The Disposition of Intravenous Potassium in Normal Man: The Role of Insulin

1981 ◽  
Vol 61 (1) ◽  
pp. 23-28 ◽  
Author(s):  
R. H. Sterns ◽  
J. Guzzo ◽  
P. U. Feig
Keyword(s):  
Plasma Insulin ◽  
Normal Volunteer ◽  
Immunoreactive Insulin ◽  
K Uptake ◽  
Insulin Levels ◽  
Urinary Potassium ◽  
Plasma Insulin Levels ◽  
Normal Man ◽  
K Concentration

1. Potassium infusion causes an increase in immunoreactive insulin levels in dogs, but either a small (30%) or no increase in humans. Since insulin stimulates the uptake of K+ by cells, a regulatory role for K+-induced insulin release has been postulated. To study the role of insulin in regulating cellular K+ uptake, six fasting normal volunteer subjects underwent two K+ infusions on separate days. Both infusions delivered 0.6 mmol h−1 kg−1 for 3 h. In one subject glucose was simultaneously infused at 0.67 mmol h−1 kg−1 (a rate known to increase peripheral insulin levels by 40–100%); the other infusion contained no glucose. 2. Plasma insulin levels did not increase during the glucose-free infusions. During glucose-containing infusions, insulin levels were 40% higher than those during glucose-free infusions. Despite this, neither urinary potassium excretion nor the increment in plasma K+ concentration or the calculated cellular K+ uptake differed significantly during the 3 h of glucose-free and glucose-containing infusions respectively. 3. These data do not support the view that potassium-induced insulin secretion regulates cellular potassium uptake within the physiological range of plasma K+ concentration.

Insulin response in rats acutely exposed to cold

1984 ◽  
Vol 62 (8) ◽  
pp. 924-927 ◽  
Author(s):  
Ora L. K. Smith
Keyword(s):  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Blocking Agent ◽  
Intravenous Glucose ◽  
Insulin Levels ◽  
Glucose Challenge ◽  
Plasma Insulin Levels ◽  
Adrenergic Blocking

To examine the role of insulin during shivering thermogenesis, rats (unacclimatized) were exposed to 4 °C for 24 h and compared with control rats kept at 25 °C. Cold exposure lowered plasma insulin levels by one half, despite unchanged plasma glucose concentrations. Adrenodemedullation 2 weeks prior to cold exposure partially restored the ability of cold rats' plasma insulin levels to respond to a glucose load, unless it was accompanied by a subcutaneous injection of epinephrine. When additional normal rats were cold stressed and injected immediately after exposure with an α-adrenergic blocking agent (phentolamine), an intravenous glucose challenge caused a mean peak insulin value that was 50% higher than that of untreated controls, while the glucose level was less elevated. The results suggest that cold depresses blood insulin levels through activation of the sympathetic adrenal system, an effect most likely mediated by α-adrenergic inhibition of the pancreatic insulin response.

scholarly journals miR-467 regulates inflammation and blood insulin and glucose

2019 ◽  
Author(s):  
Jasmine Gajeton ◽  
Irene Krukovets ◽  
Revanth Yendamuri ◽  
Dmitriy Verbovetskiy ◽  
Amit Vasanji ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Blood Glucose ◽  
Plasma Insulin ◽  
Western Diet ◽  
Insulin Levels ◽  
Glucose Clearance ◽  
Physiological Feedback ◽  
Plasma Insulin Levels ◽  
Antagonist Effect

AbstractObesity is associated with inflammation and insulin resistance (IR), but the regulation of insulin sensitivity (IS) and connections between IS and inflammation remain unclear. We investigated the role of miR-467a-5p, a miRNA induced by hyperglycemia, in regulating inflammation and blood glucose handling.We previously demonstrated that miR-467a-5p is induced by hyperglycemia and inhibits the production of thrombospondin-1 (TSP-1), a protein implicated in regulating inflammation. To investigate the role of miR-467 in blood glucose handling and tissue inflammation, WT C57/BL6 mice were fed chow or Western diet from 5 to 32 weeks of age and injected weekly with miR-467a-5p antagonist. Inhibiting miR-467a-5p resulted in 47% increase in macrophage infiltration and increased Il6 levels in adipose tissue, higher plasma insulin levels (98 vs 63 ng/mL), and 17% decrease in glucose clearance without increase in weight or HDL/LDL. The antagonist effect was lost in mice on Western diet. Mice lacking TSP-1 lost some but not all of the miR-467 effects, suggesting Thbs1−/− (and other unknown transcripts) are targeted by miR-467 to regulate inflammation.miR-467a-5p provides a physiological feedback when blood glucose is elevated to avoid inflammation and increased blood glucose and insulin levels, which may prevent IR.

Oscillations of plasma K+ and insulin during K+ infusion in awake anephric dogs

1982 ◽  
Vol 243 (1) ◽  
pp. F44-F52 ◽  
Author(s):  
R. H. Sterns
Keyword(s):  
Plasma Insulin ◽  
Average Rate ◽  
Plasma Potassium ◽  
Regulatory Control ◽  
Control Loop ◽  
K Uptake ◽  
Insulin Levels ◽  
Constant Rate ◽  
Physiological Feedback ◽  
Plasma Insulin Levels

Changes in plasma potassium ([K+]p) and insulin levels were monitored during K+ infusion in awake and anesthetized nephrectomized, splenectomized dogs. In dogs studied while anesthetized with pentobarbital, the increase in [K+]p was linear, reflecting a nearly constant rate of cellular uptake of the infused K+. In contrast, in dogs studied 18 h after nephrectomy while awake, [K+]p oscillated during infusion, reflecting an inconstant rate of cellular K+ uptake. Although these oscillations in [K+]p were associated with parallel oscillations in plasma insulin levels (suggesting the possibility of a physiological feedback control loop involving K+ and insulin), when the oscillations in insulin levels were blunted by somatostatin infusion or abolished by pancreatectomy plus insulin replacement, oscillations in [K+]p persisted and the average rate of cellular K+ uptake was not diminished. The observed oscillations of [K+]p during K+ infusion suggest the possibility of regulatory control of cellular K+ uptake within the pathophysiologic range of [K+]p. The putative control system is independent of and quantitatively more important than K+-induced insulin secretion and is obscured by pentobarbital anesthesia.

PLASMA INSULIN LEVELS IN NORMAL HUMAN FOETUSES

1970 ◽  
Vol 63 (1) ◽  
pp. 134-140 ◽  
Author(s):  
Jan I. Thorell
Keyword(s):  
Plasma Insulin ◽  
Insulin Level ◽  
Immunoreactive Insulin ◽  
Foetal Heart ◽  
Glucose Load ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Normal Human ◽  
The Mean ◽  
Human Foetuses

ABSTRACT Immunoreactive insulin was measured in plasma collected from human foetuses at gestational ages of 15-26 weeks, as well as from their mothers. In the fasting stage, the mean insulin concentration in the foetal heart was 29 μU/ml (range 6-74 μU/ml) and in the umbilical vessels 19 μU/ml (range 10-36 μU/ml. The corresponding maternal value was 11 μU/ml (range 6-30 μU/ml). After giving the mothers a glucose load, the maternal insulin level increased considerably, but no change was found in the foetal plasma. There was no correlation between foetal weight and foetal plasma insulin level.

scholarly journals Lower plasma insulin levels during overnight closed-loop in school children with type 1 diabetes: Potential advantage? A randomized cross-over trial

PLoS ONE ◽  
2019 ◽  
Vol 14 (3) ◽  
pp. e0212013 ◽  
Author(s):  
Ulrike Schierloh ◽  
Malgorzata E. Wilinska ◽  
Ineke M. Pit-ten Cate ◽  
Petra Baumann ◽  
Roman Hovorka ◽  
...  
Keyword(s):  
Type 1 Diabetes ◽  
School Children ◽  
Plasma Insulin ◽  
Closed Loop ◽  
Lower Plasma ◽  
Insulin Levels ◽  
Plasma Insulin Levels

Metformin decreases plasma insulin levels and systolic blood pressure in spontaneously hypertensive rats

1994 ◽  
Vol 267 (4) ◽  
pp. H1250-H1253 ◽  
Author(s):  
S. Verma ◽  
S. Bhanot ◽  
J. H. McNeill
Keyword(s):  
Blood Pressure ◽  
Systolic Blood Pressure ◽  
Spontaneously Hypertensive Rats ◽  
Plasma Insulin ◽  
Metformin Treatment ◽  
Hypertensive Rats ◽  
Spontaneously Hypertensive ◽  
Insulin Levels ◽  
Plasma Insulin Levels ◽  
Wistar Kyoto

To determine the relationship between hyperinsulinemia and hypertension in spontaneously hypertensive rats (SHR), the antihyperglycemic agent metformin was administered to SHR and their Wistar-Kyoto (WKY) controls, and its effects on plasma insulin levels and blood pressure were examined. Five-week-old rats were started on oral metformin treatment (350 mg.kg-1.day-1, which was gradually increased to 500 mg.kg-1.day-1 over a 2-wk period). Metformin treatment caused sustained decreases in plasma insulin levels in the SHR (27.1 +/- 2.3 vs. untreated SHR 53.5 +/- 2.7 microU/ml, P < 0.001) without having any effect in the WKY (30.7 +/- 2.2 vs. untreated WKY 37.8 +/- 1.6 microU/ml, P > 0.05). The treatment did not affect the plasma glucose levels in any group. Metformin treatment also attenuated the increase in systolic blood pressure in the SHR (157 +/- 6.0 vs. untreated SHR 196 +/- 9.0 mmHg, P < 0.001) but had no effect in the WKY (134 +/- 3 vs. untreated WKY 136 +/- 4 mmHg, P > 0.05). Furthermore, raising plasma insulin levels in the metformin-treated SHR to levels that existed in the untreated SHR reversed the effect of metformin on blood pressure (189 +/- 3 vs. untreated SHR 208 +/- 5.0 mmHg, P > 0.05). These findings suggest that either hyperinsulinemia may contribute toward the increase in blood pressure in the SHR or that the underlying mechanism is closely associated with the expression of both these disorders.

Interactions of cold exposure and starvation on glucose tolerance and insulin response

1983 ◽  
Vol 245 (6) ◽  
pp. E575-E581 ◽  
Author(s):  
A. L. Vallerand ◽  
J. Lupien ◽  
L. J. Bukowiecki
Keyword(s):  
Glucose Tolerance ◽  
Cold Acclimation ◽  
Cold Exposure ◽  
Plasma Insulin ◽  
Insulin Response ◽  
Insulinogenic Index ◽  
Intravenous Glucose ◽  
Peripheral Tissues ◽  
Insulin Levels ◽  
Plasma Insulin Levels

The metabolic interactions of cold exposure, cold acclimation, and starvation on glucose tolerance and plasma insulin levels were studied in precannulated, unrestrained, and unanesthetized rats. Cold exposure (48 h at 5 degrees C) significantly reduced the insulin response to intravenous glucose injection (P less than 0.01) while improving glucose tolerance (P less than 0.01). Starvation (48 h at 25 degrees C) also reduced the insulin response (P less than 0.01) but did not significantly alter glucose tolerance. “Accelerated starvation” induced by starving rats for 48 h at 5 degrees C dramatically reduced both basal and glucose-stimulated insulin levels while even improving glucose tolerance, resulting in a 15-fold reduction in the insulinogenic index. Cold acclimation (3 wk at 5 degrees C) induced essentially the same alterations as cold exposure. Approximately reversed changes were observed when cold-acclimated rats were returned to a warm environment for 15–18 h. Results from these studies indicate that 1) cold exposure and starvation, but not cold acclimation, act synergistically in decreasing the sensitivity and/or the capacity of pancreatic islets for secreting insulin in response to glucose stimulation; 2) glucose tolerance and possibly insulin sensitivity of peripheral tissues are enhanced by cold exposure and starvation, although glucose tolerance is improved by cold exposure only, not by starvation; 3) an improved glucose tolerance with barely detectable plasma insulin levels was obtained in cold-starved rats under normal physiological conditions.

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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