SPONTANEOUS HYPOGLYCAEMIA AND SARCOMA

1965 ◽  
Vol 50 (2) ◽  
pp. 233-238 ◽  
Author(s):  
J. A. R. Friend ◽  
C. N. Hales
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Slow Growing ◽  
Insulin Like Activity

ABSTRACT A patient with a slow-growing fibrosarcoma of ovarian origin developed attacks of hypoglycaemia. Estimations of plasma insulin-like activity and immunoassay of plasma insulin under a variety of conditions showed no evidence of abnormal insulin secretion. In addition, the responses to glucagon, tolbutamide, and L-leucine showed no definite abnormality. Possible mechanisms for the occurrence of the hypoglycaemia are discussed.

Insulin secretion and substrate homeostasis in prolonged hypothermia in rats

1988 ◽  
Vol 255 (6) ◽  
pp. R1035-R1040
Author(s):  
R. Hoo-Paris ◽  
M. L. Jourdan ◽  
L. C. Wang ◽  
R. Rajotte
Keyword(s):  
Insulin Secretion ◽  
Plasma Glucose ◽  
Low Temperatures ◽  
Plasma Insulin ◽  
Glucose Utilization ◽  
Exogenous Insulin ◽  
Metabolic Substrate ◽  
Endogenous Insulin ◽  
Dose Dependent Decrease ◽  
Dose Dependent

In hypothermia, impairment of metabolic substrate mobilization and utilization may be a factor limiting survival. By use of a newly developed technique, substrate profiles and their regulation by insulin were examined in hypothermic rats (body temperature 19 degrees C) over 24 h. Plasma glucose concentrations increased to approximately 300 mg/dl during cooling and remained high throughout the period of hypothermia. Free fatty acid (FFA) concentration was not altered during cooling or during the first 10 h of hypothermia (approximately 700 mu eq/l) but progressively decreased thereafter, reaching 420 mu eq/l by 20 h. Plasma insulin decreased dramatically during cooling and remained very low (9 +/- 2 microU/ml) during the whole period of hypothermia, reflecting the suppression of insulin secretion by isolated islets at low temperatures. To test he hypothesis that suppression of endogenous insulin secretion may hamper glucose utilization and thus limit survival in hypothermia, exogenous insulin was administered. At doses of 0.1, 0.5, and 1 U/kg intravenously, insulin slowly decreased plasma glucose and FFA. However, at 0.1 and 1 U/kg intraperitoneally, insulin resulted in a dose-dependent decrease in survival time in the hypothermic rat. It is possible that the antilipolytic effect of insulin may have outweighed any beneficial effect of improving glucose utilization in hypothermia.

Insulin secretion, body composition and pig performance are altered by feeding pattern

2014 ◽  
Vol 54 (3) ◽  
pp. 319 ◽  
Author(s):  
Ronald E. Newman ◽  
Jeffery A. Downing ◽  
Peter C. Thomson ◽  
Cherie L. Collins ◽  
David J. Henman ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Feed Intake ◽  
Plasma Insulin ◽  
Feeding Strategy ◽  
Growing Pigs ◽  
Carcass Composition ◽  
Production Performance ◽  
Feed Conversion ◽  
Ad Libitum ◽  
Entire Male

Three studies investigated the effect of feeding strategy on production performance and endocrine status of growing pigs. For Experiment 1, 20 entire male pigs (70.0 ± 4.6 kg) were allocated randomly to individual pens in one of four climate-controlled rooms. Pigs were fed for 23 days either ad libitum or entrained to feed bi-phasically for two 90-min periods. For Experiment 2, 20 entire male pigs (41.2 ± 3.5 kg) were housed as per Experiment 1. Pigs were fed for 49 days either ad libitum or fed bi-phasically for two 60-min periods. For Experiment 3, 100 female pigs (66.1 ± 3.5 kg) were randomly allocated to individual pens within a commercial piggery and fed for 42 days either ad libitum or bi-phasically for two 60-min periods. Ear vein catheters were inserted into 10 pigs from each group and hourly blood samples were collected for 24 h in Experiments 1 and 2 and for 11 h in Experiment 3. Plasma insulin, non-esterified fatty acid and glucose concentrations were determined in Experiments 1 and 2, and glucose and insulin concentrations in Experiment 3. Feed intake and performance were recorded in all experiments and carcass composition was assessed by computed tomography for Experiment 2. There were no differences in final liveweight between the two treatment groups for all experiments. Pigs fed for two 90-min periods (Experiment 1) showed no difference in feed intake when compared with feeding ad libitum. Pigs in Experiment 2 fed for two 60-min intervals consumed 2.49 kg/pig.day compared with those fed ad libitum that consumed 2.68 kg/day (P = 0.057). In Experiment 3, pigs fed twice daily consumed 2.82 kg/pig.day compared with 2.91 kg/pig.day in ad libitum-fed pigs (P = 0.051). Bi-phasic fed pigs in Experiment 2 had improved (P < 0.05) feed conversion efficiency compared with pigs fed ad libitum. For all experiments, there was no difference in plasma glucose concentrations between the two treatments. In all three experiments, the circulating insulin concentrations for pigs fed ad libitum remained at a constant level throughout the sampling period. However, plasma insulin concentrations for the bi-phasic fed pigs significantly increased ~1 h after both feeding periods during all three experiments. Insulin secretion of pigs fed for two 90-min periods differed from that of pigs fed for two 60-min periods. Plasma insulin concentration increased five-fold following feeding for 60 min, compared with that in pigs fed for 90 min, which increased two-fold. Bi-phasic-fed pigs from Experiment 2 had reduced (P < 0.05) total carcass fat and significantly increased muscle when compared with pigs fed ad libitum. The data showed that feeding pigs at two succinct periods aligned insulin secretion to the time of feeding. Pigs fed for 60 min, unlike those fed for 90-min intervals, had reduced feed intake in comparison to those fed ad libitum. This may suggest that the duration of the feeding bout is important for this response and this may in turn influence both energy balance and the way energy is partitioned.

scholarly journals Plasma Insulin Like Activity in Relation with the treatment of Diabetes Mellitus

1965 ◽  
Vol 41 (5) ◽  
pp. 604-609,580
Author(s):  
Kozo YAMADA ◽  
Nobuo SAKAMOTO ◽  
Tadataka KOIDE ◽  
Katsumi AOYAMA ◽  
Tutomu Kuno ◽  
...  
Keyword(s):  
Diabetes Mellitus ◽  
Plasma Insulin ◽  
Treatment Of Diabetes ◽  
Insulin Like Activity

Insulin secretion in fetal and newborn sheep.

1978 ◽  
Vol 235 (5) ◽  
pp. E467 ◽  
Author(s):  
A F Philipps ◽  
B S Carson ◽  
G Meschia ◽  
F C Battaglia
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Induced Response ◽  
Response Curves ◽  
Fasted State ◽  
Early Insulin Response ◽  
Arterial Plasma ◽  
Fetal Response ◽  
Maternal Glucose

The relationships between arterial plasma insulin, glucose, and fructose concentrations during the fed and fasted state were studied in seven fetal lambs and their mothers. A significant correlation between insulin and glucose concentration was noted in all fetal lambs and in their mothers. Fetal sensitivity to glucose, as measured by the slopes of the insulin-response curves, was equal to that of the adult although the fetal response was shifted to the left of the maternal. Glucose infusion in four fetal lambs caused significant insulin elevations but no early insulin response (phase I). Maternal fasting caused no alteration in glucose-induced response in the fetus. Similar glucose infusions in newborn and 1-mo-old lambs demonstrated significant early-phase insulin secretion. Basal insulin to glucose ratios were consistent with an adult pattern as early as 3 days after birth.

EFFECT OF DECAPITATION ON THE DEVELOPMENT OF INSULIN SECRETION IN THE FOETAL RABBIT

1973 ◽  
Vol 57 (1) ◽  
pp. 23-31 ◽  
Author(s):  
P. M. B. JACK ◽  
R. D. G. MILNER
Keyword(s):  
Insulin Secretion ◽  
Plasma Insulin ◽  
Insulin Concentration ◽  
Β Cell ◽  
Plasma Insulin Concentration ◽  
Intrauterine Development ◽  
Foetal Head ◽  
Significant Difference ◽  
The Mean ◽  
Control Litter

SUMMARY One rabbit foetus in a litter was decapitated on day 24 of gestation. On day 29 the litter was killed and blood was collected from all foetuses for the measurement of plasma insulin concentration. The pancreas of the decapitated foetus and that of the control litter-mate with the nearest headless body weight were cut into pieces and incubated in a physiological buffer containing 0·6 or 3·0 mg glucose/ml. The pancreas of the decapitated foetus secreted significantly more insulin than that of the control foetus in either concentration of glucose in the medium. Higher insulin secretion from the decapitated foetus persisted for 4·5 h of incubation and was demonstrable in both the first 5 and subsequent 25 min of incubation when the pancreas was initially transferred to incubation medium containing 3·0 mg glucose/ml. The mean plasma insulin concentration of the foetuses decapitated on day 24 was higher on day 29 than that of the control foetuses but there was no significant difference between the concentration of insulin in the pancreas of the two groups of animals. The results indicate that removal of the foetal head influences the intrauterine development of the rabbit β-cell.

Divergent Effects of Leptin on Luteinizing Hormone and Insulin Secretion are Dose Dependent

2003 ◽  
Vol 228 (3) ◽  
pp. 325-330 ◽  
Author(s):  
Dorota A. Zieba ◽  
Marcel Amstalden ◽  
Marlon N. Maciel ◽  
Duane H. Keisler ◽  
Nina Raver ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Luteinizing Hormone ◽  
Plasma Insulin ◽  
Beef Cows ◽  
Saline Control ◽  
Free Access ◽  
Treatment Groups ◽  
Positive Effects ◽  
Pulse Characteristics ◽  
Dose Dependent

We have shown recently that fasting permits leptin to modulate both luteinizing hormone (LH) and insulin secretion in cows. In rodents, leptin causes divergent effects on LH and insulin release that are dose dependent. To test the hypothesis that leptin effects on LH and insulin secretion in fasted cows are dose related, we examined the effects of various doses of recombinant ovine leptin (oleptin) in mature cows. Twenty ovariectomized beef cows, each bearing an estradiol implant to maintain basal estradiol concentrations, were used. All cows were fasted for 60 hr with free access to water and were assigned randomly to one of four groups (n = 5/group): 1) saline control; 2) leptin, 0.2 μg/kg; 3) leptin, 2.0 μg/kg; and 4) leptin, 20 μg/kg body wt. Blood samples were collected at 10-min intervals for 6 hr on Days 0 and 2, with saline or oleptin injected intravenously immediately after the first intensive sample on Day 2 (54 hr). Leptin caused a dose-related increase (P < 0.001) in mean concentrations of circulating LH. Stimulation of LH release by leptin was significant at the lowest (141% of control) and middle (122% of control) doses used, but no increase was observed for the highest dose. Increased mean concentrations of LH appeared to result from an augmentation of basal secretion, as pulse characteristics were not affected. After 54 hr of fasting, plasma insulin concentrations were lowered (P < 0.01) in all treatment groups compared to Day 0. After leptin injections, plasma insulin concentrations increased (P < 0.01) and reached highest concentrations during the first hour of sampling. However, this increase was sustained for several hours only in the intermediate (2.0 μg/kg) dose group. Collectively, our results show that leptin has potent positive effects on both LH and insulin secretion in fasted cows, but the anterior pituitary and endocrine pancreas appear to become downregulated in the presence of excess ligand.

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.

Effects of acute α2-blockade on insulin action and secretion in humans

1998 ◽  
Vol 274 (1) ◽  
pp. E57-E64 ◽  
Author(s):  
Andrea Natali ◽  
Amalia Gastaldelli ◽  
Alfredo Quiñones Galvan ◽  
Anna Maria Sironi ◽  
Demetrio Ciociaro ◽  
...  
Keyword(s):  
Insulin Secretion ◽  
Energy Expenditure ◽  
Plasma Insulin ◽  
Time Course ◽  
Resting Energy Expenditure ◽  
Oral Glucose ◽  
Cardiac Work ◽  
C Peptide ◽  
Glucose Ingestion ◽  
Resting Energy

We tested whether acute α2-blockade affects insulin secretion, glucose and fat metabolism, thermogenesis, and hemodynamics in humans. During a 5-h epinephrine infusion (50 ng ⋅ min−1 ⋅ kg−1) in five volunteers, deriglidole, a selective α2-receptor inhibitor, led to a more sustained rise in plasma insulin and C-peptide levels (+59 ± 14 vs. +28 ± 6, and +273 ± 18 vs. +53 ± 14 pM, P < 0.01 vs. placebo) despite a smaller rise in plasma glucose (+0.90 ± 0.4 vs. +1.5 ± 0.3 mM, P < 0.01). Another 10 subjects were studied in the postabsorptive state and during a 4-h hyperglycemic (+4 mM) clamp, coupled with the ingestion of 75 g of glucose at 2 h. In the postabsorptive state, hepatic glucose production, resting energy expenditure, and plasma insulin, free fatty acid (FFA), and potassium concentrations were not affected by acute α2-blockade. Hyperglycemia elicited a biphasic rise in plasma insulin (to a peak of 140 ± 24 pM), C-peptide levels (1,520 ± 344 pM), and insulin secretion (to 410 ± 22 pmol/min); superimposed glucose ingestion elicited a further twofold rise in insulin and C-peptide levels, and insulin secretion. However, α2-blockade failed to change these secretory responses. Fasting blood β-hydroxybutyrate and glycerol and plasma FFA and potassium concentrations all declined with hyperglycemia; time course and extent of these changes were not affected by α2-blockade. Resting energy expenditure (+25 vs. +16%, P < 0.01) and external cardiac work (+28% vs. +19%, P < 0.01) showed larger increments after α2-blockade. We conclude that acute α2-blockade in humans 1) prevents epinephrine-induced inhibition of insulin secretion, 2) does not potentiate basal or intravenous- or oral glucose-induced insulin release, 3) enhances thermogenesis, and 4) increases cardiac work.

ANF inhibits glucose-stimulated insulin secretion in mouse and rat

1988 ◽  
Vol 255 (5) ◽  
pp. E579-E582 ◽  
Author(s):  
B. Ahren
Keyword(s):  
Insulin Secretion ◽  
Atrial Natriuretic Factor ◽  
Plasma Insulin ◽  
Glucagon Secretion ◽  
Insulin Levels ◽  
Atrial Cells ◽  
Insulin And Glucagon Secretion ◽  
Plasma Insulin Levels ◽  
Glucose Stimulated Insulin Secretion ◽  
Dose Levels

Atrial natriuretic factor (ANF) is synthesized in atrial cells and was recently demonstrated to also occur within islet glucagon cells. Therefore, we investigated the possible effects of synthetic rat ANF-(1-28) on basal and stimulated insulin and glucagon secretion in the mouse and on glucose-induced insulin secretion in the rat. We found that ANF did not affect basal levels of insulin, glucagon, or glucose when injected intravenously at dose levels between 0.25 and 4.0 nmol/kg in mice. However, when injected together with glucose (2.8 mmol/kg), ANF (4.0 nmol/kg) inhibited the increase in plasma insulin levels by 40%, from 114 +/- 8 microU/ml in controls to 81 +/- 8 microU/ml (P less than 0.01). Likewise, the increase in plasma insulin levels during an intravenous infusion of glucose in rats (10 mg/min) was significantly reduced by ANF (100 pmol.kg-1.min-1; P less than 0.001). In contrast, the increase in plasma levels of insulin and glucagon after the intravenous injection of the cholinergic agonist carbachol in mice (0.16 mumol/kg) was not significantly affected by ANF. We conclude that ANF inhibits glucose-stimulated insulin secretion in the mouse and the rat. The peptide may therefore be a modulator of insulin secretion.

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