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Ketosis In Cattle Merck Manual

Is Propylene Glycol In Food Making Us Fat?

Is Propylene Glycol In Food Making Us Fat?

Most of you are probably wondering, "What the heck is propylene glycol?" Propylene glycol may sound fancy and scientific, but it's really just a clear, odorless liquid made from petroleum. It's used as a stabilizer (to keep things held together, and keep them from evaporating), and to keep foods moist. It's used in many of the foods that we eat, and the FDA deems it safe for human consumption. Sounds harmless enough, right? But I stumbled upon a little something that you may not know about propylene glycol. I promise this is the only other scientific word I will use: ketosis. Ketosis is simply a fancy medical term for when your body burns fat. So if you're overweight and you start to lose fat, it's called ketosis. I'm sure most of us can agree that ketosis is a good thing — especially here in America, where we have the most overweight population on the planet. So what do ketosis and propylene glycol have to do with being fat? Good question! There is an industry where fat is money. It's the cattle industry. Simply put, the cattle ranchers don't want cows to get skinny. When an overweight American goes into ketosis, we congratulate them and tell them how good they're looking. But when a cow starts to lose fat, the veterinarian is called immediately. According to the Merck Veterinary Manual, "Ketosis is a common disease of adult cattle." And according to this manual, one of the treatments for this condition is propylene glycol. The cow is injected twice per day with propylene glycol until it gets fat again. This stops the cow from losing fat and keeps them nice and plump. The cow can then be sold and butchered so a beautiful, fatty rib eye steak can be enjoyed. I am definitely not against a big fatty steak with proper marbling (the fatty beads throughout the steak). But Continue reading >>

Subclinical Ketosis

Subclinical Ketosis

Subclinical ketosis is defined as high serum ketone body concentrations without observed clinical signs. Subclinically affected cows are at increased risk of clinical ketosis and displaced abomasum and are also less fertile than those with normal serum ketone body concentrations. Furthermore, they appear to have reduced milk production. Determination of serum β-hydroxybutyrate (BHB) concentrations is considered the best way to detect and monitor subclinical ketosis, because the cow-side tests mentioned above are insufficiently sensitive and specific in detecting subclinical increases in serum BHB concentrations. Serum concentrations may be determined spectrophotometrically by traditional clinical laboratory means. The BHB concentrations in blood or serum samples are reasonably stable; thus, rigorous sample handling precautions are not necessary to transport the specimens to the laboratory. The test is sensitive to hemolysis, however, so hemolysis should be avoided during sample collection, and serum should be separated from the clot before shipment to the laboratory. In addition to laboratory determination by spectrophotometry, handheld devices manufactured to monitor blood ketone body concentrations in human diabetic patients have been evaluated for use in monitoring subclinical ketosis in cows. These instruments use whole blood rather than serum for BHB determination, making them particularly practical for on-farm use. The whole blood BHB concentration is very close to the serum concentration, so the interpretation of results obtained from either the handheld device or laboratory analysis is similar. Diagnosis of subclinical ketosis requires definition of a concentration above which cows are considered to be subclinically ketotic. Concentrations between 1,000 µM (10 Continue reading >>

Incidence And Clinical Vital Parameters In Primary Ketosis Of Murrah Buffaloes

Incidence And Clinical Vital Parameters In Primary Ketosis Of Murrah Buffaloes

Go to: Abstract The present study was undertaken to ascertain the incidence and clinical vital parameters in cases of primary ketosis in Murrah buffaloes brought to teaching veterinary clinical complex, Lala Lajpat Rai University of Veterinary and Animal Sciences, Hisar and from adjoining villages of the district Hisar, Haryana, India. The investigation was conducted on 24 clinical cases (out of total 145 screened) of primary ketosis. The diagnosis was confirmed on the basis of clinical signs and significantly positive two tests for ketone bodies in urine (Rothera’s and Keto-Diastix strip test). Data collected were statistically analyzed using independent Student’s t-test. Overall incidence of disease in these areas was found to be 16.55% and all the animals were recently parturited (mean: 1.42±0.14 month), on an average in their third lactation (mean: 2.38±0.30) and exhibited clinical signs such as selective anorexia (refusal to feed on concentrate diet), drastic reduction in milk yield (mean: 64.4±5.35%), ketotic odor from urine, breath, and milk and rapid loss of body condition. All the clinical vital parameters in ketotic buffaloes (body temperature, heart rate, respiration rate, and rumen movements) were within normal range. Primary ketosis in Murrah buffaloes was the most common seen in the third lactation, within the first 2 months after parturition with characteristics clinical signs and no variability in vital parameters. The disease has severe effect on the production status of affected animal. Keywords: buffaloes, incidence, Keto-Diastix strip test, primary ketosis, Rothera’s test History (related to lactation) in buffaloes suffering from primary ketosis. Continue reading >>

A Brief Review And Observations On Clinical Ketosis In Non-lactating Pregnant Dairy Cattle

A Brief Review And Observations On Clinical Ketosis In Non-lactating Pregnant Dairy Cattle

Abstract The carbohydrate and glucose metabolism is briefly discussed. A review is given of the aetiology of the different types of ketosis in ruminants with the emphasis on the cow. Clinical ketosis in non-lactating pregnant animals is highlighted in a study of 20 cases, 16 in-calf heifers and four three-year-old cows. Fourteen animals had primary clinical ketosis thought to be mainly due to underfeeding. Six animals-had secondary clinical ketosis and were suffering from accompanying primary diseases. Treatment and possible causative factors are discussed. The introduction of heifers into mobs of older cows together with the change from free grazing to being break fed seems to be a major cause of underfeeding and stress. The whole of the literary matter of the New Zealand Veterinary Journal is copyright Taylor and Francis, Downloading this article signifies agreement with the terms and conditions of electronic access. Continue reading >>

Ketosis

Ketosis

Ketosis is a metabolic disease that occurs when the cow is in severe state of negative energy balance. In this state, the cow mobilises large quantities of body fat but cannot convert this to energy through the usual pathways. Instead, ketone bodies are produced which in small amounts can be used by the cow for energy. However, when ketone production is high, the cow cannot use all the ketone bodies for energy and ketone levels increase in the blood. When this occurs the cow may suffer from ketosis. Types of Ketosis Type 1 ketosis is a result of a sudden drop in energy intake. This can be due to underfeeding or adverse weather events (e.g. snow storms) that prevent the cows from eating sufficient amounts of dry matter. Type 2 ketosis generally occurs post-calving, when the cow is mobilising excess body fat to meet the demands of milk production. Cows that are too fat at calving (BCS > 5) or cows that have been overfed pre-calving are particularly at risk. Silage ketosis is due to cows ingesting poor quality silage. The silage undergoes a secondary fermentation and when ingested will increase the risk of ketosis. Symptoms Ketosis can be displayed in two ways: Wasting form Lethargy (head down, lack of energy) Decreased dry matter intake Decreased milk production Often a sweet smell on the breath (acetone) Nervous form Excitable, uncoordinated and can become aggressive Strange behaviour such as eating soil, licking fence posts and gates, walking in circles, or standing with heads raised up and pushed into a corner etc. If a cow shows signs of ketosis seek advice from your veterinarian Prevention It is important to prevent ketosis from occurring, rather than treating cases as they appear. Prevention depends on adequate feeding and management of body condition score (BCS). E Continue reading >>

Ketotic Cows: Treatment And Prognosis (proceedings)

Ketotic Cows: Treatment And Prognosis (proceedings)

12Next An absolute requirement for treating ketosis in cattle is to identify and treat the primary cause for the negative energy balance. Symptomatic treatment for ketosis without attacking the primary cause is doomed to failure. Propylene glycol is a routine treatment for ketosis. Only 2 oral formulations are approved for use in cattle as a treatment and the dose rate is 8 oz, q 12 h, for up to 10 days (2 other formulations labeled for use as preventive treatment). Research suggests that 296 ml once/day as on oral drench is just as effective as 887 ml once/day. Propylene glycol is absorbed from the rumen as propylene glycol, some propylene glycol is metabolized to propionate in the rumen, but most is absorbed intact and metabolized to glucose in liver. Propylene glycol increases serum [glucose], decreases serum β-OH butyrate & NEFA concentrations but only if a functional liver as propylene glycol must be metabolized. Propylene glycol is only beneficial if rumen motility to aid mixing and absorption. Glycerol (same dose rate as propylene glycol) and sodium propionate (uncertain dose rate) also reported to be of use but are both considered inferior to propylene glycol. Sodium propionate may have palatability problems. Calcium propionate has been examined, but the evidence is not convincing that it is superior to propylene glycol, even though it also has calcium. Not very soluble, and large volumes need to be administered. 500 ml of 50% Dextrose IV is also a routine treatment (one time administration of 250 g). Numerous approved products for treating ketosis in cattle. A cow uses 50-70 g glucose/hour for maintenance and 200 g glucose/hour high production, from a total blood glucose pool <40 g. Milk is 4.5% lactose, 50 kg of milk contains 2.25 kg lactose (glucose and gala Continue reading >>

Ketosis In Cattle

Ketosis In Cattle

MSD and the MSD Veterinary Manual Merck & Co., Inc., Kenilworth, NJ, USA (known as MSD outside of the US and Canada) is a global healthcare leader working to help the world be well. From developing new therapies that treat and prevent disease to helping people in need, we are committed to improving health and well-being around the world. The Veterinary Manual was first published in 1955 as a service to the community. The legacy of this great resource continues as the Merck Veterinary Manual in the US and Canada and the MSD Veterinary Manual outside of North America. © 2016 Merck Sharp & Dohme Corp., a subsidiary of Merck & Co., Inc., Kenilworth, NJ, USA Continue reading >>

Pregnancy Toxaemia

Pregnancy Toxaemia

Also known as: Twin Lamb Disease A disease affecting ewes during the last few weeks of gestation. Mainly affects twin or multiple bearing ewes. The condition occurs when the ewe does not receive an adequate energy supply during a time when the rapidly growing foetuses drain carbohydrate stores. This results in a sub-clinical ketosis which can quickly progress to a clinical pregnancy toxaemia. It is a serious condition which can be fatal and most frequently affects lowland flocks. Very similar to ketosis in cows. Signalment It is seen more frequently in older ewes and those carrying multiple lambs who are in poor body condition score. Can often be diagnosed on history and a clinical exam. Differential diagnoses include listeriosis, pneumonia, and hypocalcaemia. Clinical Signs Mainly neurological signs are apparent as a result of the hypoglycaemic state of the animal. Ewes are often depressed and not aware of their surrounding, they can adopt an unusual posture which may progress to ataxia or recumbency. Some appear blind and there may be trembling and twitching of the face and ears. Ewes often grind their teeth and make chewing movements. They are also anorexic and may have breathing difficulties and a nasal discharge. Some ewes abort which may result in septicaemia. Laboratory Tests Biochemistry will often reveal a hypoglycaemia and a hyperkalaemia due to ketoacidosis. Additionally a high ß hydroxybutyrate (BHB) (which is one of the ketone bodies) level will also be evident. BHB is a more reliable measure of disease as not all animals show hypoglycaemia on blood work and some even are hyperglycaemic. On urine analysis ketones may be present. Treatment of advanced cases of pregnancy toxemia is often unsuccessful. Propylene glycol can be given orally that acts as a precu Continue reading >>

Prevalence Of Subclinical Ketosis And Relationships With Postpartum Diseases In European Dairy Cows

Prevalence Of Subclinical Ketosis And Relationships With Postpartum Diseases In European Dairy Cows

Abstract Subclinical ketosis (SCK) is defined as concentrations of β-hydroxybutyrate (BHBA) ≥ 1.2 to 1.4 mmol/L and it is considered a gateway condition for other metabolic and infectious disorders such as metritis, mastitis, clinical ketosis, and displaced abomasum. Reported prevalence rates range from 6.9 to 43% in the first 2 mo of lactation. However, there is a dearth of information on prevalence rates considering the diversity of European dairy farms. The objectives of this study were to (1) determine prevalence of SCK, (2) identify thresholds of BHBA, and (3) study their relationships with postpartum metritis, clinical ketosis, displaced abomasum, lameness, and mastitis in European dairy farms. From May to October 2011, a convenience sample of 528 dairy herds from Croatia, Germany, Hungary, Italy, Poland, Portugal, Serbia, Slovenia, Spain, and Turkey was studied. β-Hydroxybutyrate levels were measured in 5,884 cows with a handheld meter within 2 to 15 d in milk (DIM). On average, 11 cows were enrolled per farm and relevant information (e.g., DIM, postpartum diseases, herd size) was recorded. Using receiver operator characteristic curve analyses, blood BHBA thresholds were determined for the occurrence of metritis, mastitis, clinical ketosis, displaced abomasum, and lameness. Multivariate binary logistic regression models were built for each disease, considering cow as the experimental unit and herd as a random effect. Overall prevalence of SCK (i.e., blood BHBA ≥ 1.2 mmol/L) within 10 countries was 21.8%, ranging from 11.2 to 36.6%. Cows with SCK had 1.5, 9.5, and 5.0 times greater odds of developing metritis, clinical ketosis, and displaced abomasum, respectively. Multivariate binary logistic regression models demonstrated that cows with blood BHBA levels o Continue reading >>

Pregnancy Toxemia In The Ewe Leanne M. Schulz Iowa State University

Pregnancy Toxemia In The Ewe Leanne M. Schulz Iowa State University

Volume 45 | Issue 1 Article 2 Richard L. Riese Iowa State University Follow this and additional works at: Part of the Large or Food Animal and Equine Medicine Commons, and the Obstetrics and Gynecology Commons This Article is brought to you for free and open access by the Student Publications at Iowa State University Digital Repository. It has been accepted for inclusion in Iowa State University Veterinarian by an authorized editor of Iowa State University Digital Repository. For more information, please contact [email protected] Recommended Citation Schulz, Leanne M. and Riese, Richard L. (1983) "Pregnancy Toxemia in the Ewe," Iowa State University Veterinarian: Vol. 45 : Iss. 1 , Article 2. Available at: Pregnancy Toxemia in the Ewe Leanne M. Schulz· Richard L. Riese, DVM ** INTRODUCTION Pregnancy toxemia, also known as ovine ketosis, lambing sickness, twin lamb disease, or domzietke, is a widespread, usually fatal disease of sheep. I. l.3.4. 5 The disease also occurs occasionally in goats, and the clinical course is very similar to that in sheep.6.7 Pregnancy toxemia occurs during late preg- nancy, and although death losses in a given flock are usually sporadic, they can exceed 13 % . I Among severely affected ewes, the death rate often approaches 95 %. I These fac- tors, combined with the prevalence of the disease, make pregnancy toxemia of major economic importance to the sheep industry. Pregnancy toxemia is significantly different from bovine ketosis, even though ketosis is a major factor in both diseases and the clinical signs are often similar. 7.8 The two major differences are the time of onset and the re- sponse to treatment.9 •IO Pregnancy toxemia occurs prior to lambing, while bovine ketosis occurs from a few days to several weeks post- calving. Continue reading >>

Metabolic Alkalosis

Metabolic Alkalosis

Metabolic alkalosis is primary increase in bicarbonate (HCO3−) with or without compensatory increase in carbon dioxide partial pressure (Pco2); pH may be high or nearly normal. Common causes include prolonged vomiting, hypovolemia, diuretic use, and hypokalemia. Renal impairment of HCO3− excretion must be present to sustain alkalosis. Symptoms and signs in severe cases include headache, lethargy, and tetany. Diagnosis is clinical and with ABG and serum electrolyte measurement. The underlying condition is treated; oral or IV acetazolamide or hydrochloric acid is sometimes indicated. Metabolic alkalosis is bicarbonate HCO3− accumulation due to Regardless of initial cause, persistence of metabolic alkalosis indicates that the kidneys have increased their HCO3− reabsorption, because HCO3− is normally freely filtered by the kidneys and hence excreted. Volume depletion and hypokalemia are the most common stimuli for increased HCO3− reabsorption, but any condition that elevates aldosterone or mineralocorticoids (which enhance sodium [Na] reabsorption and potassium [K] and H+ excretion) can elevate HCO3−. Thus, hypokalemia is both a cause and a frequent consequence of metabolic alkalosis. Causes are listed; the most common are volume depletion (particularly when involving loss of gastric acid and chloride [Cl] due to recurrent vomiting or nasogastric suction) and diuretic use (see Table: Causes of Metabolic Alkalosis). Causes of Metabolic Alkalosis Cause Comments GI acid loss* Gastric acid loss due to vomiting or nasogastric suction Loss of HCl and acid coupled with contraction alkalosis due to release of aldosterone and subsequent resorption of HCO3 Congenital chloridorrhea Fecal Cl loss and HCO3 retention Villous adenoma Probably secondary to K depletion Renal a Continue reading >>

Ketosis

Ketosis

Not to be confused with Ketoacidosis. Ketosis is a metabolic state in which some of the body's energy supply comes from ketone bodies in the blood, in contrast to a state of glycolysis in which blood glucose provides energy. Ketosis is a result of metabolizing fat to provide energy. Ketosis is a nutritional process characterised by serum concentrations of ketone bodies over 0.5 mM, with low and stable levels of insulin and blood glucose.[1][2] It is almost always generalized with hyperketonemia, that is, an elevated level of ketone bodies in the blood throughout the body. Ketone bodies are formed by ketogenesis when liver glycogen stores are depleted (or from metabolising medium-chain triglycerides[3]). The main ketone bodies used for energy are acetoacetate and β-hydroxybutyrate,[4] and the levels of ketone bodies are regulated mainly by insulin and glucagon.[5] Most cells in the body can use both glucose and ketone bodies for fuel, and during ketosis, free fatty acids and glucose synthesis (gluconeogenesis) fuel the remainder. Longer-term ketosis may result from fasting or staying on a low-carbohydrate diet (ketogenic diet), and deliberately induced ketosis serves as a medical intervention for various conditions, such as intractable epilepsy, and the various types of diabetes.[6] In glycolysis, higher levels of insulin promote storage of body fat and block release of fat from adipose tissues, while in ketosis, fat reserves are readily released and consumed.[5][7] For this reason, ketosis is sometimes referred to as the body's "fat burning" mode.[8] Ketosis and ketoacidosis are similar, but ketoacidosis is an acute life-threatening state requiring prompt medical intervention while ketosis can be physiological. However, there are situations (such as treatment-resistant Continue reading >>

Fatty Liver Disease Of Cattle

Fatty Liver Disease Of Cattle

By Walter Gruenberg, DrMedVet, MS, PhD, DECAR, DECBHM, Assistant Professor, Department of Farm Animal Health, Utrecht University Fatty liver results from a state of negative energy balance and is one of the important metabolic diseases of postparturient dairy cows. Although often considered a postpartum disorder, it usually develops before and during parturition. Periparturient depression of feed intake, and endocrine changes associated with parturition and lactogenesis contribute to development of fatty liver. Cows that are overconditioned at calving are at highest risk. Fatty liver can develop whenever there is a decrease in feed intake and may occur secondary to the onset of another disorder. Fatty liver at calving is commonly associated with ketosis (see Ketosis in Cattle). Etiology: Mobilization of body fat reserves that is triggered by hormonal cues in states of negative energy balance results in the release of nonesterified fatty acids (NEFAs) from adipose tissue. The liver retains ~15%–20% of the NEFAs circulating in blood and thus accumulates increased amounts during periods when blood NEFA concentrations are increased. The most dramatic increase occurs at calving, when plasma concentrations are often >1,000 μEq/L. Concentrations can reach that level if the animal goes off feed. NEFAs taken up by the liver can either be oxidized or esterified. The primary esterification product is triglyceride, which can either be exported as part of a very low density lipoprotein (VLDL) or be stored in liver cells. In ruminants, export occurs at a very slow rate relative to many other species because of impaired VLDL synthesis. Therefore, under conditions of increased hepatic NEFA uptake and esterification, triglycerides accumulate. Oxidation of NEFAs leads either to the pr Continue reading >>

Ketosis

Ketosis

Ketosis (Acetonemia, Ketonemia) is a common multifactorial disease resulting in downer cow syndrome in adult cattle worldwide[1]. Causes which predisposed to ketosis include: Ketosis is a common disease of dairy cows in early lactation caused by a negative energy balance that results in high concentrations of circulating nonesterified fatty acids (NEFAs) (acetone, acetoacetate, and β-hydroxybutyrate (BHB)). This disease is usually associated with fatty liver. Clinical signs Clinically affected cattle shows signs of anorexia, reduced milk yield and may present as downer cows. Neurological signs of restlessness and ataxia may sometimes be noted. A sweet breath may be observed by an observant farmer or veterinarian. Diagnosis is based on presenting clinical signs supported by laboratory tests such as urinalysis and milk detection of ketones. During the first month of lactation, ratios of glycerophosphocholine:phosphocholine less than 2.5 in the milk indicate a high risk for developing ketosis[2]. Blood tests showing elevated NEFAs can assist diagnosis in more valuable cattle[3]. Bolus IV administration of 500 mL of 50% dextrose solution is a common therapy[4]. Glucocorticoids including dexamethasone or isoflupredone acetate at 5–20 mg/dose, IM, generally results in a more sustained response. Oral propylene glycol (250–400 g) may be effective as ketosis therapy[5]. Continue reading >>

Incidence And Clinical Vital Parameters In Primary Ketosis Of Murrah Buffaloes

Incidence And Clinical Vital Parameters In Primary Ketosis Of Murrah Buffaloes

Ankit Kumar: Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Neelesh Sindhu: Teaching Veterinary Clinical Complex, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Parmod Kumar: Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Tarun Kumar: Teaching Veterinary Clinical Complex, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Gaurav Charaya: Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Surbhi: Department of Veterinary Physiology and Biochemistry, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] V. K. Jain: Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Sridhar: Department of Veterinary Medicine, Lala Lajpat Rai University of Veterinary & Animal Sciences, Hisar - 125 004, Haryana, India; [email protected] Continue reading >>

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