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At least 19 recordsLinked to original sources
PubMed1994

Bovine ketosis and somatotrophin: risk factors for ketosis and effects of ketosis on health and production.

Aspects of the metabolism and health of 63 cows which had been treated with different amounts of bovine somatotrophin (BST) daily in the preceding lactation and 25 control cows were studied. The aims of the study were first, to identify cows with ketotic conditions, either by measurements of blood metabolite concentrations or by clinical observations, secondly, to evaluate the risk of such conditions in cows treated with BST in the preceding lactation, and thirdly, to examine the metabolic and production consequences of the ketotic conditions in an environment in which the cows' health, body condition and nutrition were closely observed. The cows were categorised objectively by the use of cluster analysis into non-ketotic cows and ketonaemic cows, on the basis of their plasma metabolite concentrations. Twelve of the control cows and none of the cows previously treated with BST were classified as ketonaemic. Similarly, nine of the control cows but only two of the cows previously treated with BST had clinical ketosis. Some, but not all, of the decrease in the risk of clinical ketosis was attributable to the lower body condition score of the cows previously treated with BST. The clinically ketotic cows had a greater risk of other illness in the first 10 days post partum than their herdmates, but the ketonaemic cows had a significantly lower risk of other disease in the first 10 days post partum. The ketonaemic control cows were significantly heavier than the non-ketotic control cows, but they maintained a higher dry matter intake than the latter cows, probably a key factor in reducing the risk of clinical ketosis.

3-Hydroxybutyric Acid↗
PubMed1988

beta-Adrenergic blockade counteracts starvational ketosis, but aggravates post-exercise ketosis in non-athletes.

Post-exercise ketosis is not abolished by glucose ingestion immediately after exercise but is counteracted by simultaneous beta-adrenergic blockade. To investigate the effect of beta-adrenergic blockade on post-exercise ketosis without the ingestion of glucose, we administered propranolol (1 mg/kg body mass) to 15 carbohydrate-starved people, of whom five had just walked 9 km in 2 h. There were 43 control subjects (no propranolol). The blood concentration of 3-hydroxybutyrate rose from 0.18 +/- 0.02 (S.E.M.) mmol/l at 07.00 h to 0.35 +/- 0.04 mmol/l at 09.00 h whether the subjects had exercised during those 2 h or not (d.f. = 57). The blood concentration of 3-hydroxybutyrate at 15.00 h in the groups not treated with propranolol was not affected by exercise (0.95 +/- 0.90 mmol/l; d.f. = 42). Propranolol significantly raised the concentration of 3-hydroxybutyrate at 15.00 h to 1.68 +/- 0.26 mmol/l when given after exercise (d.f. = 4), but lowered it to 0.46 +/- 0.07 mmol/l in the non-exercised group (d.f. = 9). This was not accompanied by significant differences in the blood concentrations of glucose, free fatty acid, insulin or glucagon. The difference in response to propranolol administration is probably determined by the alanine and lactate flux from muscle for hepatic oxaloacetate synthesis.

3-Hydroxybutyric Acid↗
PubMed1985

Ketone body production and disposal in diabetic ketosis. A comparison with fasting ketosis.

This work compares the metabolism of total ketone bodies in 13 insulin-deprived, type I diabetic subjects and 26 control subjects fasted for 15 h to 23 days, with the two groups showing a similar range of ketone body levels (1-12 mM). Ketone turnover rate was measured using a primed, constant infusion of either 14C-acetoacetate or 14C-beta-hydroxybutyrate, both tracers yielding comparable results. The major conclusions of this study are the following: the kinetics of ketone bodies are comparable in the two groups within the range of concentrations tested. The hyperketonemia of fasting and diabetes is primarily caused by an increased production of ketone bodies, but the phenomenon is amplified by a progressive limitation in the ability of tissues to remove ketones from blood as the concentration rises. The inverse relationship between the metabolic clearance and the plasma levels of ketones, which underlies this process, represents a general characteristic of ketone body metabolism that applies to both types of ketosis. A maximal metabolic disposal rate of about 2.3 mmol/min/1.73 m2 is attained in both groups at concentrations of 10-12 mM, which correspond to the highest ketone body levels encountered during prolonged fasting. Thus, up to these levels, there is no evidence for the existence of a ketone body removal defect specific to diabetes.

3-Hydroxybutyric Acid↗
PubMed1991

Metabolic changes in blood and liver during development and early treatment of experimental fatty liver and ketosis in cows.

Eighteen cows were assigned in equal numbers to three groups: control, ketosis induction by using feed restriction plus dietary 1,3-butanediol to provide ketone bodies, and glucose treatment with 484 g/d of glucose infused intraduodenally starting 7 d after beginning ketosis induction. Ketosis induction, begun at d 15 postpartum, caused ketonemia and gradual development of clinical ketosis by d 40 to 45. None of the cows in the control or glucose-treated groups became ketotic. Concentrations of NEFA in plasma of cows that became ketotic increased 3.0-, 2.6-, and 1.9-fold at 3 wk before, 2 wk before, and at ketosis, respectively, but increased nonsignificantly for glucose-treated cows. Concurrently, beta-hydroxybutyrate increased 3.5-, 5.8- and 8.4-fold for cows that became ketotic but 1.6-fold or less for glucose-treated cows. Plasma acetate increased dramatically 2 wk before ketosis. Liver glycogen content decreased to nearly 0 by 2 wk before ketosis occurred, but it increased to prepartal values in glucose-treated cows. Liver triglycerides averaged 2.0% of wet weight at d 5 for all cows but increased to 8 to 10% for about 2 wk before ketosis occurred. Microscopy of liver samples demonstrated progressive accumulation of lipid globules, which began in hepatocytes near the central vein and progressed toward the portal triad. Visible lipid content reached a peak 2 wk before ketosis. Hepatic in vitro gluconeogenic capacity decreased significantly for ketosis induction protocol cows when clinical ketosis was detected. Results indicate that experimental ketosis was preceded by metabolic abnormalities up to 2 wk before clinical ketosis occurred. The key events for onset of clinical ketosis, however, were not elucidated.

3-Hydroxybutyric Acid↗
PubMed2001

Neonatal ketosis is not rare: experience of neonatal screening using gas chromatography-mass spectrometry.

The causes and effects of transient neonatal ketosis, discovered during a pilot study of screening for abnormalities in neonatal metabolism using gas chromatography-mass spectrometry, were investigated. Of the 21,342 neonates that were screened, 47 had significant ketosis. The organic acid profile accompanying ketosis in the urine of neonates followed the pattern of ketotic dicarboxylic aciduria in approximately half of the cases. Ketosis was more often found in neonates nourished by breast feeding (33 out of 47). Over half of the neonates showing ketosis (28 out of 47) were asymptomatic. When normal neonates and neonates testing positive for ketosis were compared, no statistically significant correlations were found with regard to birth mass, gestational period, or gender. However, neonates with ketosis tended to have low mass gain rates in the 5 days from birth and a statistically significant difference was found in this regard in comparison to normal neonates (P<0.0001). From the above results, development of ketosis in neonates was found to be possible even in normal subjects. Most ketosis in neonates was also found to depend largely on nourishment after birth. Existence of an asymptomatic ketosis category was also suggested.

Gas Chromatography-Mass Spectrometry↗
PubMed2004

Ketosis-prone type 2 diabetes in patients of sub-Saharan African origin: clinical pathophysiology and natural history of beta-cell dysfunction and insulin resistance.

Nonautoimmune ketosis-prone diabetic syndromes are increasingly frequent in nonwhite populations. We have characterized a cohort of patients of sub-Saharan African origin who had ketosis-prone type 2 diabetes (n = 111), type 1 diabetes (n = 21), and type 2 diabetes (n = 88) and were admitted to a hospital for management of uncontrolled diabetes. We compared epidemiological, clinical, and metabolic features at diabetes onset and measured insulin secretion (glucagon-stimulated C-peptide) and insulin action (short intravenous insulin tolerance test) during a 10-year follow-up. Ketosis-prone type 2 diabetes shows a strong male predominance, stronger family history, higher age and BMI, and more severe metabolic decompensation than type 1 diabetes. In ketosis-prone type 2 diabetes, discontinuation of insulin therapy with development of remission of insulin dependence is achieved in 76% of patients (non-insulin dependent), whereas only 24% of patients remain insulin dependent. During evolution, ketosis-prone type 2 diabetes exhibit specific beta-cell dysfunction features that distinguish it from type 1 and type 2 diabetes. The clinical course of non-insulin-dependent ketosis-prone type 2 diabetes is characterized by ketotic relapses followed or not by a new remission. Progressive hyperglycemia precedes and is a strong risk factor for ketotic relapses (hazard ratio 38). The probability for non-insulin-dependent ketosis-prone type 2 diabetes to relapse is 90% within 10 years, of whom approximately 50% will become definitively insulin dependent. Insulin sensitivity is decreased in equal proportion in both ketosis-prone type 2 diabetes and type 2 diabetes, but improves significantly in non-insulin-dependent ketosis-prone type 2 diabetes, only after correction of hyperglycemia. In conclusion, ketosis-prone type 2 diabetes can be distinguished from type 1 diabetes and classical type 2 diabetes by specific features of clinical pathophysiology and also by the natural history of beta-cell dysfunction and insulin resistance reflecting a propensity to glucose toxicity.

Adult↗
PubMed1986

Evidence for impaired metabolism in liver during induced lactation ketosis of dairy cows.

Ketosis was induced in four lactating dairy cows at an average of 36 d postpartum and 24 d after initiation of a protocol for inducing ketosis. Liver and adipose biopsies were taken at five stages; once prepartal, once early postpartal, once during an induction protocol, once during ketosis, and once during recovery after treatment of ketosis. At each stage, in vitro estimates were made of capacities of liver slices for gluconeogenesis, fatty acid oxidation, and ketogenesis and of capacities of adipose tissue slices for lipogenesis and lipolysis. There were no significant differences for any metabolic capacity between prepartal and early postpartal stages; however, a significant decrease in hepatic metabolic activity was associated with ketosis. Gluconeogenic rates from all substrates tested were decreased significantly during ketosis, and similar decreases were measured for oxidation of gluconeogenic substrates and fatty acids. Treatment of ketosis resulted in complete recovery from impairments of metabolism in liver. Results suggest that a prolonged energy deficit, plus a major influx of ketone precursors, is accompanied by eventual hepatic impairment, that clinical ketosis is associated with this impairment, and that the impairment is reversed by effective treatment of ketosis.

Acidosis↗
PubMed1988

Subclinical ketosis in dairy cows.

Subclinical ketosis is defined as a preclinical stage of ketosis. The peak prevalence of subclinical ketosis occurs during the fourth week of lactation. Herd-related factors, breed, parity, and season are other important determinants. Subclinical ketosis can be revealed by determining levels of plasma glucose, plasma NEFA and blood, and milk or urine ketone body concentration. There are theoretical and practical advantages of using milk ketone bodies. Most authors are agreed on approximate lower and upper borderlines for subclinical ketosis. The risk of an outbreak of clinical symptoms has been evaluated by some authors. Most authors have found significant negative relationships between energy balance and ketone body concentration. Some disagreement may be attributable to the fact that the diets used in different experiments can have different glucogenic potential, even if the energy content is the same. This affects the relationship between energy balance and ketone body concentration, as the ketone body level is influenced by both the energy balance and plasma glucose. Feeding silage with high butyric acid content increases the risk of subclinical ketosis. There are indications that cows with the highest milk yield directly after calving are at greatest risk for developing ketosis. Increased ketone body level secondarily reduces milk production, a decrease that has been quantified by some authors. Subclinical ketosis causes delayed reproductive functions return to normal after calving, increased intervals from calving to first and last service, and an increased frequency of ovarian cysts. The routine determination of milk acetone levels in control programs can be used to evaluate the status of individual cows, to indicate the energy feeding in early lactation at a herd level, and to evaluate sires for breeding. The heritability and the tendency toward a positive genetic correlation between milk acetone and milk yield have also been discussed, as have aspects of nutritional prevention. Factors such as energy- and protein-rich roughage, tasty high-energy concentrates, suitable feeding during the dry period, and division of the concentrates into at least four meals are considered to be important.

Acidosis↗
PubMed1998

Comparative analysis of blood chemical values in primary ketosis and abomasal displacement in cows.

Blood chemical values, including ketone bodies, were measured in 25 cows with abomasal displacement (displacement group), 16 cows with primary ketosis (ketosis group), and nine normal controls to investigate the pathophysiology of abomasal displacement. Increases in aspartate aminotransferase, gamma-glutamyl transpeptidase, non-esterified fatty acid (NEFA), and ketone bodies (3-hydroxybutyric acid and acetoacetic acid) were observed in the displacement and ketosis groups. Total cholesterol increased significantly in the ketosis group but decreased in the displacement group. Glucose was significantly low and reversely correlated to ketone bodies in the ketosis group but was not low and was not correlated with ketone bodies in the displacement group. While NEFA was correlated to ketone bodies in the ketosis group, it was not in the displacement group. A correlation between the values of acetoacetic acid and 3-hydroxybutyric acid was seen in both the ketosis and displacement groups. The fact that blood chemical values in ketosis cows were clearly different from those in displacement cows suggest that the biochemical mechanism of ketogenesis is different between these two groups.

Abomasum↗
PubMed2001

Body condition related to ketosis and reproductive performance in Norwegian dairy cows.

The relationships between body condition score (BCS) and ketosis, and between BCS and reproductive performance in 732 moderate yielding, dual-purpose cows were studied. The cows were of the breed Norwegian Cattle. Farms with tie-stall barns and a history of high ketosis incidence were chosen for the study. Sixteen assessors visited the farms monthly and the same assessor assigned a BCS to each cow once a month. A BCS of 3.5 or higher at calving was associated with increased risk for ketosis. Cows that subsequently developed ketosis had higher BCS than healthy cows before the disease was diagnosed, and they lost more body condition than did the latter after ketosis had occurred. Summer calving cows and primiparous cows showed the lowest risk of ketosis. A history of ketosis before first service decreased the likelihood of conception to that service. Loss in body condition during the postpartum period was associated with decreased likelihood of conception to first service, prolonged calving to conception intervals and increased number of artificial inseminations per conception. Reproductive performance was not associated with BCS at calving. We concluded that BCS is a useful method of monitoring relations among nutritional management, reproduction, and ketosis in moderate yielding dual-purpose cows.

Animal Husbandry↗
PubMed1982

Primary ketosis in the high-producing dairy cow: clinical and subclinical disorders, treatment, prevention, and outlook.

Bovine ketosis typically occurs in early lactation. Clinical signs include diminished appetite, decreased milk production, loss of weight, hypoglycemia, and hyperketonemia. Susceptibility to ketosis is probably due to the combination of appetite limitation and a high degree of precedence given to the demand of the mammary gland for nutrients, in particular glucose. The precipitating cause is likely to be development of a marked imbalance between glucose supply and glucose requirement. This imbalance then leads to decreased carbohydrate status, decreased insulin secretion, increased fat mobilization, and increased hepatic ketogenesis. Hepatic ketogenesis may be augmented by the diminished carbohydrate status. The role of hormones other than insulin in the etiology of ketosis, although probably important, has not yet been elucidated satisfactorily. Treatment of ketosis involves increasing glucose supply relative to glucose demand. Incidence of clinical ketosis can be minimized by correct nutrition and management as outlined in recommended guidelines. Besides decreasing milk field, clinical ketosis may affect productivity adversely in other ways, for example, by impairing fertility. Subclinical ketosis is important because it may remain undetected and yet have effects on productivity which parallel those elicited by clinical ketosis. Future research should be directed toward understanding mechanisms conferring priority on milk production and regulating appetite.

Acetates↗
PubMed1991

Clinical ketosis: phenotypic and genetic correlations between occurrences and with milk yield.

The repeatability and heritability of ketosis were estimated using data from 28,277 Finnish Ayrshire cows. A four-trait linear model including community-year, calving age and month, genetic group, and random sire effects was used to describe first and second lactation milk yields and veterinary diagnoses of ketosis. Variance components were estimated using REML. The disease traits were also analyzed with a categorical model including the same effects except that community and year were separate factors. Variance components were estimated with marginal maximum likelihood. Genetic relationships between 339 sires analyzed were included in models. The phenotypic correlation between the first and second lactation was defined as a repeatability of trait. The lactational incidence risk of ketosis was .05 in both the first and the second lactation. Average milk production was 4956 and 5547 kg in the first and second lactations, respectively. Estimates of heritabilities were .09 and .07 for ketosis and .23 and .19 for milk in the first and second lactations, respectively. Genetic correlations between first and second lactation recordings were .64 for ketosis and .93 for milk. Repeatabilities between subsequent lactations were .36 (.13 in linear analysis) for ketosis and .68 for milk. In the first lactation, genetic relationship between milk yield and ketosis was unfavorable, but in the second lactation ketosis and milk yield were genetically and phenotypically unrelated.

Animals↗