenhydramine in diabetic rats

2020 ◽  
Vol 11 (4) ◽  
pp. 5067-5070
Author(s):  
Pang Jyh Chayng ◽  
Nurul Ain ◽  
Kaswandi Md Ambia ◽  
Rahim Md Noah
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Fasting Blood Glucose ◽  
Insulin Level ◽  
Diabetic Rats ◽  
Group Iv ◽  
Diabetic Rat ◽  
Control Group ◽  
Group I

The purpose of this project is to study the anti-diabetic effect of on a diabetic rat model. A total of Twenty male Sprague rats were used and it randomly distributed into four groups which are Group I: , Group II: negative control, Group III: and Group IV: and . In diabetic model were induced with via injection at the dosage of 65mg/kg. and FBG (Fasting Blood Glucose) level of diabetic rats were assessed every three days. Blood was collected via cardiac puncture at day 21 after the induction of treatment. Insulin level of the rats was assessed with the Mercodia Rat Insulin ELISA kit. FBG level of group I (12.16 ±3.96, p&lt;0.05) and group IV (11.34 ±3.67, p&lt;0.05) were significantly decreased. Meanwhile, the for all rats did not show any significant increase. However, the insulin level was escalated in group IV (0.74+0.25, p&lt;0.05) significantly. The present study shows that the and the combination of and lowered blood glucose level and enhanced insulin secretion.

scholarly journals Fetal growth, glucose tolerance and plasma insulin concentration in rats given a marginal-zinc diet in the latter stages of pregnancy

1988 ◽  
Vol 59 (2) ◽  
pp. 315-322 ◽  
Author(s):  
Susan Southon ◽  
Susan J. Fairweather-Tait ◽  
Christine M. Williams
Keyword(s):  
Blood Glucose ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Oral Glucose ◽  
Fetal Blood ◽  
Plasma Insulin Concentration ◽  
Pregnant Rats ◽  
Zn Content ◽  
Tail Blood

1. Wistar rats were fed on a control semi-synthetic diet throughout pregnancy, or a control diet in the first 2 weeks and a marginal-zinc diet in the 3rd week of pregnancy. On day 20, after an overnight fast, half the animals in each group were given glucose by gavage and the 0–30 min rise in blood glucose measured in tail blood. After 60 min blood was taken by cardiac puncture for glucose and insulin assay. Maternal pancreases were removed and the Zn contents measured. Fetuses from each litter were combined for wet/dry weights, protein and DNA determinations.2. Plasma insulin concentration was higher, and glucose concentration and pancreatic Zn content lower, in pregnantv. non-pregnant animals of similar age, fed on the same diet. Pancreatic Zn content was lowest in the marginal-Zn group of pregnant rats. Fetuses from mothers fed on the marginal-Zn diet during the last week of pregnancy were slightly heavier than controls and had a significantly higher protein: DNA ratio. The 0–30 min rise in blood glucose was significantly greater in the marginal-Zn animals.3. In a second experiment, pregnant rats were given similar diets to those used in the first study, but the marginal-Zn diet was given for a shorter period (days 15–19 of pregnancy). On day 19 the rats were meal-fed and on day 20, after an overnight fast, an oral glucose dose was administered. Tail-blood was taken at timed intervals up to 60 min post-dosing for glucose assay. Both maternal and fetal blood glucose and insulin concentration was measured 70 min post-dosing.4. Values for maternal and fetal blood glucose and plasma insulin, measured 70 min after the administration of a glucose dose, were similar in the two groups, but the initial rise in blood glucose concentration was again significantly higher in pregnant rats given the marginal-Zn diet towards term.5. It is suggested that the change in growth and composition, observed in fetuses from rats given a marginal-Zn diet in later pregnancy, is associated with altered maternal carbohydrate metabolism.

scholarly journals The effect of acetoacetate on plasma insulin concentration

1971 ◽  
Vol 125 (2) ◽  
pp. 541-544 ◽  
Author(s):  
R. A. Hawkins ◽  
K. G. M. M. Alberti ◽  
C. R. S. Houghton ◽  
D. H. Williamson ◽  
H. A. Krebs
Keyword(s):  
Fatty Acids ◽  
Blood Glucose ◽  
Free Fatty Acids ◽  
Glucose Concentration ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
Diabetic Rats ◽  
Insulin Concentration ◽  
Plasma Insulin Concentration ◽  
Arterial Blood

1. Sodium acetoacetate was infused into the inferior vena cava of fed rats, 48h-starved rats, and fed streptozotocin-diabetic rats treated with insulin. Arterial blood was obtained from a femoral artery catheter. 2. Acetoacetate infusion caused a fall in blood glucose concentration in fed rats from 6.16 to 5.11mm in 1h, whereas no change occurred in starved or fed–diabetic rats. 3. Plasma free fatty acids decreased within 10min, from 0.82 to 0.64mequiv./l in fed rats, 1.16 to 0.79mequiv./l in starved rats and 0.83 to 0.65mequiv./l in fed–diabetic rats. 4. At 10min the plasma concentration rose from 20 to 49.9μunits/ml in fed unanaesthetized rats and from 6.4 to 18.5μunits/ml in starved rats. There was no change in insulin concentration in the diabetic rats. 5. Nembutal-anaesthetized fed rats had a more marked increase in plasma insulin concentration, from 30 to 101μunits/ml within 10min. 6. A fall in blood glucose concentration in fed rats and a decrease in free fatty acids in both fed and starved rats is to be expected as a consequence of the increase in plasma insulin. 7. The fall in the concentration of free fatty acids in diabetic rats may be due to a direct effect of ketone bodies on adipose tissue. A similar effect on free fatty acids could also be operative in normal fed or starved rats.

scholarly journals Effect of Sago Analog Rice and Red Bean Diet to β Cells Pancreas Refinement in STZ-NA Induced Diabetic Rats

2020 ◽  
pp. 667-673
Author(s):  
Sri Budi Wahjuningsih ◽  
Haslina Haslina ◽  
Agus Tri Putranto ◽  
Mita Nurul Azkia
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Insulin Level ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Pancreatic Β Cell ◽  
Β Cells ◽  
Β Cell ◽  
Red Bean

The study aims to determine the effect of sago analogue rice and red beans in diabetic rats to repair pancreatic β-cells. Thirty-five males Wistar rats were divided into 5 groups: normal group diet (STD), the diabetic group (STDD) with a standard feed diet, the diabetic group with mentik wangi rice (MWRD), the diabetic group with sago analogue rice (SARD) and the diabetic group with sago analogue rice with the addition of 10% red bean flour (SARKBD). All groups were analysed for dietary interventions, blood glucose level, insulin level for HOMA-β and HOMA S indices and measurement of insulin level by using IHC analysis. In addition, short-chain fatty acids (SCFA) analysis was performed in the caecum. This study showed that decreasing blood glucose level shown in SARD and RASKBD groups. The pancreatic β-cell number indicated an increase in the SARD group compares to the STDD group. The pool total of SCFA in SARD group was the highest among of all groups, as well as the acetate, propionate and butyrate pools. These results indicate that the sago analogue rice diet could repair and increase the expression of pancreatic β-cell through absorption inhibition mechanisms and by increasing insulin sensitivity and the SCFA level.

scholarly journals Consecutive Low Doses of Streptozotocin Induce Polycystic Ovary Syndrome Features in Mice

2021 ◽  
Vol 22 (3) ◽  
pp. 1299
Author(s):  
Youngjae Ryu ◽  
Yong Jin Kim ◽  
Yoon Young Kim ◽  
Jungwoo Kim ◽  
Sung Woo Kim ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Polycystic Ovary ◽  
Insulin Level ◽  
Experimental Period ◽  
Reproductive Age ◽  
Total Testosterone ◽  
Low Doses ◽  
Glucose Levels

Polycystic ovarian syndrome (PCOS) is a common reproductive endocrine disorder in reproductive-age women. Due to its various pathophysiological properties and clinical heterophenotypes, the mechanism of PCOS pathogenesis is still unclear. Several animal models have been used to study PCOS and allow the exploration of the specific mechanism underlying PCOS. We focused on streptozotocin (STZ) to develop a non-steroidal and non-diabetic PCOS model. We administered multiple STZ injections to female C57BL/6 mice (3–4 weeks old) at different concentrations: STZ-15 (15 mg/kg), STZ-30 (30 mg/kg), and STZ-60 (60 mg/kg) treatments. During the experimental period, we analyzed body weight, blood glucose levels, and estrous cycle pattern. Furthermore, five weeks after STZ administration, we examined hormone levels and the morphology of ovarian tissues. Mice in the STZ-15 group did not show differences in body weights, blood glucose level, insulin level, and insulin tolerance compared to wild-type and control groups whereas those in the STZ-60 group presented a typical diabetes phenotype. In the case of the STZ-30 group, only increased blood glucose level was observed. Total testosterone levels were significantly elevated in STZ-15 and STZ-30 groups. Luteinizing hormone (LH) and estradiol levels were not significantly changed in the STZ-treated groups. The number of ovarian antral follicles and atretic follicles significantly increased in the ovary of mice in the STZ-15 and STZ-30 groups. All STZ-treated groups manifested irregular estrus cycles. However, the patterns of estrous cycles were different between mice treated with different STZ concentrations. We found that PI3K-AKT and IRS-1 signaling in the ovary was enhanced by low doses of STZ treatment. Taken together, our finding indicates that multiple injections of STZ at low doses induce PCOS features in mice without induction of diabetes features.

GLUCOSE-INDUCED INCREASE OF PLASMA INSULIN IN THE RAT FOETUS IN UTERO

1974 ◽  
Vol 62 (3) ◽  
pp. 545-551 ◽  
Author(s):  
A. KERVRAN ◽  
J. R. GIRARD
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Plasma Insulin ◽  
Blood Glucose Concentration ◽  
In Utero ◽  
Plasma Insulin Concentration ◽  
Pregnant Rats ◽  
Plasma Insulin Levels ◽  
Effect Of Glucose ◽  
Foetal Blood

SUMMARY The effect of glucose on the release of insulin from the pancreas of 18·5 to 21·5-day-old rat foetuses has been studied in utero. Foetal hyperglycaemia was induced by a 1 h glucose infusion into pregnant rats. In foetuses from mother rats infused with saline, the blood glucose and the plasma insulin concentrations increased up to day 21·5 of gestation. The blood glucose level of the foetuses never exceeded that of the mothers which remained stable from day 18·5 to day 21·5 of gestation. The infusion of glucose raised the foetal blood glucose concentration to that of the mothers and induced a significant increase of plasma insulin levels both in the mothers and their foetuses. The enhanced plasma insulin concentration observed in the 18·5-day-old foetuses of glucose-infused pregnant rats became greater each day up to 21·5 days.

BLOOD GLUCOSE LEVEL IN MICE

1967 ◽  
Vol 56 (4) ◽  
pp. 713-725 ◽  
Author(s):  
Ingmar Lundquist ◽  
Claus Rerup
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Glucose Level ◽  
Pancreatic Beta Cells ◽  
Plasma Insulin ◽  
Alloxan Diabetes ◽  
Physiological Significance ◽  
Measurable Effect ◽  
Hypoglycaemic Effect ◽  
Plasma Insulin Levels

ABSTRACT The hypoglycaemic effect of synthetic tetraicosapeptide corticotrophin was investigated in NMRI mice in order to determine its physiological significance as well as its mechanism of action. It was found that in normal non-fasting mice corticotrophin produced a maximal hypoglycaemic response at a dose level of about 5 μg per 20 g mouse (1250 milliunits per 20 g mouse). The ED50 of the hypoglycaemic effect was about 1000 times larger than the ED50 for adrenal cortical stimulation. Immunoassayable insulin was markedly increased 15 minutes following 5 μg of corticotrophin, whereas following a maximal steroidogenic dose (1.6 nanogram) or following ether stress the plasma insulin levels were normal. In adrenalectomized mice the administration of 5 μg of corticotrophin had practically no effect on the blood glucose level, whereas pretreatment with a glucocorticosteroid in adrenalectomized mice markedly restored the hypoglycaemic response. Acutely hypophysectomized mice showed a hypoglycaemic response to corticotrophin indistinguishable from that found in normal mice, whereas animals hypophysectomized 3–7 days before corticotrophin injection showed a smaller response. Corticotrophin in a dose of 5 μg per 20 g mouse had no hypoglycaemic effect in mice with manifest alloxan diabetes. Corticotrophin injected 5 minutes following a diabetogenic dose of alloxan hardly had any measurable effect on the acute initial alloxan hyperglycaemia, whereas the latter was greatly reduced when corticotrophin was given 5 minutes before alloxan administration. Pretreatment with corticotrophin did not change the frequency or intensity of the ensuing diabetic condition in mice. It is concluded that the corticotrophin induced hypoglycaemia is dependent on 1) the presence of normally functioning pancreatic beta-cells; and 2) the presence of glucocorticosteroids. It is doubtful whether the observed hypoglycaemia has any physiological significance.

scholarly journals Correlation of Estrogen with Serum Insulin and Blood Glucose Levels in Post-menopausal Women

2017 ◽  
Vol 46 (1) ◽  
pp. 32-37
Author(s):  
Nahid Yeasmin ◽  
Qazi Shamima Akhter ◽  
Sayeeda Mahmuda ◽  
Mahmudul Hasan ◽  
Rukhshana Rabbani ◽  
...  
Keyword(s):  
Blood Glucose ◽  
Blood Glucose Level ◽  
Postmenopausal Women ◽  
Glucose Level ◽  
Serum Insulin ◽  
Fasting Blood Glucose ◽  
Insulin Level ◽  
Fasting Insulin ◽  
Glucose Levels ◽  
Estrogen Level

Hyperglycemia is a major risk factor for cardiovascular diseases in postmenopausal women. Increased incidence of cardiovascular diseases in postmenopausal women may be due to hyperglycemia caused by lower level of estrogen hormone. This cross sectional study was conducted in the Department of Physiology, Dhaka Medical College, Dhaka, Bangladesh during the period of January to December 2011 to observe the correlation of estrogen with fasting serum insulin (FSI) and fasting blood glucose (FBG) levels in postmenopausal women. A total of 90 women were selected from different areas of Dhaka city, among them, 60 postmenopausal women of age group 50 to 60 years were taken as study group and 30 apparently healthy premenopausal women of age group 20 to 30 years were included as comparison group. The study parameters fasting blood glucose level was estimated by enzymatic method in both groups. Serum insulin level was estimated by Enzyme Linked Immunosorbent Assay (ELISA) and serum estrogen level by RIA method in order to assess the hormonal level of both groups. Data was analyzed by Unpaired Student’s‘t’ test and Pearson's correlation co-effcient (r) test as applicable. Mean serum fasting insulin level and mean blood glucose level was higher in postmenopausal women than premenopausal and result was statistically significant. In postmenopausal women serum estrogen level was lower than premenopausal and serum estrogen level showed negative correlation with serum fasting insulin level. Blood glucose level also showed negative correlation with serum estrogen level. All these correlation were statistically non-significant. It may be concluded that the serum fasting insulin and blood glucose levels are significantly higher in postmenopausal women that may be due to low level of estrogen.Bangladesh Med J. 2017 Jan; 46 (1): 32-37

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