scholarly journals Inhibitory Effects of Intranasal Administration of Insulin on Fat Oxidation during Exercise Are Diminished in Young Overweight Individuals

2018 ◽  
Vol 7 (10) ◽  
pp. 308 ◽  
Author(s):  
Hisayo Yokoyama ◽  
Ryosuke Takeda ◽  
Eriko Kawai ◽  
Akemi Ota ◽  
Emiko Morita ◽  
...  
Keyword(s):  
Intranasal Administration ◽  
Fat Oxidation ◽  
Inhibitory Effect ◽  
Normal Weight ◽  
Inhibitory Effects ◽  
Glucose Levels ◽  
Graded Exercise ◽  
High Insulin ◽  
Exercise Induced ◽  
The Brain

It remains unknown whether the high insulin (INS) levels in the brain affect fat oxidation during exercise. We examined the effects of the intranasal administration of INS, which increases the INS concentration in the cerebrospinal fluid when peripheral effects are lacking, on the maximum fat oxidation rate (maxFOR) and its intensity (FATmax) during exercise in 15 young normal-weight (N group) and eight young overweight (O group) individuals. On two separate days, either INS or placebo (PL) was randomly administered intranasally before a graded exercise test. Indirect calorimetry was used to assess maxFOR and FATmax during exercise. Blood INS and glucose levels did not change after INS administration. In the N group, maxFOR and FATmax were significantly smaller in the INS trial than in the PL trial. MaxFOR was significantly smaller in the O group than in the N group and was not influenced by INS administration. Exercise-induced elevation in blood epinephrine levels tended to be reduced by INS administration only in the N group. Intranasal INS administration reduces fat oxidation during exercise without any peripheral effects, possibly by suppressing sympathetic nerve activity. This inhibitory effect is diminished in overweight subjects, suggesting that cerebral insulin effects are attenuated in this population.

BIOCHEMICAL STUDIES ON CHLORPROMAZINE: 1. THE EFFECT OF CHLORPROMAZINE ON RESPIRATORY ACTIVITY OF ISOLATED RAT BRAIN CORTEX

1957 ◽  
Vol 35 (12) ◽  
pp. 1135-1144 ◽  
Author(s):  
O. Lindan ◽  
J. H. Quastel ◽  
S. Sved
Keyword(s):  
Plasma Proteins ◽  
Brain Cortex ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Acid Dyes ◽  
Highly Sensitive ◽  
Binding Power ◽  
The Brain

Chlorpromazine exerts a progressive inhibitory activity (at 0.3–0.6 mM) on the respiration of brain cortex in presence of either glucose, fructose, pyruvate, or L-glutamate. A similar progressive inhibition occurs with other phenothiazine derivatives such as methylene blue and phenergan. However, chlorpromazine does not inhibit oxygen uptake in the presence of succinate. Potassium-stimulated respiration is highly sensitive to chlorpromazine, as it is markedly diminished by 0.2 mM concentration of the drug, a concentration which does not affect the unstimulated respiration. The increased inhibition of potassium-stimulated respiration is only clearly seen during the early part of the experiment.Chlorpromazine is bound by tissue constituents. At a constant concentration of chlorpromazine (0.6 mM), its inhibitory effect on cortical respiration may be abolished by markedly increasing the amount of tissue present. The inhibitory effect of chlorpromazine may be diminished by addition of plasma proteins (αβ-globulin) or by addition of heated homogenized brain, liver, or kidney. No binding occurs with polyglutamic acid, ribonucleic, and deoxyribonucleic acids, but binding does occur with certain acid dyes such as trypan red. Trypan red may be used to immobilize free chlorpromazine. When the latter drug is absorbed, however, by the nervous tissue, the addition of trypan red has no effect on the metabolic inhibitions brought about by the absorbed chlorpromazine.It is concluded that chlorpromazine resembles a large variety of narcotics and anaesthetics in its marked inhibitory effects on potassium-stimulated respiration of the brain. Its action, in vitro, however, differs from that of the narcotics in bringing about progressive, apparently irreversible, inhibitions and in its high binding power with tissue proteins. Such apparently irreversible inhibition is consistent with the conclusion that the drug, after combination with the tissue, gradually diffuses into the cell bringing about metabolic inhibitions.

Maximal fat oxidation rate is higher in fit women and unfit women with obesity, compared to normal weight unfit women

2021 ◽  
Author(s):  
Jacob Frandsen ◽  
Ida Marie Dahlgaard Hansen ◽  
Julie Fensmark Wismann ◽  
Maria Høyer Olsen ◽  
Morten Runge Brage-Andersen ◽  
...  
Keyword(s):  
Young Women ◽  
Exercise Test ◽  
Oxidation Rate ◽  
Fat Oxidation ◽  
Cycle Ergometer ◽  
Normal Weight ◽  
Middle Aged ◽  
Graded Exercise ◽  
Maximal Fat Oxidation ◽  
Related Increase

Abstract Introduction Maximal fat oxidation rate (MFO) is higher in aerobically fit vs. unfit young men, but this training related increase in MFO is attenuated in middle-aged men. Further, it has also been found that unfit men with obesity may have an elevated MFO compared to unfit normal-weight men. Aim/Hypothesis Based hereupon, we aimed to investigate whether a fitness related higher MFO were attenuated in middle-aged women compared to young women. Also, we aimed to investigate if unfit women with obesity have a higher MFO compared to unfit normal-weight women. We hypothezised that the training related elevated MFO was attenuated in middle-aged women, but that unfit women with obesity would have an elevated MFO compared to unfit normal-weight women. Methods We recruited a total of 70 women stratified into six groups: Young fit (n=12), young unfit (n=12) middle-aged fit (n=12), middle-aged unfit (n=12), unfit young women with obesity (n=12) and unfit middle-aged women with obesity (n=10). Body composition and resting blood samples were obtained and MFO was measured by a graded exercise test on a cycle ergometer via indirect calorimetry. Subsequently, a maximal exercise test was performed to establish V̇O2peak. Results Young and middle-aged fit women had a higher MFO compared to age-matched unfit women, and young fit women had a higher MFO compared to fit middle-aged women. Unfit women with obesity, independent of age, had a higher MFO compared to their normal-weight and unfit counterparts. Conclusion The training related increase in MFO seems maintained in middle-aged women and secondly, we find that unfit women with obesity, independent of age have a higher MFO compared to unfit normal-weight women.

Modulatory effect of glucose on VIP-induced gastric somatostatin release

1988 ◽  
Vol 254 (6) ◽  
pp. E756-E759 ◽  
Author(s):  
R. Schmid ◽  
V. Schusdziarra ◽  
M. Classen
Keyword(s):  
Cell Function ◽  
Inhibitory Effect ◽  
Maximal Effect ◽  
Inhibitory Effects ◽  
Glucose Levels ◽  
Normal Glucose ◽  
D Cell ◽  
First Time ◽  
Effect Of Glucose ◽  
Fasted Rats

The present study was designed to examine the effect of increasing perfusate glucose concentrations on vasoactive intestinal peptide (VIP)-induced somatostatin (SLI) release from the isolated rat stomach. The stomach of overnight-fasted rats was perfused with Krebs-Ringer buffer containing 100, 150, or 200 mg/dl glucose, respectively. VIP was administered at 10(-12), 10(-11), 10(-9), and 10(-8) M. At a normal glucose concentration of 100 mg/dl, VIP at doses of 10(-12), 10(-11), and 10(-9) M elicited a small inhibitory effect on SLI release by 200-300 pg/min (P less than 0.01). As reported previously at 10(-8) M, VIP stimulated gastric SLI secretion by 500 pg/min (P less than 0.01). Increasing perfusate glucose to 150 mg/dl resulted in a stimulation of SLI release by all four concentrations of VIP with a maximal effect at 10(-9) M. During 200 mg/dl glucose, VIP had no effect in concentrations below 10(-9) M, and only the two highest doses (10(-9) and 10(-8) M) stimulated SLI release significantly. In the absence of VIP, glucose had no effect on gastric SLI release. In conclusion, the present data demonstrate for the first time that at normal glucose levels VIP has not only stimulatory but also inhibitory effects on gastric SLI, and second, a modest elevation of glucose has a modulatory effect on gastric D-cell function.

BIOCHEMICAL STUDIES ON CHLORPROMAZINE: 1. THE EFFECT OF CHLORPROMAZINE ON RESPIRATORY ACTIVITY OF ISOLATED RAT BRAIN CORTEX

1957 ◽  
Vol 35 (1) ◽  
pp. 1135-1144 ◽  
Author(s):  
O. Lindan ◽  
J. H. Quastel ◽  
S. Sved
Keyword(s):  
Plasma Proteins ◽  
Brain Cortex ◽  
Inhibitory Effect ◽  
Inhibitory Effects ◽  
Acid Dyes ◽  
Highly Sensitive ◽  
Binding Power ◽  
The Brain

Chlorpromazine exerts a progressive inhibitory activity (at 0.3–0.6 mM) on the respiration of brain cortex in presence of either glucose, fructose, pyruvate, or L-glutamate. A similar progressive inhibition occurs with other phenothiazine derivatives such as methylene blue and phenergan. However, chlorpromazine does not inhibit oxygen uptake in the presence of succinate. Potassium-stimulated respiration is highly sensitive to chlorpromazine, as it is markedly diminished by 0.2 mM concentration of the drug, a concentration which does not affect the unstimulated respiration. The increased inhibition of potassium-stimulated respiration is only clearly seen during the early part of the experiment.Chlorpromazine is bound by tissue constituents. At a constant concentration of chlorpromazine (0.6 mM), its inhibitory effect on cortical respiration may be abolished by markedly increasing the amount of tissue present. The inhibitory effect of chlorpromazine may be diminished by addition of plasma proteins (αβ-globulin) or by addition of heated homogenized brain, liver, or kidney. No binding occurs with polyglutamic acid, ribonucleic, and deoxyribonucleic acids, but binding does occur with certain acid dyes such as trypan red. Trypan red may be used to immobilize free chlorpromazine. When the latter drug is absorbed, however, by the nervous tissue, the addition of trypan red has no effect on the metabolic inhibitions brought about by the absorbed chlorpromazine.It is concluded that chlorpromazine resembles a large variety of narcotics and anaesthetics in its marked inhibitory effects on potassium-stimulated respiration of the brain. Its action, in vitro, however, differs from that of the narcotics in bringing about progressive, apparently irreversible, inhibitions and in its high binding power with tissue proteins. Such apparently irreversible inhibition is consistent with the conclusion that the drug, after combination with the tissue, gradually diffuses into the cell bringing about metabolic inhibitions.

Inhibition of dorsal-horn cell responses by stimulation of the Kölliker-Fuse nucleus

1986 ◽  
Vol 65 (6) ◽  
pp. 825-833 ◽  
Author(s):  
Charles J. Hodge ◽  
A. Vania Apkarian ◽  
Richard T. Stevens
Keyword(s):  
Brain Stem ◽  
Biogenic Amines ◽  
Dorsal Horn ◽  
Inhibitory Effect ◽  
Control Mechanisms ◽  
Inhibitory Effects ◽  
Content Type ◽  
Cell Responses ◽  
The Brain ◽  
Stimulation Of

✓ The Kölliker-Fuse nucleus (KF) in the dorsolateral pons has been shown to be the major source of catecholamine innervation of the spinal cord. This has important implications in terms of pain control mechanisms, since catecholamine-mediated mechanisms are essential for the expression of opiate and other varieties of antinociception. This study examines the effects of KF stimulation on responses of dorsal-horn cells to innocuous and noxious cutaneous stimuli in anesthetized cats. Stimulation of the KF potently inhibits the responses of dorsal-horn cells to both noxious and innocuous stimuli. The threshold for the inhibitory effect is significantly lower for responses to noxious stimuli as opposed to innocuous stimuli. The inhibitory effect is specific to the stimulus site, as evidenced by a marked decrease in the effect following small changes in the position of the stimulating electrode in the brain stem. The latency of the effects indicates a bulbospinal conduction velocity of 4 to 5 m/sec, which is much slower than usual reticulospinal effects and is consistent with a catecholamine-mediated system. The dependence of KF-spinal inhibition on intact biogenic amines was tested by depleting the animals of these amines with reserpine pretreatment. Depletion of biogenic amines resulted in a significant decrease in the KF spinal inhibitory effects, suggesting their dependence on intact noradrenergic stores. The results of these studies are consistent with the idea that the KF-spinal system plays an important noradrenergic-dependent role in the brain-stem modulation of spinal processing of noxious, potentially painful stimuli.

In Vitro Effects of Ethanol on Rabbit Platelet Aggregation, Secretion of Granule Contents, and Cyclic AMP Levels in the Presence of Prostacyclin

1989 ◽  
Vol 61 (02) ◽  
pp. 254-258 ◽  
Author(s):  
Margaret L Rand ◽  
Peter L Gross ◽  
Donna M Jakowec ◽  
Marian A Packham ◽  
J Fraser Mustard
Keyword(s):  
Cyclic Amp ◽  
Inhibitory Effect ◽  
Rabbit Platelet ◽  
Inhibitory Effects ◽  
Low Concentrations ◽  
Rabbit Platelets ◽  
High Concentrations ◽  
In Vitro Effects ◽  
Aggregation Of Platelets

SummaryEthanol, at physiologically tolerable concentrations, inhibits platelet responses to low concentrations of collagen or thrombin, but does not inhibit responses of washed rabbit platelets stimulated with high concentrations of ADP, collagen, or thrombin. However, when platelet responses to high concentrations of collagen or thrombin had been partially inhibited by prostacyclin (PGI2), ethanol had additional inhibitory effects on aggregation and secretion. These effects were also observed with aspirin- treated platelets stimulated with thrombin. Ethanol had no further inhibitory effect on aggregation of platelets stimulated with ADP, or the combination of ADP and epinephrine. Thus, the inhibitory effects of ethanol on platelet responses in the presence of PGI2 were very similar to its inhibitory effects in the absence of PGI2, when platelets were stimulated with lower concentrations of collagen or thrombin. Ethanol did not appear to exert its inhibitory effects by increasing cyclic AMP above basal levels and the additional inhibitory effects of ethanol in the presence of PGI2 did not appear to be brought about by further increases in platelet cyclic AMP levels.

Inhibition of ADP-Induced Responses in Human Platelets by Agents Elevating the Cyclic AMP Level: Comparison of Aggregation and Shape Change

1984 ◽  
Vol 52 (03) ◽  
pp. 333-335 ◽  
Author(s):  
Vider M Steen ◽  
Holm Holmsen
Keyword(s):  
Inhibitory Action ◽  
Human Platelet ◽  
Platelet Rich Plasma ◽  
Shape Change ◽  
Inhibitory Effect ◽  
Human Platelets ◽  
Inhibitory Effects ◽  
Early Step ◽  
Stimulus Response ◽  
Sequential Relationship

SummaryThe inhibitory effect of cAMP-elevating agents on shape change and aggregation in human platelets was studied to improve the understanding of the sequential relationship between these two responses.Human platelet-rich plasma was preincubated for 2 min at 37° C with prostaglandin E1 or adenosine, agents known to elevate the intracellular level of cAMP. Their inhibitory effects on ADP-induced shape change and aggregation were determined both separately and simultaneously. The dose-inhibition patterns for shape change and aggregation were similar for both PGE1 and adenosine. There was no distinct difference between the inhibitory action of these two inhibitors.These observations suggest that elevation of the intracellular concentration of cAMP interferes with an early step in the stimulus-response coupling that is common for aggregation and shape change.

The Inhibitory Effect of Heparin and Related Glycosaminoglycans on Neutrophil Chemotaxis

1984 ◽  
Vol 52 (02) ◽  
pp. 134-137 ◽  
Author(s):  
Yaacov Matzner ◽  
Gerard Marx ◽  
Ruth Drexler ◽  
Amiram Eldor
Keyword(s):  
Specific Binding ◽  
Anticoagulant Activity ◽  
Neutrophil Migration ◽  
Inhibitory Effect ◽  
Chemotactic Factor ◽  
Human Neutrophils ◽  
Boyden Chamber ◽  
Neutrophil Chemotaxis ◽  
Inhibitory Effects ◽  
Chemotactic Factors

SummaryClinical observations have shown that heparin has antiinflammatory activities. The effect of heparin on neutrophil chemotaxis was evaluated in vitro in the Boyden Chamber. This method enabled differentiation between the direct effects of heparin on neutrophil migration and locomotion, and its effects on chemotactic factors. Heparin inhibited both the random migration and directed locomotion of human neutrophils toward zymosan-activated serum (ZAS) and F-met-leu-phe (FMLP). Inhibition was found to be dependent on the concentrations of the heparin and of the chemotactic factors. No specific binding of heparin to the neutrophils could be demonstrated, and heparin’s inhibitory effects were eliminated by simple washing of the cells. When added directly to the chamber containing chemotactic factor, heparin inhibited the chemotactic activity of ZAS but not that of FMLP, suggesting a direct inhibitory effect against C5a, the principal chemotactic factor in ZAS.Experiments performed with low-molecular-weight heparin, N-desulfated heparin, dextran sulfate, chondroitin sulfate and dextran indicated that the inhibitory effects of heparin on neutrophil chemotaxis are not related to its anticoagulant activity, but probably depend on the degree of sulfation of the heparin molecule.

ADRENERGIC CONTROL MECHANISM FOR ACTH SECRETION IN MAN

1973 ◽  
Vol 74 (2) ◽  
pp. 263-270 ◽  
Author(s):  
Yoshikatsu Nakai ◽  
Hiroo Imura ◽  
Teruya Yoshimi ◽  
Shigeru Matsukura
Keyword(s):  
Intravenous Infusion ◽  
Human Subjects ◽  
Blocking Agent ◽  
Inhibitory Effect ◽  
Plasma Acth ◽  
Acth Secretion ◽  
Glucose Levels ◽  
Alpha Receptors ◽  
Normal Human ◽  
Adrenergic Blocking

ABSTRACT In order to determine if an adrenergic mechanism is involved in the secretion of corticotrophin (ACTH), the effect of adrenergic-blocking or -stimulating agent on plasma ACTH, cortisol and glucose levels was studied in normal human subjects. The intravenous infusion of methoxamine, an alpha adrenergic-stimulating agent, caused a rise in plasma ACTH and cortisol. This increase in plasma ACTH and cortisol was significantly inhibited by the simultaneous administration of phentolamine, an alpha adrenergic-blocking agent, in combination with methoxamine. The intravenous infusion of propranolol, a beta adrenergic-blocking agent, caused no significant change in plasma ACTH and cortisol, although it enhanced the plasma ACTH response to insulin-induced hypoglycaemia. On the other hand, alpha adrenergicblockade by intravenous infusion of phentolamine significantly suppressed the plasma ACTH response to insulin-induced hypoglycaemia. These studies suggest a stimulatory effect of alpha receptors and a possible inhibitory effect of beta receptors on ACTH secretion in man.

Inhibitory Effects of Intranasal Insulin Administration on Fat Oxidation during Exercise Are Diminished in Overweight Young Individuals

Diabetes ◽  
2018 ◽  
Vol 67 (Supplement 1) ◽  
pp. 736-P
Author(s):  
HISAYO YOKOYAMA ◽  
RYOSUKE TAKEDA ◽  
ERIKO KAWAI ◽  
AKEMI OTA ◽  
EMIKO MORITA ◽  
...  
Keyword(s):  
Fat Oxidation ◽  
Insulin Administration ◽  
Intranasal Insulin ◽  
Inhibitory Effects
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