Lack of effect of acute ethanol consumption on active cation fluxes of leucocytes and erythrocytes in healthy humans

1987 ◽  
Vol 73 (4) ◽  
pp. 387-393 ◽  
Author(s):  
Rachel J. Green ◽  
D. N. Baron
Keyword(s):  
Neutrophil Count ◽  
Serum Insulin ◽  
Ethanol Consumption ◽  
Electrolyte Excretion ◽  
Plasma Adrenaline ◽  
Healthy Humans ◽  
Human Volunteers ◽  
Acute Ethanol ◽  
Intracellular Electrolyte Concentrations

1. Acute ethanol consumption in human volunteers did not appear to alter active cation fluxes by Na+,K+-ATPase, or intracellular electrolyte concentrations, in peripheral leucocytes or erythrocytes. 2. Urinary electrolyte excretion was decreased after ethanol consumption, compared with controls. 3. Neither plasma glucose nor serum insulin was altered by ethanol. 4. After ethanol consumption there was an elevation of endogenous plasma adrenaline levels. This was accompanied by a leucocytosis, which could be attributed to a raised neutrophil count. 5. The raised adrenaline levels were not associated with hypokalaemia. 6. It is possible that in vivo ethanol may prevent adrenaline-induced hypokalaemia by fluidizing the membrane and/or decreasing the affinity of β-receptors for adrenaline.

scholarly journals Antagonism of GluK1-containing Kainate Receptors Reduces Ethanol Consumption by Modulating Ethanol Reward and Withdrawal

2021 ◽  
Author(s):  
Natalia Quijano-Carde' ◽  
Erika E. Perez ◽  
Richard Feinn ◽  
Henry R. Kranzler ◽  
Mariella De Biasi
Keyword(s):  
Association Studies ◽  
Genetic Association Studies ◽  
Ethanol Consumption ◽  
In Vivo Microdialysis ◽  
Ethanol Withdrawal ◽  
Kainate Receptors ◽  
Dependent Manner ◽  
Receptor System ◽  
Acute Ethanol

Alcohol use disorder (AUD) is a neuropsychiatric condition affecting millions of people worldwide. Topiramate (TPM) is an antiepileptic drug that has been shown to reduce ethanol drinking in humans. However, TPM is associated with a variety of adverse effects due to its interaction with many receptor systems and intracellular pathways. Thus, a better understanding of the role of TPM's main molecular targets in AUD could yield better therapeutic tools. GluK1-containing kainate receptors (GluK1*KARs) are non-selectively inhibited by TPM, and genetic association studies suggest that this receptor system could be targeted to reduce drinking in AUD patients. We examined the efficacy of LY466195, a selective inhibitor of GluK1*KAR, in reducing ethanol consumption in the intermittent two-bottle choice paradigm in mice. The effect of LY466195 on various ethanol-related phenotypes was investigated by quantification of alcohol intake, physical signs of withdrawal, conditioned place preference (CPP) and in vivo microdialysis in the nucleus accumbens. Selective GluK1*KAR inhibition reduced ethanol intake and preference in a dose-dependent manner. LY466195 treatment attenuated the physical manifestations of ethanol withdrawal and influenced the rewarding properties of ethanol. Interestingly, LY466195 injection also normalized changes in dopamine levels in response to acute ethanol in ethanol-dependent mice, but had no effect in ethanol-naive mice, suggesting ethanol state-dependent effects. The data point to GluK1*KARs as an attractive pharmacological target for the treatment of AUD.

Acute hypoxia decreases plasma VEGF concentration in healthy humans

2006 ◽  
Vol 290 (3) ◽  
pp. E434-E439 ◽  
Author(s):  
Kerstin M. Oltmanns ◽  
Hartmut Gehring ◽  
Sebastian Rudolf ◽  
Bernd Schultes ◽  
Claudia Hackenberg ◽  
...  
Keyword(s):  
Serum Insulin ◽  
Acute Hypoxia ◽  
Vascular Endothelial ◽  
Double Blind ◽  
Healthy Humans ◽  
Normoxic Control ◽  
Endothelial Growth Factor ◽  
Double Blind Crossover Study

Vascular endothelial growth factor (VEGF) is known to be upregulated by hypoxia in vitro. However, in vivo data about VEGF regulation in chronic hypoxic diseases are conflicting. We investigated the effects of hypoxia on plasma VEGF concentration in healthy subjects. To control known confounders, such as insulin, glucose concentrations, or exercise, hypoxic effects on VEGF were studied during experimentally clamping glucose concentrations at rest. In a double-blind crossover study design, we induced hypoxia for 30 min by decreasing oxygen saturation to 75% (vs. normoxic control) in 14 healthy men. Plasma VEGF concentration was determined at baseline, immediately after hypoxia had ended, and after a further 150 min. Levels of its soluble (s)Flt-1 receptor were assessed at baseline and at the end of the clamp. In parallel, catecholamine and cortisol levels were monitored. To investigate potential effects of glucose administration on the release of VEGF, we performed a third session, reducing glucose infusion for 30 min while serum insulin was held stable thereby inducing hypoglycemia. Hypoxia decreased VEGF levels compared with the normoxic control ( P < 0.05). VEGF concentrations increased during hypoglycemia ( P < 0.02) but were comparable to the normoglycemic control at the end of the clamp ( P > 0.80). sFlt-1 receptor concentration remained unchanged during hypoxia and hypoglycemia compared with control (both P > 0.4). Epinephrine concentration ( P < 0.01) increased upon hypoxia, whereas norepinephrine and cortisol did not change. Contrary to in vitro studies, in healthy humans hypoxia decreases plasma VEGF concentration, suggesting that systemic VEGF concentration may be differently regulated than the expression on cellular basis.

scholarly journals Effects of ethanol consumption on the B-group vitamin contents of liver, blood and urine in rats

2011 ◽  
Vol 108 (6) ◽  
pp. 1034-1041 ◽  
Author(s):  
Aiko Miyazaki ◽  
Mitsue Sano ◽  
Tsutomu Fukuwatari ◽  
Katsumi Shibata
Keyword(s):  
Pantothenic Acid ◽  
Ethanol Consumption ◽  
Ethanol Exposure ◽  
Ethanol Solution ◽  
Acute Ethanol ◽  
Sufficient Vitamin ◽  
And Control ◽  
Vitamin Mixture

Several studies have shown that blood vitamin levels are lower in alcoholic patients than in control subjects. Acute ethanol exposure enhances the release of vitamins from liver cells in vitro. The aim of the present study is to confirm the effects of ethanol consumption on vitamin contents in vivo. We compared the contents of B-group vitamins in the liver, blood and urine between ethanol-fed and control rats fed a diet containing a sufficient- and low-vitamin mixture. The experimental rats were fed a 15 % ethanol solution freely for 28 d, and then 24 h urine samples were collected, after which the animals were killed. The B-group vitamin contents in the liver, blood and urine were measured. No differences in liver, blood and urine contents were observed between the control and ethanol-fed rats fed a diet containing a sufficient-vitamin mixture. On the contrary, in rats fed a diet containing a low-vitamin mixture, consumption of ethanol caused a decrease in the contents of vitamins B1, B2 and pantothenic acid in the liver; however, the contents of the other vitamins did not decrease. In the blood, the contents of vitamins B1, B2, B6 and pantothenic acid were lower in the ethanol-fed rats than in the controls. Urinary excretion of the B-group vitamins, except for niacin, was lower in the ethanol-fed rats. These results show that ethanol consumption affects the absorption, distribution and excretion of each of the vitamins in rats fed a diet containing a low-vitamin mixture.

Topical application of solubilized Reseda luteola extract inhibits ultraviolet B-induced inflammation in human volunteers in vivo

Planta Medica ◽  
2009 ◽  
Vol 75 (09) ◽  
Author(s):  
F Casetti ◽  
W Jung ◽  
U Wölfle ◽  
J Reuter ◽  
K Neumann ◽  
...  
Keyword(s):  
Topical Application ◽  
Ultraviolet B ◽  
Human Volunteers

Short‐Term Repeatability of in Vivo Cardiac Intravoxel Incoherent Motion Tensor Imaging in Healthy Human Volunteers

2021 ◽  
Author(s):  
Xiu‐Shi Zhang ◽  
En‐Hui Liu ◽  
Xin‐Yu Wang ◽  
Xin‐Xiang Zhou ◽  
Hong‐Xia Zhang ◽  
...  
Keyword(s):  
Intravoxel Incoherent Motion ◽  
Short Term ◽  
Healthy Human ◽  
Human Volunteers

In vivo pharmacokinetics in human volunteers: oral administered guar gum-based colon-targeted 5-fluorouracil tablets

2003 ◽  
Vol 19 (5) ◽  
pp. 355-362 ◽  
Author(s):  
Y.S.R Krishnaiah ◽  
V Satyanarayana ◽  
B Dinesh Kumar ◽  
R.S Karthikeyan ◽  
P Bhaskar
Keyword(s):  
Guar Gum ◽  
Human Volunteers ◽  
In Vivo Pharmacokinetics

Increased high-frequency heart rate variability during insulin-induced hypoglycaemia in healthy humans

2004 ◽  
Vol 106 (6) ◽  
pp. 583-588 ◽  
Author(s):  
Hartmut SCHÄCHINGER ◽  
Johannes PORT ◽  
Stuart BRODY ◽  
Lilly LINDER ◽  
Frank H. WILHELM ◽  
...  
Keyword(s):  
Heart Rate ◽  
High Frequency ◽  
Concomitant Increase ◽  
Plasma Adrenaline ◽  
Non Invasive ◽  
Hyperinsulinaemic Clamp ◽  
Healthy Humans ◽  
Plasma Insulin Levels ◽  
Single Blind ◽  
Cardiac Autonomic Activity

Despite causing sympathetic activation, prolonged hypoglycaemia produces little change in HR (heart rate) in healthy young adults. One explanation could be concurrent parasympathetic activation, resulting in unchanged net effects of autonomic influences. In the present study, hypoglycaemic (2.7 mmol/l) and normoglycaemic (4.7 mmol/l) hyperinsulinaemic clamp studies were performed after normoglycaemic baseline clamp periods with 15 healthy volunteers (seven male; mean age, 27 years) on two occasions in a randomized single-blind cross-over design. Non-invasive indices of cardiac autonomic activity and hormones were measured at baseline and 1 h after the beginning of hypoglycaemia or control normoglycaemia. Plasma insulin levels and mean HR were similar during both conditions. During hypoglycaemia, there was a 485% increase in plasma adrenaline (epinephrine). A shortening of the pre-ejection period by 45% suggested strong sympathetic cardiac activation. High-frequency (0.15–0.45 Hz) HRV (HR variability) increased, indicating a concomitant increase in parasympathetic tone. Thus, during hypoglycaemia-induced sympathetic cardiac activation in healthy adults, parasympathetic mechanisms are involved in stabilizing mean HR.

scholarly journals Glucose Transporter 8 (GLUT8) Regulates Enterocyte Fructose Transport and Global Mammalian Fructose Utilization

Endocrinology ◽  
2012 ◽  
Vol 153 (9) ◽  
pp. 4181-4191 ◽  
Author(s):  
Brian J. DeBosch ◽  
Maggie Chi ◽  
Kelle H. Moley
Keyword(s):  
Glucose Transporter ◽  
Serum Insulin ◽  
Density Lipoprotein ◽  
Wild Type ◽  
In Vivo Models ◽  
The Metabolic Syndrome ◽  
High Fructose

Enterocyte fructose absorption is a tightly regulated process that precedes the deleterious effects of excess dietary fructose in mammals. Glucose transporter (GLUT)8 is a glucose/fructose transporter previously shown to be expressed in murine intestine. The in vivo function of GLUT8, however, remains unclear. Here, we demonstrate enhanced fructose-induced fructose transport in both in vitro and in vivo models of enterocyte GLUT8 deficiency. Fructose exposure stimulated [14C]-fructose uptake and decreased GLUT8 protein abundance in Caco2 colonocytes, whereas direct short hairpin RNA-mediated GLUT8 knockdown also stimulated fructose uptake. To assess GLUT8 function in vivo, we generated GLUT8-deficient (GLUT8KO) mice. GLUT8KO mice exhibited significantly greater jejunal fructose uptake at baseline and after high-fructose diet (HFrD) feeding vs. wild-type mice. Strikingly, long-term HFrD feeding in GLUT8KO mice exacerbated fructose-induced increases in blood pressure, serum insulin, low-density lipoprotein and total cholesterol vs. wild-type controls. Enhanced fructose uptake paralleled with increased abundance of the fructose and glucose transporter, GLUT12, in HFrD-fed GLUT8KO mouse enterocytes and in Caco2 cultures exposed to high-fructose medium. We conclude that GLUT8 regulates enterocyte fructose transport by regulating GLUT12, and that disrupted GLUT8 function has deleterious long-term metabolic sequelae. GLUT8 may thus represent a modifiable target in the prevention and treatment of malnutrition or the metabolic syndrome.

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