Increased ethanol consumption and blood ethanol levels in rats with portacaval shunts

1985 ◽  
Vol 248 (3) ◽  
pp. G287-G292
Author(s):  
J. R. Martin ◽  
H. Porchet ◽  
R. Buhler ◽  
J. Bircher

In a series of experiments, it was demonstrated that male rats with end-to-side portacaval shunts (PCS) consumed more ethanol and exhibited higher blood ethanol levels than sham-operated control animals in chronic tests with 2% ethanol and water ad libitum. Ethanol intake in the 6 h prior to blood sampling was 2-5 times and blood ethanol 10-50 times higher in PCS than control rats. These effects were not due to the feminization of male rats occurring after a PCS, since female PCS rats exhibited comparable increases of ethanol intake and blood ethanol. In both sexes ethanol elimination rate and alcohol dehydrogenase activity per total liver were lower after PCS than in control rats, explaining the disproportionate increase in blood ethanol relative to ethanol intake. Interestingly, ethanol intake was not abnormal in PCS rats fed a low-protein, low-tryptophan diet (corn) alone or as a supplement to the usual chow diet. Such dietary modulation of ethanol preference in this animal model of chronic liver dysfunction merits further attention.

1980 ◽  
Vol 58 (3) ◽  
pp. 231-236 ◽  
Author(s):  
Daya R. Varma

Influence of dietary protein on the disposition and metabolism of phenylbutazone was investigated in male rats fed ad libitum a 21% (control) or a 5% (low) protein diet for 3 weeks. Phenylbutazone and its metabolites were assayed by high-pressure liquid chromatography. Dietary protein deficiency was associated with a decrease in the conversion of phenylbutazone into oxyphenbutazone by 9000 × g liver supernatant of protein-deficient rats. Also, dietary protein deficiency was associated with a decrease in the urinary excretion of various metabolites of phenylbutazone, namely, oxyphenbutazone γ-hydroxyphenylbutazone, β-hydroxyphenylbutazone, p,γ-dihydroxyphenylbutazone, and an unknown metabolite (not identified). Pretreatment with phenobarbitone or phenylbutazone led to an increase in the hepatic metabolism of phenylbutazone and the urinary excretion of various metabolites in both groups of animals. Within 5 min after an injection of phenylbutazone, plasma contained oxyphenbutazone; the area under the curve of oxyphenbutazone was significantly greater in protein-deficient rats than in controls possibly due to a greater accumulation. It is concluded that dietary protein deficiency is associated with a decrease in the disposition and metabolism of phenylbutazone in rats.


1978 ◽  
Vol 40 (1) ◽  
pp. 103-113 ◽  
Author(s):  
Leena Pekkanen ◽  
K. Eriksson ◽  
Marja-Liisa Sihvonen

1. The voluntary ethanol consumption, ethanol elimination rate and blood acetaldehyde level after intraperitoneal injection of ethanol were studied in rats receiving diets with highly imbalanced proportions of dietary protein, carbohydrate and fat.2. The rats, which received the low-protein diet containing 0.05 of the total energy as protein, 0.80 as carbohydrate and 0.15 as fat, drank only approximately half as much ethanol as did the control group, which received 0.30 of its total food energy from protein, 0.55 from carbohydrate and 0.15 from fat. Ethanol elimination rate in the low-protein group was decreased and the blood acetaldehyde level after ethanol injection was markedly increased.3. On the high-fat diet, which contained 0.30 of the total energy from protein, 0.05 from carbohydrate and 0.65 from fat, the rats drank significantly more ethanol than did the rats on the control diet; their ethanol elimination rate was decreased but their blood acetaldehyde level was not affected.4. In conclusion, the strong decrease in voluntary ethanol drinking by the low-protein group may have been caused by the increased acetaldehyde accumulation in the blood, but a particularly low blood acetaldehyde level was not one of the factors inducing excessive ethanol drinking in the high-fat group.


2007 ◽  
Vol 97 (1) ◽  
pp. 104-110 ◽  
Author(s):  
Heidi Normanton ◽  
Jos G. M. Houdijk ◽  
Neil S. Jessop ◽  
Dave P. Knox ◽  
Ilias Kyriazakis

Lactating rats experience a breakdown of immunity to parasites, i.e. they carry larger worm burdens after re-infection compared to their non-lactating counterparts. Feeding high-protein foods to lactating rats results in reduced worm burdens. This could be attributed to changes in gastrointestinal environment or to overcoming effects of nutrient scarcity on host immunity. The latter hypothesis was addressed through a manipulation of nutrient demand by manipulating litter size. Twenty-three rats were immunized prior to mating and re-infected on day 2 of lactation with 1600 infective Nippostrongylus brasiliensis larvae. From parturition onwards, rats received ad libitum a low-protein food (100 g crude protein/kg). Litter sizes were standardised to nine (LS9), six (LS6) or three (LS3) pups, by day 2 of lactation. After a further 10 d, LS9 and LS6 rats carried more worms than LS3 rats. However, feeding treatments did not affect concentrations of mucosal inflammatory cells. Achieved feed intake did not differ consistently between the treatment groups. However, LS9 and LS6 rats lost weight, whilst LS3 rats gained weight during lactation. The results support the view that resistance to N. brasiliensis is sensitive to changes in nutrient demand, and the improved resistance to N. brasiliensis is likely due to effects of overcoming nutrient scarcity on host immunity.


2003 ◽  
Vol 27 (9) ◽  
pp. 1459-1462 ◽  
Author(s):  
S??mia H. Zidi ◽  
Klas Linderborg ◽  
Satu V??kev??inen ◽  
Mikko Salaspuro ◽  
Kalle Jokelainen

1959 ◽  
Vol 196 (5) ◽  
pp. 965-968 ◽  
Author(s):  
Clarence Cohn ◽  
Dorothy Joseph

Normal young adult male rats were either force-fed or allowed to eat ad libitum a moderate carbohydrate diet for 3–4 weeks. The force-fed animals were given either the amount of diet consumed by the animals eating ad libitum (pair-fed) or 80% of this amount (underfed). After a 2-week period of observation, we found that the rats eating ad libitum gained 65 gm of body weight, the pair-fed, force-fed 62 gm and the underfed, force-fed 40 gm. On the basis of the water, fat and protein content of the skin, viscera and carcass of control animals killed at the beginning of the feeding regimen and of similar constituents of the experimental animals after 2 weeks of feeding, the composition of the newly formed tissues of the various groups of animals consisted of the following: a) the rat with free access to food—water = 67.8%, fat = 7.8% and protein = 22.4%; b) the pair-fed, force-fed animal—water = 55.5%, fat = 23.6% and protein = 17.7%; c) the underfed, force-fed animal—water = 64.4%, fat = 7.9% and protein = 20.0%. The ratio of calories retained in newly formed tissue to the calories ingested over the 2-week period was 11.9% for the animals eating ad libitum, 20.6% for the pair-fed, force-fed animals and 9.5% for the underfed, force-fed rats. Force feeding appears to change intermediary metabolic pathways in the direction of increased ‘efficiency’ with resultant greater fat deposition.


Alcohol ◽  
2019 ◽  
Vol 76 ◽  
pp. 65-71 ◽  
Author(s):  
Jessica Hollander ◽  
Megan McNivens ◽  
Ricardo M. Pautassi ◽  
Michael E. Nizhnikov

2021 ◽  
Vol 12 ◽  
Author(s):  
Chloe G. Henderson ◽  
Damian L. Turner ◽  
Steven J. Swoap

Alternate day fasting (ADF) induces weight loss and improves various markers of health in rodents and humans. However, it is unclear whether the benefits of ADF are derived from the lower caloric intake of ADF or from the 24-h fasting period. Therefore, this study directly compared selected markers for health – such as glucose control, body weight, liver triglycerides, T cell frequencies, and others – in high-fat (60% calories from fat) diet-induced obese mice subjected to either ADF or caloric restriction (CR). Obese mice were randomly assigned to one of four groups: (1) ADF: remained on the high-fat diet, but fed on alternate days (n = 5), (2) PF: remained on the high-fat diet, but pair-fed to the ADF group (n = 5), (3) LF: moved to a chow ad libitum diet (n = 5; 17% calories from fat), and (4) HF: remained on the high-fat ad libitum diet (n = 5). An additional group of non-obese mice maintained on a chow diet since weaning were used as controls (CON: n = 5). After 10 weeks, ADF, PF, and LF mice ate fewer kcals, had a lower body mass, had smaller epididymal fat pads, improved glucose tolerance, and had a lower hepatic triglyceride content relative to HF mice (p < 0.05), but none reached that of CON mice in these measures. T cell frequencies of the spleen, blood, and mesenteric lymph nodes were reduced in ADF, PF, and HF compared to the CON group. Importantly, there were no significant differences between the ADF and PF groups in any of the measurements made in the current study. These data suggest that ADF, PF, and LF diets each lead to improved markers of health relative to high-fat diet-induced obese mice, and that the caloric restriction associated with ADF is the major factor for the noted improvements.


2021 ◽  
Vol 15 (1) ◽  
pp. 3-14
Author(s):  
T. S. Petryn ◽  
◽  
M. R. Nagalievska ◽  
N. O. Sybirna ◽  
◽  
...  

Introduction. Metabolic syndrome is a cluster of metabolic abnormalities that includes hypertension, central obesity, insulin resistance and atherogenic dyslipidemia. Given the wide geographical distribution and growing number of people suffering from this disease, there is an urgent need in developing animal models that would accurately reproduce the development of all symptoms of human metabolic syndrome (insulin resistance, dyslipidemia, obesity and hypertension). The most cost-effective method related to the real causes of metabolic syndrome is the use of different types of diets. Materials and Methods. The study was performed on white outbred male rats about 6 months old and weighing 300–400 g. The metabolic syndrome was induced by high-fat and high-carbohydrate diets. The lipid-enriched diet involved the consumption of regular chow diet for laboratory animals with additional fat content (40 % by weight of chow). The source of additional lipids was olive oil, which is rich in monounsaturated fatty acids (MUFAs). Animals on the diet enriched in carbohydrates together with regular chow diet for laboratory animals consumed 10 % fructose solution instead of drinking water. Glucose tolerance tests were conducted and areas under the glycemic curves were calculated. We determined the content of glycated hemoglobin and glucose concent­ration, the concentration of low-density lipoproteins (LDL), high-density lipoproteins (HDL), triglycerides and cholesterol in the blood plasma of rats. Results. The development of metabolic syndrome induced by an excessive consumption of carbohydrates and lipids for 42 days was accompanied by impaired glucose tolerance, increased glycosylated hemoglobin, triglycerides and cholesterol concentrations, as well as a decreased HDL content. An increase in the concentrations of LDL and activity of paraoxonase were found due to the induction of the pathological condition by an excessive fat intake, while a high carbohydrate diet caused a decrease in paraoxonase activity. Conclusions. The use of fructose for 42 days causes the most pronounced manifestations of the studied pathology. The use of this model will allow determining the biochemical and molecular changes that accompany the development of this pathological condition. It will also facilitate the development and evaluation of the effectiveness of new therapeutic approaches to the treatment of metabolic syndrome.


1992 ◽  
Vol 285 (1) ◽  
pp. 167-172 ◽  
Author(s):  
Y Zhao ◽  
J Jaskiewicz ◽  
R A Harris

Feeding clofibric acid to rats caused little or no change in total activity of the liver branched-chain 2-oxo acid dehydrogenase complex (BCODC). No change in mass of liver BCODC was detected by immunoblot analysis in response to dietary clofibric acid. No changes in abundance of mRNAs for the BCODC E1 alpha, E1 beta and E2 subunits were detected by Northern-blot analysis. Likewise, dietary clofibric acid had no effect on the activity state of liver BCODC (percentage of enzyme in the dephosphorylated, active, form) of rats fed on a chow diet. However, dietary clofibric acid greatly increased the activity state of liver BCODC of rats fed on a diet deficient in protein. No stable change in liver BCODC kinase activity was found in response to clofibric acid in either chow-fed or low-protein-fed rats. Clofibric acid had a biphasic effect on flux through BCODC in hepatocytes prepared from low-protein-fed rats. Stimulation of BCODC flux at low concentrations was due to clofibric acid inhibition of BCODC kinase, which in turn allowed activation of BCODC by BCODC phosphatase. Inhibition of BCODC flux at high concentrations was due to direct inhibition of BCODC by clofibric acid. The results suggest that the effects of clofibric acid in vivo on branched-chain amino acid metabolism can be explained by the inhibitory effects of this drug on BCODC kinase.


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