Severity of experimental escherichia-coli mastitis in ketonemic and nonketonemic dairy-cows.

The severity of experimental Escherichia coli mastitis in relation to in vitro chemotaxis of polymorphonuclear leukocytes was investigated in cows during negative energy balance. The negative energy balance was induced by feed restriction. Cows were classified into two groups, ketonemic and nonketonemic, based on the beta-hydroxybutyrate concentration in the peripheral blood at the moment of inoculation. Bacterial growth in the inoculated quarter was used as a parameter to indicate the severity of experimental mastitis. In the nonketonemic cows, experimental mastitis ranged from moderate to severe. Severity of experimental mastitis was negatively related to preinfection chemotactic response of polymorphonuclear leukocytes. In contrast, the course of experimental mastitis in the ketonemic group was relatively severe in all cows, regardless of preinfection chemotactic response

Beneficial effects of the ketogenic diet on nonalcoholic fatty liver disease: A comprehensive review of the literature

Nonalcoholic fatty liver disease (NAFLD) is a major cause of chronic liver disease, characterized by hepatic fat accumulation and possible development of inflammation, fibrosis, and cancer. The ketogenic diet (KD), with its drastic carbohydrate reduction, is a now popular weight loss intervention, despite safety concerns on a possible association with fatty liver. However, KDs were also reported to be beneficial on hepatic pathology, with ketone bodies recently proposed as effective modulators of inflammation and fibrosis. If the beneficial impact of weight loss on NAFLD is established, less is known on the effect of macronutrient distribution on such outcome. In a hypocaloric regimen, the latter seems not to be crucial, whereas at higher calorie intake, macronutrient ratio and, theoretically, ketosis, may become important. KDs could positively impact NAFLD for their very low carbohydrate content, and whether ketosis plays an additional role is unknown. Indeed, several mechanisms may directly link ketosis and NAFLD improvement, and elucidating these aspects would pave the way for new therapeutic strategies. We herein aimed at providing an accurate revision of current literature on KDs and NAFLD, focusing on clinical evidence, metabolic pathways involved, and strict categorization of dietary interventions

Diet-induced Ketoacidosis in a Non-diabetic: A Case Report

Introduction: Anion gap metabolic acidosis is a common disorder seen in the emergency department. The differential can include toxicological, renal, endocrine, infectious, and cardiogenic disorders. Ketosis, however, is one of the rarer causes of metabolic acidosis seen by the emergency physician in developed nations.Case Report: A 53-year-old female presented after starting a low-carbohydrate ketogenic diet for weight loss. She reported xerostomia, nausea with abdominal pain and a 17-pound weight loss over the previous 22 days. Labs revealed an anion-gap metabolic acidosis with ketosis. She was treated with 5% dextrose in normal saline and a sliding scale insulin coverage. Her anion gap corrected during her hospital course and was discharged on hospital day three.Discussion: The ketogenic diet typically consists of a high-fat, adequate protein and low carbohydrate diet that has previously been thought to be relatively safe for weight loss. However, when carbohydrates are completely removed from the diet an overproduction of ketones bodies results in ketoacidosis. Treatment should be aimed at halting the ketogenic process and patient education.Conclusion: Although rarely included in the differential for metabolic acidosis, diet-induced ketosis should be included by the emergency physician when faced with a patient who recently changed their eating patterns

Progressive changes in metabolism of cows during induction of ketosis and treatment of ketosis with intestinal administration of glucose

During the 9 wk immediately after parturition, 18 high-producing cows were distributed equally among three treatments: ad-lib fed control, ketosis-induced, and glucose-treated cows. Ketosis was induced at an average of 44 d postpartum and 29 d after initiation of a protocol that included feed restriction to 80% of ad lib intake and supplemental 1,3-butanediol at 8% of dry matter intake. Treated cows were given the ketosis-induction protocol but also received 500 g glucose/d infused continuously into the duodenum from d 25 to 40 postpartum. Liver and blood samples for ketosis-induced cows were taken at eight stages, which were usually about 7 days apart: prepartal, early postpartum, preinduction, three stages of induction, ketotic, and recovery;Ketosis-induced cows decreased milk production by 31% at ketosis, but values for glucose-treated cows remained constant. Plasma free fatty acid concentrations increased 2.6- and 1.9-fold at two weeks before and at ketosis, whereas glucose-treated cow values increased slightly then returned to baseline. Beta-hydroxybutyrate also increased 5.8- and 8.4-fold for the same time periods for ketosis-induced cows, but only a maximum of 1.6-fold for glucose-treated cows. Plasma glucose was decreased by 20% for ketosis and increased by 9% for treated cows. After parturition, liver glycogen percentages decreased across all treatments and reached essentially zero for ketosis-induced cows two weeks before ketosis. However, values for glucose-treated cows returned to prepartal amounts during glucose infusions. Liver triglyceride increased to 8.5 and 9.8% for two weeks before and at ketosis. Values for glucose-treated cows during the same time periods were 1.3 and 1.1%. Gluconeogenic rates were not different until the ketosis stage when ketotic cows decreased four-fold. Detrimental effects of ketosis therefore seem to begin up to two weeks before clinical ketosis is detected;In vivo kinetic techniques were used to estimate irreversible loss of rumen propionate and plasma glucose at 20, 30, 41, 49, and 60 d postpartum in a subset of four cows from the main experiment. Both glucose and propionate irreversible loss were decreased at the ketosis stage for the ketosis-induced

Tropical calcific pancreatitis.........An overview

Tropical calcific pancreatitis is a nonalcoholic type of chronic pancreatitis affecting the childrens and young adults characterized clinically by recurrent abdominal pain in childhood, diabetes in adolescent and death in early childhood. Although the exact etiology is not known, malnutrition and chronic cassava toxicity either singly or in combination are presumed to be the prime factor in pancreatic injury unopposed by detoxification of free radical. Moreover micronutrients deficiency, oxidant stress and antioxidant deficiency might play substantial role. Diabetes secondary to tropical calcific pancreatitis is a distinctive and frequent problem, being named by W.H.O. study group as 'fibrocalculous pancreatic diabetes (FCPD) and classified as one of the variant of the so-called malnutrition related diabetes mellitus (MRDM).熱帯地方の貧困層の小児や若干成人にみられる非アルコール性の慢性膵炎で,小児期に反復する腹痛で発症し,10～20歳で膵性糖尿病になり,20～ 30歳で死亡する類似の病像を示す症例をTropical calcific pancreatitis(熱帯性石灰化慢性膵炎)という｡高率に膵石を伴う｡成因は乳幼児期からの熱量,蛋白貰,micronutrients(亜鉛,銅,セレニウム)の摂取不足に加えて食事中シアン産生物質や環境中oxidantsなど複合因子によると推測されている｡病理像は世界各国にみられる慢性膵炎典型例に類似する｡最近は,生活環境や医療事情の改善により,全身栄養障害の減少や生存期間 の延長など病像が変貌しっつある｡糖尿病を重視する立場からはFibrocalculous pancreatic diabetesと呼ばれ,同一地域にみられるProtein-deficient pancreatic diabetesと合わせてMalnutrition-related diabetes mellitus(MRDM)と総称し,糖尿病の一亜型に分類されている

Trial Protocol: Randomised controlled trial of the effects of very low calorie diet, modest dietary restriction, and sequential behavioural programme on hunger, urges to smoke, abstinence and weight gain in overweight smokers stopping smoking

Background\ud Weight gain accompanies smoking cessation, but dieting during quitting is controversial as hunger may increase urges to smoke. This is a feasibility trial for the investigation of a very low calorie diet (VLCD), individual modest energy restriction, and usual advice on hunger, ketosis, urges to smoke, abstinence and weight gain in overweight smokers trying to quit. \ud \ud Methods\ud This is a 3 armed, unblinded, randomized controlled trial in overweight (BMI > 25 kg/$m^2$), daily smokers (CO > 10 ppm); with at least 30 participants in each group. Each group receives identical behavioural support and NRT patches (25 mg(8 weeks),15 mg(2 weeks),10 mg(2 weeks)). The VLCD group receive a 429-559 kcal/day liquid formula beginning 1 week before quitting and continuing for 4 weeks afterwards. The modest energy restricted group (termed individual dietary and activity planning(IDAP)) engage in goal-setting and receive an energy prescription based on individual basal metabolic rate(BMR) aiming for daily reduction of 600 kcal. The control group receive usual dietary advice that accompanies smoking cessation i.e. avoiding feeling hungry but eating healthy snacks. After this, the VLCD participants receive IDAP to provide support for changing eating habits in the longer term; the IDAP group continues receiving this support. The control group receive IDAP 8 weeks after quitting. This allows us to compare IDAP following a successful quit attempt with dieting concurrently during quitting. It also aims to prevent attrition in the unblinded, control group by meeting their need for weight management. Follow-up occurs at 6 and 12 months. \ud \ud Outcome measures include participant acceptability, measured qualitatively by semi-structured interviewing and quantitatively by recruitment and attrition rates. Feasibility of running the trial within primary care is measured by interview and questionnaire of the treatment providers. Adherence to the VLCD is verified by the presence of urinary ketones measured weekly. Daily urges to smoke, hunger and withdrawal are measured using the Mood and Physical Symptoms Scale-Combined (MPSS-C) and a Hunger Craving Score (HCS). 24 hour, 7 day point prevalence and 4-week prolonged abstinence (Russell Standard) is confirmed by CO < 10 ppm. Weight, waist and hip circumference and percentage body fat are measured at each visit. \ud \ud Trial Registration\ud Current controlled trials ISRCTN83865809\ud \u