Evaluation of hepatic injury in acute carbon monoxide-poisoned patients in emergency department.

INTRODUCTION: The affinity of hemoglobin for carbon monoxide (CO) is 250 times higher than that for oxygen. Therefore, exposure to CO leads to a reduction in oxygen delivery to tissues, resulting in cellular hypoxia and affects whole body. Hepatic dysfunction in critically ill patients is related to poor outcome, but few studies have been conducted on this subject that occurs after CO poisoning. This study aims to conduct a study of hepatic injury in CO-poisoned patients in emergency department (ED). METHODS: This retrospective observational study collected data from patients who were diagnosed with acute CO poisoning at the ED between June 2011 and May 2018 in local tertiary-care hospital (Wonju, Republic of Korea). The primary end point of this study was to describe the prevalence of hepatic injury in acute CO-poisoned patients. The secondary goals were to investigate the recovery trends of hepatic injury caused by acute CO poisoning and the relation to neurologic outcome and mortality. RESULTS: Eight hundred ninety-four patients were enrolled in the final analysis, 128 cases (14.3%) had subclinical hepatic injury and 15 (1.6%) cases had hepatic injury. The relationship with mortality was not statistically significant. However, the hepatic injury group was higher incidence of intensive care unit admission and other complications. Patients in the hepatic injury group recovered through conservative management within 1 week of being admitted to the ED. CONCLUSIONS: While CO-induced hepatic injury is relatively uncommon, it can be associated with complications and poor neurologic outcome. However, CO-induced hepatic injury was not found to have a statistically significant effect on mortality rate.

Serum ammonia as an early predictor of in-hospital mortality in patients with glufosinate poisoning.

BACKGROUND: The mortality rate associated with human glufosinate poisoning is high. We evaluated the usefulness of serum ammonia and sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation II (APACHE II) scores for early prediction of in-hospital mortality in glufosinate ammonium poisoning. METHODS: A prospectively collected pesticide poisoning registry at a single academic medical center was retrospectively analyzed. Data were collected from consecutive patients diagnosed with glufosinate ammonium poisoning between May 2007 and February 2018. The initial serum ammonia level was defined as the highest serum ammonia level measured within 12 h after emergency department (ED) arrival. The SOFA and APACHE II scores were calculated using data obtained within the first 12 h after ED arrival. The patients were divided into survivor and nonsurvivor groups by in-hospital death status. RESULTS: In total, 110 patients were included. Ten patients (9.1%) died in the hospital despite treatment. Median initial serum ammonia level was significantly higher in the nonsurvivor group than in the survivor group (219 (range: 158-792) versus 100.5 (range: 25-317) µg/dL, p < 0.001). Median SOFA and APACHE II scores in the survivor and nonsurvivor groups were 2 (range: 0-10) versus 5 (range: 1-8) (p = 0.044) and 7 (range: 0-28) versus 16 (range: 8-22) (p = 0.001), respectively. In the multiple logistic regression analysis, the initial serum ammonia level was the only independent predictor (cutoff value: 151 µg/dL). CONCLUSION: An initial serum ammonia level >151 µg/dL was an independent early predictor of in-hospital mortality in glufosinate ammonium poisoning.

The usefulness of the SOFA and APACHE II scoring systems for the early prediction of mortality in patients with dapsone poisoning.

The rate of mortality from dapsone poisoning is high because of the long absorption half-life of dapsone. This study aimed to evaluate the usefulness of the sequential organ failure assessment (SOFA) and acute physiology and chronic health evaluation II (APACHE II) scoring systems for the early prediction of mortality in patients with dapsone poisoning. This is a retrospective and observational study of consecutive patients diagnosed with dapsone poisoning. The SOFA and APACHE II scores were obtained within the first 24 h of admission. Patients were divided into survivor and non-survivor groups. In total, 106 patients were included. The SOFA scores of the survivor and non-survivor groups were 1 (0-8) and 4 (1-10), respectively (p < 0.001). The APACHE II scores of the survivor and non-survivor groups were 9 (1-25) and 14 (3-23), respectively (p < 0.001). Based on these scores and in-hospital mortality cases, the standardized mortality ratios for the APACHE II and SOFA were 1.00 (95% confidence interval (CI): 0.64-1.48) and 1.00 (95% CI: 0.64-1.49), respectively. In the model adjusted for clinically important variables and variables with significant differences between the survivor and non-survivor groups, the area under the curve of the SOFA (0.907; 95% CI: 0.834-0.955) was significantly higher than that of the APACHE II (0.793; 95% CI: 0.703-0.867) (p = 0.008). The SOFA and APACHE II score systems had good discrimination and satisfactory calibration performance in patients with dapsone poisoning. However, the SOFA score was a more useful method in predicting mortality than the APACHE II score.

The usefulness of diffusion-weighted magnetic resonance imaging performed in the acute phase as an early predictor of delayed neuropsychiatric sequelae in acute carbon monoxide poisoning.

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). No previous study has determined whether early use of diffusion-weighted magnetic resonance imaging (DWI) can predict which patients will develop DNS in the acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 17-month period. All included patients with acute CO poisoning underwent DWI to evaluate brain injury within 72 h after CO exposure. DWI was evaluated as follows: (1) presence of pathology, (2) number of pathologies, (3) asymmetry, and (4) location of pathology. Patients were divided into two groups. The DNS group was composed of patients with delayed sequelae, while the non-DNS group included patients with no sequelae. A total of 102 patients with acute CO poisoning were finally enrolled in this study. DNS developed in 10 patients (9.8%). Between the DNS group and the non-DNS group, presence of pathology on DWI and initial Glasgow Coma Scale (GCS) showed significant difference. There was also a statistical difference between the non-DNS group and DNS group in terms of CO exposure time, troponin I, rhabdomyolysis, acute kidney injury, and pneumonia. The presence of pathology in DWI and initial GCS (cutoff: <12) at the emergency department served as an early predictors of DNS.

The relationship between serum ammonia level and neurologic complications in patients with acute glufosinate ammonium poisoning: A prospective observational study.

Glufosinate ammonium poisoning can cause neurological complications even after a symptom-free period. We prospectively investigated the predictors of neurologic complications in acute glufosinate ammonium poisoning and the change of serum ammonia level as a predictor of patient's presence and recovery of neurologic complication. This prospective observational study collected data from consecutive patients diagnosed with acute glufosinate ammonium poisoning between September 2014 and June 2016. Serum ammonia was serially measured. The patients were divided into two groups: the neurologic complication group and the nonneurologic complication group. We also defined 25 other insecticide- or herbicide-poisoned patients as controls. The neurologic complication group included 18 patients (72.0%). The latency period for neurologic complications was within 48-h postingestion. The peak ammonia level was statistically higher in the neurologic complication group than in the control group ( p < 0.001) and the nonneurologic complication groups ( p = 0.001). There was a statistical difference between the nonneurologic complication group and the neurologic complication group ( p = 0.0085) in terms of ingested amount. The peak ammonia was the only predictor for the development of neurologic complications (the optimal cutoff: 90 µg/dL). In patients with mental changes, the mean serum ammonia levels before and after recovery of the mental changes were statistically different ( p = 0.0019). In acute glufosinate ammonium poisoning, serial serum ammonia level measurements are needed and a serum peak ammonia level greater than 90 µg/dL is a predictor of neurologic complications. Also, it is important to treat the hyperammonemia in acute glufosinate ammonium poisoning.

Serum neuron-specific enolase as an early predictor of delayed neuropsychiatric sequelae in patients with acute carbon monoxide poisoning.

Delayed onset of neuropsychiatric symptoms after apparent recovery from acute carbon monoxide (CO) poisoning has been described as delayed neuropsychiatric sequelae (DNS). To date, there have been no studies on the utility of serum neuron-specific enolase (NSE), a marker of neuronal cell damage, as a predictive marker of DNS in acute CO poisoning. This retrospective observational study was performed on adult patients with acute CO poisoning consecutively treated over a 9-month period. Serum NSE was measured after emergency department arrival, and patients were divided into two groups. The DNS group comprised patients with delayed sequelae, while the non-DNS group included patients with none of these sequelae. A total of 98 patients with acute CO poisoning were enrolled in this study. DNS developed in eight patients. The median NSE value was significantly higher in the DNS group than in the non-DNS group. There was a statistical difference between the non-DNS group and the DNS group in terms of CO exposure time, Glasgow Coma Scale (GCS), loss of consciousness, creatinine kinase, and troponin I. GCS and NSE were the early predictors of development of DNS. The area under the curve according to the receiver operating characteristic curves of GCS, serum NSE, and GCS combined with serum NSE were 0.922, 0.836, and 0.969, respectively. In conclusion, initial GCS and NSE served as early predictors of development of DNS. Also, NSE might be a useful additional parameter that could improve the prediction accuracy of initial GCS.

Korean traditional Chungkookjang improves body composition, lipid profiles and atherogenic indices in overweight/obese subjects: a double-blind, randomized, crossover, placebo-controlled clinical trial.

BACKGROUND/OBJECTIVES: Chungkookjang is a Korean representative fermented soybean food. In this study, we investigated the effect of Korean traditional Chungkookjang compared with placebo on body composition, dyslipidemia and risk factors for atherosclerosis in overweight/obese subjects. SUBJECTS/METHODS: This double-blind, randomized, controlled crossover trial was conducted on 120 overweight/obese subjects, aged 19-29 years. Subjects were randomly divided into a Chungkookjang (n=60) or a placebo (n=60) group. After 12 weeks, the groups were crossed over for an additional 12 weeks. During the intervention period, subjects were asked to maintain their usual diet and activity and not to take any functional foods or dietary supplements. The anthropometric measures, lipid profiles and atherogenic indices were determined at baseline and at the end of each 12-week period. RESULTS: The anthropometry measurements, percentage body fat, lean body mass, waist circumference and waist-to-hip ratio of women in the Chungkookjang group were significantly improved compared with the placebo group. Lipid profiles and high-sensitivity C-reactive protein of women in Chungkookjang were significantly improved. The atherogenic indices of apolipoprotein B/apolipoprotein A1 decreased in both the placebo and the Chungkookjang group, and it also decreased below 0.55 for all the men and women in the Chungkookjang group. CONCLUSIONS: In conclusion, these results suggest that supplementation with Chungkookjang may improve body composition and risk factors for cardiovascular disease in overweight and obese adults.

Features of myocardial injury in severe organophosphate poisoning.

BACKGROUND: In organophosphate (OP) poisoning cardiac complications may occur. However, the current body of knowledge largely consists of limited studies, and case reports are mainly on electrocardiogram (ECG) abnormalities. As definite myocardial injury is difficult to assess through ECG, we investigated the prevalence of myocardial injury through cardiac biochemical markers such as troponin I (TnI) in severe OP poisoning. METHODS: We conducted a retrospective review of 99 consecutive OP insecticide poisoning cases that were diagnosed and treated at the emergency department of the Wonju Severance Christian Hospital between March 2008 and December 2013. RESULTS: Based on Namba classification for OP poisoning, there were no patients with mild toxicity, 9 patients (9.1%) with moderate toxicity and 90 patients (90.9%) with severe toxicity. On ECG, normal sinus rhythm was most common, and ST depression and elevation were seen in 11 patients (11.1%). Elevation of TnI within 48 h was seen in 34 patients (34.3%). The median peak level and peak time of TnI were 0.305 (IQR, 0.078-2.335) ng/mL and 15 (IQR 6.9-34.4) hours, respectively. There were differences between patients with normal TnI and elevated TnI in terms of age (yrs), number of patients who were exposed to OP via the oral route, and initial Glasgow Coma Scale (GCS; 58 ± 17 vs. 66 ± 16, p = 0.015, 56 [87.5%] vs. 33 [97.1%], p = 0.048 and 12.0 [IQR, 8.0-15.0] vs. 9.0 [IQR, 5.8-12.0], p = 0.019). CONCLUSIONS: OP can cause direct myocardial injury during the acute early phase in severe OP poisoning. Monitoring of TnI may be needed in severe OP poisoning.

Lactobacillus plantarum LG42 isolated from gajami sik-hae decreases body and fat pad weights in diet-induced obese mice.

AIMS: This study investigated the antiobesity effect of lactic acid bacteria (Lactobacillus plantarum LG42) isolated from gajami sik-hae. METHODS AND RESULTS: Male C57BL/6J mice were divided into four groups (n = 10); NDC (normal diet & DW), HDC (high-fat diet & DW), LGLAB (high-fat diet & Lactobacillus plantarum LG42, 1 × 10(7) CFU per mouse), HGLAB (high-fat diet & L. plantarum LG42, 1 × 10(9) CFU per mouse). After 12 weeks, GLAB supplemented groups showed lower body weight, with a significant reduction in epididymal and back fat. Serum and hepatic triglyceride, serum insulin and leptin levels were significantly lowered in GLAB supplemented groups. The hepatic mRNA expression of PPARα and CPT-I were significantly increased in GLAB groups, whereas the level of ACC, SREBP-1 and LXRα were significantly decreased in GLAB groups compared with HDC group. Additionally, GLAB reduces the expression of PPARγ in the epididymal adipose tissue resulting in inhibition of genes regulated by PPARγ. CONCLUSION: These results suggest that the Lactobacillus plantarum LG42 has antiobesity effects in high-fat-diet-induced obese mice. SIGNIFICANCE AND IMPACT OF THE STUDY: These results may contribute to nutraceutical and food industries in developing functional food and probiotics based therapies for the treatment and prevention of obesity.

Anti-obesity effect of kimchi fermented with Weissella koreensis OK1-6 as starter in high-fat diet-induced obese C57BL/6J mice.

AIMS: In this study, we investigated the anti-obesity effects of kimchi (Korean traditional fermented vegetable) fermented either without starter culture or with a specific starter culture, Weissella koreensis OK1-6. METHODS AND RESULTS: C57BL/6J mice were divided into four groups (n = 7); normal diet, HF (high-fat diet), HF-KC (high-fat diet containing 3% kimchi manufactured without starter) and HF-KCO (high-fat diet containing 3% kimchi manufactured with the starter culture W. koreensis OK1-6). After 12 weeks of dietary intervention, the mice were killed, and serum and tissue samples were examined. Serum and hepatic lipid profile, insulin, leptin concentration and expression level of lipid anabolic genes like peroxisome proliferator-activated receptor γ, stearoyl-CoA desaturase-1, liver X receptor α and SREBP2 were significantly decreased (<0.05) along with body and epididymal fat pad weight in the HF-KCO group compared with the HF-KC and HF group. CONCLUSIONS: These results suggested that kimchi fermented with the starter W. koreensis OK1-6 has anti-obesity effects in HF-induced obese mice. SIGNIFICANCE AND IMPACT OF THE STUDY: These results may contribute to nutraceutical and food industries in developing functional food and probiotics based therapies for the treatment and prevention of obesity.

Intracellular lipid accumulation inhibitory effect of Weissella koreensis OK1-6 isolated from Kimchi on differentiating adipocyte.

AIMS: To investigate the intracellular lipid accumulation inhibitory effect of spent culture medium extract and the cytoplasmic fraction of Weissella koreensis OK1-6 cells isolated from kimchi in differentiating 3T3-L1 cells. METHODS AND RESULTS: Differentiating 3T3-L1 cells were treated with either cytoplasmic fraction of W. koreensis OK1-6 cells or its spent media for 4 days. Both the spent culture medium extract and cytoplasmic fraction of W. koreensis OK1-6 cells significantly decreased the triglyceride concentration and intracellular lipid accumulation in the treated groups compared with the control group. The mRNA expression levels of C/EBP-α, one of the major transcriptional factors involved in adipocyte differentiation, were significantly less expressed in 3T3-L1 cells treated with the spent medium and cytoplasmic fraction. The expressions of aP2, fatty acid synthase (FAS) and SREBP1 genes were also decreased significantly. CONCLUSIONS: These results suggested that W. koreensis OK1-6 could play a crucial role in preventing intracellular lipid accumulation by down-regulating the expression of adipocyte-specific genes C/EBPα, aP2, SREBP1 and FAS. SIGNIFICANCE AND IMPACT OF THE STUDY: These results may contribute to nutraceutical and food industries in developing probiotic-based therapies for the treatment and prevention of obesity.

Factors associated with early onset post-traumatic syringomyelia.

STUDY DESIGN: Retrospective study. OBJECTIVES: To identify factors associated with the development of early onset post-traumatic syringomyelia within 5 years of spinal cord injury. SETTING: Department of Rehabilitation Medicine, Pusan National University School of Medicine, Korea. METHODS: We retrospectively examined the records of 502 patients with traumatic cervical or thoracic spinal cord injury who underwent follow-up magnetic resonance imaging (MRI) examinations more than once a year for at least 5 years. Patients were assessed in terms of the neurological level of injury, the severity of initial spinal cord injury, the use of surgery and the extent of spinal canal involvement. The latter was evaluated by calculating the shortest antero-posterior diameter of the injured vertebral canal and the spinal reserve capacity as shown on MRI at the time of trauma onset and at the time of diagnosis of syringomyelia. RESULTS: Syringomyelia developed within 5 years in 37 (7.3%) of the 502 patients. The mean age of these 37 patients was 44.6 years (range, 17-67 years) and the mean interval from spinal cord injury to onset of syringomyelia was 38.8 months (range, 2-54 months). The development of post-traumatic syringomyelia within 5 years was not significantly related to the severity or level of injury, the use of spinal surgery or the extent of spinal canal encroachment (P≥0.05 for each comparison). CONCLUSION: Early onset syringomyelia occurring within 5 years after spinal cord injury was not associated with neurological injury level, severity of injury, the use of spinal surgery or canal encroachment.

Caffeine as a lipolytic food component increases endurance performance in rats and athletes.

Caffeine is one of the famous ergogenic aids in the athletic field. Caffeine has been known to stimulate lipolysis that spares stored glycogen utilization during moderate intensity exercise. Therefore, we investigated the effects of caffeine ingestion on exercise performance in rats and athletes. Rats were administered the caffeine (6 mg/kg) 1 h prior to the exercise then were run on a treadmill at a speed of 20 m/min. They were decapitated at 0 min, 30 min, 60 min of exercise, and exhausted time point. Human subjects ingested the caffeine (5 mg/kg) 1 h prior to the exercise. They exercised on a cycle ergometer at 60% of their VO2max for 45 min, and then the exercise intensity was increased to 80% of their VO2max until exhaustion. Blood and breathing gas samples were collected and calculated every 10 min during exercise. Respiratory exchange ratio of the caffeine trial was significantly lower than that of the placebo trial in the athletes' study (p<0.05). Blood free fatty acid (FFA) levels in studies of both rats and athletes were increased by caffeine ingestion during exercise (p<0.05). Blood lactate levels were also increased during exercise in both rats and athletes (p<0.05). Increased FFA and glycerol concentrations reduced glycogen utilization during exercise compared with placebo group in rats. In addition, endurance time to exhaustion was significantly increased by the caffeine ingestion in both rats and athletes (p<0.05). These results suggest that the caffeine ingestion enhanced endurance performance resulting from spare stored glycogen with increasing lipolysis from adipose tissues and fat oxidation during exercise both in rats and in athletes.

L-Carnitine changes the levels of insulin-like growth factors (IGFs) and IGF binding proteins in streptozotocin-induced diabetic rat.

This study investigated the effects of L-carnitine on insulin-like growth factor-I/II (IGF-I/II) and insulin-like growth factor binding proteins (IGFBPs) in streptozotocin (STZ)-induced diabetic rats. Each rat in the three L-carnitine-treated groups was injected subcutaneously with L-carnitine, 50 (D50), 100 (D100), or 200 (D200) mg/kg body weight every other day for four weeks, and animals in normal (N) and diabetic (DM) groups received saline by the same method. Diabetic rats had significantly lower carnitine concentrations in serum and liver compared with normal rats. Total carnitine concentrations were increased dose-dependently by carnitine treatment. Total IGF-I in serum from diabetic rats was increased dose-dependently by carnitine treatment, but was statistically significant only in the D200 group. The expression of liver IGF-I mRNA was lower in diabetic rats than in normal rats and increased by L-carnitine treatment. L-Carnitine treatment of diabetic rats had no effect on the levels of IGF-II in serum, liver, and kidney. Although the levels of IGF-II in serum and kidney of diabetic rats were increased in comparison with normal rats, IGF-II mRNA was not expressed in liver. Diabetic rats had markedly lower IGFBP-3 than normal rats did, and IGFBP-3 was increased by L-carnitine treatment. These results demonstrate that L-carnitine treatment of diabetic rats modulates the IGFs/IGFBPs axis. Especially note-worthy is that L-carnitine at a dose of 200 mg/kg/48 h for four weeks was able to restore serum total IGF-I in STZ-induced diabetic rats to nearly normal levels.

Effects of carnitine coingested caffeine on carnitine metabolism and endurance capacity in athletes.

The purpose of this study was to examine whether caffeine (CAF), carnitine (CAR), or CAF+CAR mixture administration affects exercise endurance time via carnitine metabolism. Water (CON), CAF, CAR, or CAF+CAR mixture was administered to five male rugby athletes participating in this study by a randomized double-blind fashion who were made to ride a cycle ergometer for exercise. The CAF effect on exercise endurance time was small, but the CAR trial significantly increased the exercise endurance time compared with CON trial; a further CAF+CAR mixture trial had greater effects on the exercise endurance time than those of a CON, CAF, or CAR trial. A CAR or CAF+CAR mixed trial increased urinary nonesterified carnitine (NEC) and total carnitine (TCAR), but no changes were observed in acid-soluble acylcarnitine (ASAC) and acid-insoluble acylcarnitine (AIAC) excretion. A CAR or CAF+CAR mixed trial resulted in higher levels of plasma NEC, ASAC, and TCAR fractions than the CON and CAF trials did on exhaustion time. Total cholesterol, triglyceride, and free fatty acid in blood were significantly increased at exhaustion time, but they were not affected in the CAF or the CAR trial. These results suggest that carnitine ingestion could promote fat oxidation, resulting in higher endurance performance in athletes, and especially these ergogenic effects of carnitine coingested with caffeine may be greater than those of carnitine alone.

Auto-ADP-ribosylation of NAD glycohydrolase from Neurospora crassa.

NAD glycohydrolase (NADase; EC 3.2.2.5) is an enzyme that catalyzes hydrolysis of NAD to produce ADP-ribose and nicotinamide. We recently demonstrated that self-inactivation of NADase from rabbit erythrocytes was due to an auto-ADP-ribosylation. In the present study, a mechanism of self-inactivation of NADase from Neurospora crassa by its substrate was investigated by using intact mycelia of N. crassa and purified NADase, which had molecular characteristics different from mammalian NADases. The results suggested that inactivation of NADase from N. crassa was also due to an auto-ADP-ribosylation. These findings indicate that the auto-modification of NADase is one of the universal phenomena to regulate enzyme functions.

Acetylcarnitine-mediated inhibition of ethanol oxidation in hepatocytes.

Carnitine-mediated prevention of ethanol-induced hepatic steatosis is related to the attenuation of ethanol metabolism by carnitine in the intact rat. Although carnitine retards ethanol oxidation in the intact animal, the in vitro activities of ethanol-metabolizing enzymes remain unaltered. Therefore, hepatocytes were targeted to understand the mechanism of carnitine effect on ethanol metabolism. Rat hepatocytes were isolated by a collagenase-perfusion technique and incubated in albumin-containing medium with ethanol in the presence or absence of added carnitine or related compounds. Ethanol oxidation was determined by the loss of ethanol as well as by the products formed. The rate of ethanol oxidation in the presence of carnitine was one-half the rate in the absence of carnitine (14 vs. 25 nmol.min-1.million-1 cells). It took 100 times the concentration of carnitine to equal the maximal inhibition produced by acetylcarnitine and the effect of acetylcarnitine was without a lag time. It is concluded that acetylcarnitine is the mediator of carnitine inhibition of ethanol oxidation.

Acetylcarnitine inhibits alcohol dehydrogenase.

Carnitine and acetylcarnitine are used as dietary supplements and as therapeutic agents. Carnitine attenuates ethanol metabolism in intact animals but the in vitro activities of alcohol dehydrogenase (ADH), microsomal ethanol oxidizing system (MEOS) or catalase are not significantly altered by carnitine. Since acetylcarnitine was a far more potent inhibitor of ethanol oxidation than carnitine in hepatocytes, the activities of rat liver ADH and MEOS were determined with or without acetylcarnitine. The activity of ADH, not MEOS, was significantly inhibited by acetylcarnitine at NAD: acetylcarnitine < or = 1. The inhibition is of a competitive nature where acetylcarnitine competes with NAD+ (Ki = 135 mumol.L-1). This finding is unique in that this is the first report of this function of acetylcarnitine and it is a novel interaction between two important nutrients, niacin and carnitine.

Carnitine prolongs the half-life of ethanol in broilers.

The object was to determine if carnitine attenuated ethanol metabolism in broilers similar to that reported in the rats. Two groups (n = 5) of 5-week-old broilers were given for 10 days the feed with or without 0.5% L-carnitine supplement. A single oral dose of ethanol on day 8 was followed by serial blood samples which were analysed for ethanol. Another dose of ethanol was given on day 10 and 2 hr later, plasma and liver were collected and analysed for ethanol, total lipid, triglycerides and carnitine. The carnitine supplemented diet prolonged the half-life of ethanol due to attenuation of ethanol metabolism which is similar to that reported earlier in rodents. The increases in plasma and hepatic acylcarnitines indicate that supplementary carnitine lessens the load of free acyl groups in the liver by eventual oxidation or excretion.

Opposite effects of dietary saturated and unsaturated fatty acids on ethanol-pharmacokinetics, triglycerides and carnitines.

OBJECTIVE: The objective of this study was to determine the effects of saturated fatty acid (SFA) and unsaturated fatty acid (UFA) diets on ethanol pharmacokinetics. Hepatic ADH and plasma carnitines were also evaluated as possible indicators of the mechanism involved. METHODS: Sprague-Dawley male rats were fed modified AIN76 diets containing 10% coconut oil (SFA) or corn oil (UFA) for 120 days. A single dose (3 g/kg bw) of ethanol (13% solution) was orally administered using a gastric canula on day 30, 90, 105 and 120. Tail vein blood samples were collected at various intervals following ethanol dose and were analyzed for blood-ethanol concentration (BEC). In an analogous trial rats were given these diets for 70 days and blood samples were collected on day 35 and 63 for triglycerides, cholesterol and carnitine determination. The animals were killed on day 70 to collect liver for ADH determination. RESULTS: Compared to the UFA group, the SFA group exhibited significantly higher BEC, larger area under the curve, longer half-life of ethanol, and lower rates of ethanol elimination. Plasma carnitines were also higher in the SFA vs UFA group. However, hepatic ADH activity was not different between the groups. CONCLUSION: Dietary SFA protects liver from alcohol injury by retarding ethanol metabolism, and carnitine may be involved.