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Query: UMLS:C0015695 (fatty liver)
 13,941 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Previous research has shown that a combination of feed restriction and dietary 1,3-butanediol starting at 14 d post-partum resulted in fatty liver and ketosis. Sixteen multiparous Holstein cows were used to determine effects of feed restriction or 1,3-butanediol as separate treatments. Treatments during d 14 to 42 postpartum were 1) control (ad libitum intake), 2) 20% feed restriction, or 3) control plus dietary 1,3-butanediol (5.5% of DM). From d 43 to 56, cows assigned to treatments 2 and 3 received a combination of feed restriction and butanediol. One cow on treatment 2 developed ketosis, but not fatty liver, after only 4 d of feed restriction. No other cows developed fatty liver or ketosis. Both treatments decreased milk production compared with controls. Feed restriction increased the extent of negative energy balance and caused transient increases in concentrations of NEFA, acetate, and beta-hydroxybutyrate in plasma. Concentrations of beta-hydroxybutyrate and insulin in plasma were increased by butanediol, which is a potent ketone body precursor. Concentration of glycogen in liver was less in feed-restricted cows, whereas glycogen and total lipid were greater in cows given butanediol separately. Gluconeogenic capacity of liver slices was not different among groups. Addition of 1,3-butanediol to in vitro incubation media decreased oxidation of propionate to CO2. Neither feed restriction nor dietary 1,3-butanediol as separate treatments induced the fatty liver and ketosis observed in earlier experiments in which the two treatments were given together.
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PMID:Metabolic changes in blood and liver of dairy cows during either feed restriction or administration of 1,3-butanediol. 178 95

An increase in liver fat concentration during the peripartum period is extremely common in dairy cows and, to some degree, is probably normal. When severe, it is associated with clinical problems including increased morbidity and mortality and reduced breeding efficiency. Fatty liver develops when serum NEFA concentrations rise and hepatic uptake of NEFA exceeds the liver's ability to synthesize and secrete lipoproteins. In most cases, hepatic lipid accumulation appears to commence prepartum, in association with rising serum NEFA concentrations and declining serum lipoprotein concentrations. Commonly used clinicopathologic tests of liver function do not yield clearly abnormal results except in animals with extremely high concentrations of liver fat. Clinically useful estimates of hepatic lipid concentration can be obtained in the field by determining the buoyancy of needle biopsy samples in liquids of various specific gravities. Clinically ill animals with liver fat concentrations of greater than 35 per cent by weight have a poor prognosis, and those that do survive will have a protracted convalescence. Treatment of dairy cows with clinical fatty liver should be aimed at reducing further adipose lipid mobilization and promoting hepatic lipoprotein synthesis; however, protocols for therapy have not as yet been evaluated critically. Prevention of fatty liver is more rewarding than treatment. Dry cows should be maintained in a moderately fat condition and fed high-quality, palatable feeds in amounts necessary to met or slightly exceed their energy requirements. Free-choice feeding of high-energy feeds should be avoided in late lactation and during the nonlactating period.
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PMID:Fatty liver in dairy cows. 306 11

Effects of Panax ginseng on plasma and hepatic lipids were investigated in the high cholesterol diet-fed rats and in patients with hyperlipidemia. Oral administration of red ginseng powder reduced plasma total cholesterol, triglyceride and NEFA, while plasma HDL-cholesterol was elevated. Platelet adhesiveness was also reduced by ginseng administration. The plasma lipid-improving actions were also observed in patients with hyperlipidemia. Hepatic cholesterol and triglyceride contents were decreased and phospholipid increased by ginseng administration in the high cholesterol diet-fed rats, corresponding to improvement of the fatty liver.
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PMID:Serum HDL-cholesterol-increasing and fatty liver-improving actions of Panax ginseng in high cholesterol diet-fed rats with clinical effect on hyperlipidemia in man. 666 Feb 21

Nine pregnant, nonlactating cows were used to monitor liver triglycerides before and after parturition. Estimates were made of the contribution of depressed feed intake and parturition to plasma NEFA concentrations and development of fatty liver. Liver biopsies and plasma samples were obtained on d 19, 10, 5, 3, and 1 prior to calving and on d 1, 7, 14, and 21 after calving. Depression of DMI started on d 2 prior to calving and was 40% of DMI on d 3 prior to depression of feed intake. Elevation of plasma NEFA concentrations started prior to DMI depression, on d 5 before parturition. Liver triglyceride infiltration did not occur until the concentration of plasma NEFA was maximized on d 1 after calving. This result implicated the acute rise in NEFA at calving as a contributing factor to triglyceride accumulation in the liver. The increasing plasma glucose and decreasing plasma BHBA prior to calving may have reflected metabolic changes toward gluconeogenesis. Liver glycogen decreased 70% during the final 19 d prior to calving. Hepatic triglyceride infiltration (7.7% DM basis) on d 1 post-partum and duration of DMI depression prepartum were less severe than those observed in previous studies. Frequent liver biopsies did not affect DMI.
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PMID:Peripartum liver triglyceride and plasma metabolites in dairy cows. 808 10

Plasma NEFA concentrations increase prior to and at parturition, resulting in increased fatty acid uptake by the liver, fatty acid esterification, and triglyceride storage. Liver triglyceride concentration increases four- to fivefold between d 17 prior to calving and d 1 following calving. Increases in liver triglyceride following calving do not appear to be dramatic. Severity of fatty liver 1 d postpartum is correlated negatively with feed intake 1 d prepartum. Export of newly synthesized triglyceride as very low density lipoprotein occurs slowly in ruminants and is a major factor in the development of fatty liver. Nutritional strategies to minimize the elevation in plasma NEFA prior to calving results in lower liver triglyceride at calving. Fatty liver probably precedes clinical spontaneous ketosis. Liver triglyceride to glycogen ratio may be used to predict susceptibility of cows to ketosis. Consequently, strategies to reduce liver triglyceride at calving may decrease incidence of ketosis. Research to determine methods to reduce fatty acid delivery to the liver or to enhance hepatic export of very low density lipoprotein near calving is warranted. Identification of the cause for the slow rate of assembly and secretion of hepatic very low density lipoprotein in ruminants will be required to assess the feasibility of increasing export of very low density lipoprotein.
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PMID:Etiology of lipid-related metabolic disorders in periparturient dairy cows. 813 93

Plasma glucose concentration during late gestation was thought to be important for the development of fatty liver near parturition. Thirteen multiparous cows were given a 1-L oral drench of propylene glycol once daily beginning 10 +/- 3.6 d prepartum until parturition. Eleven control cows received a 1-L water drench. Plasma glucose increased following propylene glycol administration. Plasma NEFA concentration was 403 and 234 microM, and plasma insulin concentrations were .354 and .679 ng/ml, for control cows and cows treated with propylene glycol measured from 1 to 7 d prepartum. Plasma NEFA tended to be lower in cows treated with propylene glycol from 1 to 21 d postpartum. Prepartum propylene glycol administration reduced hepatic triglyceride accumulation by 32 and 42% at 1 and 21 d postpartum, respectively. Prepartum plasma BHBA was reduced during propylene glycol administration. Prepartum plasma glucose, NEFA, BHBA, and insulin were strongly correlated with liver triglyceride at 1 d postpartum (r = -.49, .45, .36, and -.49, respectively). Pre- and postpartum DMI were not affected by treatment. Milk production and composition measured through 21 d postpartum were not different between groups.
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PMID:Effect of prepartum propylene glycol administration on periparturient fatty liver in dairy cows. 822 21

We studied development of fatty liver in high producing dairy cows with free access to feed during the dry period and thus showed the combined effects of parturition and prepartum overfeeding. Postpartum liver triacylglycerol concentrations at 1 wk postpartum, as measured in liver biopsies, had increased more than 6-fold, which was preceded or accompanied by an increase in plasma NEFA concentrations. Concentrations of hepatic phospholipid changed only slightly. The amounts of total lipids in serum, very low density lipoproteins, and high density lipoproteins significantly decreased by .5 wk after parturition, and concentrations of high density lipoproteins rose steadily. The pattern was similar for concentrations of total cholesterol and phospholipid in serum. Total lipid concentrations in low density lipoproteins were not altered after parturition. The activity of microsomal phosphatidate phosphohydrolase in the liver showed a transient increase at .5 wk after calving, but activity of microsomal glycerolphosphate acyltransferase remained relatively constant. The activities of diacylglycerol acyltransferase had increased about twice at 1 wk after calving and remained at this high level until at least 4 wk after parturition. The rise in activity of diacyglycerol acyltransferase was probably a response to the extra influx of fatty acids to channel them into triacylglycerol. Activities of microsomal cholinephosphate cytidylyltransferase initially increased after calving and then decreased slightly. Activities of hepatic choline kinase had increased after calving. This study indicates that hepatic triacylglycerol accumulates because of the increased hepatic uptake of NEFA and the simultaneous increase in activity of diacylglycerol acyltransferase.
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PMID:Time trends of plasma lipids and enzymes synthesizing hepatic triacylglycerol during postpartum development of fatty liver in dairy cows. 859 5

Limited secretion of very low density lipoproteins (VLDL) in dairy cows is strongly related to fatty liver and other metabolic disorders in the early postpartum. Currently, there is limited information on which roles apolipoprotein B(100) (ApoB(100)), apolipoprotein E (ApoE), and microsomal triglyceride transfer protein (MTP) play in that VLDL limitation. To our knowledge, no studies have simultaneously measured ApoB(100), ApoE, and MTP mRNA in periparturient dairy cows. Therefore, a trial was conducted to assess liver gene expression of these proteins in transition dairy cows and to evaluate the relationships between their expression and metabolic status. Eight multiparous Holstein cows were monitored during the transition period. To evaluate metabolic and nutritional status, body condition score was registered, and plasma indexes of energy metabolism and VLDL were determined from 35 d before to 35 d after calving. Liver biopsies were performed on d -35, 3, and 35 relative to day of calving, and gene expression of ApoB(100), ApoE, and MTP were determined on liver tissue. Body condition, plasma glucose and VLDL decreased, and plasma NEFA and BHBA increased after calving. Compared with values of d -35, on d 3 after calving the ApoB(100) mRNA synthesis was lower, whereas MTP and ApoE mRNA abundance were higher. Negative correlation (r = -0.57) between plasma NEFA concentration and ApoB(100) mRNA abundance, and positive correlation between ApoB(100) mRNA abundance and plasma cholesterol (r = 0.65) and plasma albumins (r = 0.52) were detected at 3 d postpartum. Data on changes of gene expression of the 3 main proteins involved in the regulation of synthesis and secretion of VLDL in the liver suggest that decreased mRNA for ApoB(100) may be consistent with decreased synthesis and/or secretion of VLDL from liver during the periparturient period.
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PMID:Abundance of mRNA of apolipoprotein b100, apolipoprotein e, and microsomal triglyceride transfer protein in liver from periparturient dairy cows. 1537 48

Fatty liver (i.e., hepatic lipidosis) is a major metabolic disorder of many dairy cows in early lactation and is associated with decreased health status and reproductive performance. In severe cases, milk production and feed intake are decreased. Therefore, a practical preventative or an efficacious treatment of fatty liver could save millions of dollars yearly in treatment, replacement, and production losses for dairy farmers. Fatty liver develops when the hepatic uptake of lipids exceeds the oxidation and secretion of lipids by the liver, which usually is preceded by high concentrations of plasma NEFA mobilized from adipose tissue. Excess lipids are stored as triacylglycerol in the liver and are associated with decreased metabolic functions of the liver. Liver can be categorized into normal liver or mild, moderate, or severe fatty liver; the latter can be subdivided further into nonencephalopathic severe fatty liver and hepatic encephalopathy. Insufficient or unbalanced dietary intake, obesity, and elevated estrogen concentrations are involved in the etiology of fatty liver, which is associated with greater incidence of dystocia, diseases, infections, and inflammations. Because even mild fatty liver is associated with decreased health status and reproductive performance of dairy cows, prevention of fatty liver by supplying cows with sufficient nutrients and a clean and health-promoting environment in the peripartal period would reduce production losses of cows more than would any treatment of fatty liver. This, however, might not be enough for cows that are obese or do not eat well, had calving difficulties or twins, have metabolic or infectious diseases, or are in severe negative energy balance because of high milk production immediately after calving. Potential and commonly used preventatives, as well as treatments, are discussed in the review. Currently, detection of fatty liver is possible only by minor surgery. Ultrasonic techniques offer a potential tool to noninvasively detect fatty liver. Future gene-array and proteomic studies may provide means to detect early molecular events in the etiology of fatty liver plus their connection with immune function and reproductive performance so that more effective treatments and preventatives of fatty liver can be developed. Such advances hopefully will make fatty liver a problem of the past.
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PMID:Invited review: pathology, etiology, prevention, and treatment of fatty liver in dairy cows. 1537 89

The pathway for oxidation of energy involves a balanced oxidation of C2 and C3 compounds. During early lactation in dairy cattle this C2/C3 ratio is out of balance, due to a high availability of lipogenic (C2) products and a low availability of glycogenic (C3) products relative of the C2 and C3 products required for milk production. This review compares studies which manipulated dietary energy source and shows that dietary energy source can affect the balance of the C2/C3 ratio, as indicated by plasma NEFA, beta-hydroxybutyrate (BHBA) and glucose levels. It is shown that glycogenic nutrients increase glucose and insulin concentrations and decrease NEFA and BHBA plasma levels. Extra lipogenic nutrients elevate NEFA and BHBA and decrease plasma glucose concentrations. Lipogenic nutrients generally increase milk fat percentage and decrease milk protein percentage, suggesting a surplus of C2 compounds. The inverse is the case for feeding extra glycogenic nutrients, implying reduced deamination and oxidation of glycogenic amino acids. Feeding extra glycogenic nutrients improved the energy balance (EB), in contrast to ambiguous results of lipogenic nutrients on EB. Moreover, glycogenic feed may reduce the severity of ketosis and fatty liver, but increased the incidence of (sub)clinical acidosis. Since studies are scarce, it seems difficult to draw conclusions on the effects of dietary energy source on reproduction. However, lipogenic nutrients decrease glucose and increase NEFA and BHBA plasma levels. High plasma NEFA and BHBA and low plasma glucose levels are associated with decreased reproductive performance, which might imply the C2/C3 compound balance to be important for reproductive function.
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PMID:Effect of dietary energy source on energy balance, production, metabolic disorders and reproduction in lactating dairy cattle. 1628 10


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