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At least 19 recordsLinked to original sources
PubMed1979

[Bilirubin in the blood serum of clinically healthy cows and those ill with ketosis and hepatopathies].

Studied was the bilirubin equilibrium in 62 normal cows, 52 cows with clinical ketosis, 31 cows with diffuse liver injury, and 14 cows that went off food for five days. A moderate rise of the total bilirubin of mixed type was found in ketosis-affected cows. Statistically significant proved the changes in the free fraction, however, there were no persuasive data that they were due to superproduction of bilirubin. Changes in the total bilirubin similar to those in cows with ketosis were established also in cows subjected to starvation, substantiated by the adequate rise of the free and the bound fraction. The hyperbilirubinemia in cows with diffuse liver injuries was found to be of a mixed type, with a very clear transposition in the bilirubin fractions. The direct: indirect ratio of bilirubin in this case was higher than unit, and the percent participation of the indirect fraction was brought down to 42.5. Apparently, the symptoms of liver affections were beyond the frames of what was found in the cows with ketosis. With the use of tests for the demonstration of urobilin and urobilinogen in the urine no dependable idea could be found of the status of the pigment fraction in the liver of ketosis-affected cows or the fact that this fraction was involved to a considerable extent. Discussed is the possibility of linking the state of hyperbilirubinemia in cows with ketosis with some energy deficiency with regard to the plasma glucosis and the liver glycogen.

Acidosis↗
PubMed2026

Metabolic ketosis attenuates NLRP3 inflammasome activation and is associated with improvements in hepatic steatosis and liver stiffness in MASLD: a pilot randomized controlled trial.

BACKGROUND: Metabolic dysfunction-associated steatotic liver disease (MASLD) is increasingly recognized as a systemic metabolic-inflammatory disorder in which metabolic stress and innate immune activation, particularly through the NLRP3 inflammasome, contribute to disease progression. Metabolic ketosis, characterized by increased levels of circulating ketone bodies, especially &#x3b2;-hydroxybutyrate, has emerged as a promising strategy to modulate substrate utilization, inflammatory signaling, and hepatic injury. However, clinical evidence integrating molecular, metabolic, and hepatic outcomes remains limited. METHODS: In this pilot randomized controlled trial, 20 participants with newly diagnosed MASLD were randomly assigned to either a 3-month intervention with a daily C8-enriched medium-chain fatty acid formulation (m-CAP; meta-Capridin, providing approximately 20 g/day of C8) or a standardized low-carbohydrate dietary protocol. Metabolic indices, inflammatory mediators, adipokines, and hepatic enzymes were assessed. The expression of key inflammasome components (NLRP3, caspase-1, and ASC) was evaluated in peripheral blood mononuclear cells, and hepatic steatosis and liver stiffness were measured via transient elastography. RESULTS: The C8-enriched intervention was associated with increased circulating &#x3b2;-hydroxybutyrate levels, indicating the achievement of nutritional ketosis. Changes over time were observed in metabolic parameters, including fasting serum glucose (p < 0.05), HOMA-IR (p < 0.05), body fat percentage (p < 0.05), and BMI (p < 0.05). Alterations in inflammatory mediators and adipokine-related outcomes were also observed following the intervention. At the molecular level, changes in inflammasome-related markers were detected, including caspase-1 mRNA expression (p < 0.05) and NLRP3 expression at the transcriptional (p < 0.05) and protein levels (p < 0.01), whereas ASC expression remained unchanged. Changes in hepatic steatosis (p < 0.01) and liver stiffness measurements were observed following the intervention. Given the absence of significant Group &#xd7; Time interactions for several secondary outcomes, these findings should be interpreted as exploratory and hypothesis-generating. CONCLUSIONS: Induction of metabolic ketosis was associated with changes in metabolic, inflammatory, and hepatic parameters in patients with MASLD. The observed associations between ketosis, inflammasome-related markers, and noninvasive liver outcomes warrant further investigation of ketosis-based interventions as adjunctive approaches in MASLD. Larger and longer-term clinical trials are needed to confirm these findings and to determine whether short-term changes in liver stiffness reflect sustained alterations in hepatic status rather than structural fibrosis regression. TRIAL REGISTRATION: Iranian Registry of Clinical Trials (IRCT); Unique identifier: IRCT20170315033086N12; Registration date: 19 September 2024; Registry URL: https://www.irct.ir. IRCT is a primary registry in the WHO Registry Network (https://www.who.int/tools/clinical-trials-registry-platform/network/primary-registries).

Humans↗
PubMed1977

[Serum alkaline phosphatase and transaminase activity in cows with clinical ketosis].

Studied was the activity of the alkaline phosphatase and the transaminases in the serum of clinically normal and ketosis-affected cows as well as cows with an affected liver. The changes were followed in the activity of SGOT and SGPT that had set in as a result of five-day starving and the injection of prednisolon at the rate of 0.5 mg/kg in the course of four days. The activity of serum alkaline phosphatase in ketosis-affected cows proved unchanged--1.99 +/1 0.35 VE. A moderate increase was established in cows with liver affections-- 3.73 +/- 0.35 VE. The hyperenzymemia in ketosis-affected animals, in animals with liver injuries as well as in cows subjected to starving or prednisolon treatment was substantiated by the higher activity of SGOT. Dependable higher values of SGOT were established in the serum of freshly calved cows as compared to cows of advanced lactation. The higher activity of SGOT in animals with ketosis is associated with the physiologic status, starving, enzyme induction, inadequacy of the cell energy balance--all limiting the possibility of it being ascribed with preference to the tissue proliferation or destruction, which is to be expected with cows having an affected liver.

Acidosis↗
PubMed1978

Cutaneous reactions to local traumatization with heat in alloxan diabetic rabbits with and without ketosis.

Short-term alloxan diabetic rabbits with and without ketosis were traumatized with local cutaneous application of heat. The degree of traumatization varied with regard to the temperature and duration used. The lowest degree of traumatization which caused intravenously injected Evans blue to be observed within the area of traumatization was determined. There was no difference between diabetic animals without ketosis and controls. A more pronounced traumatization of animals with ketosis was necessary if Evans blue was to be observed, but there was then a significant difference between these and controls. The traumatized skin areas were also studied histologically. The inflammatory reaction induced was judged as being weaker in animals with ketosis.

Animals↗
PubMed1978

Chronic ketosis and cerebral metabolism.

The effects of chronic ketosis on cerebral metabolism were determined in adult rats maintained on a high-fat diet for approximately three weeks and compared to a control group of animals. The fat-fed rats had statistically significantly lower blood glucose concentrations and higher blood beta-hydroxybutyrate and acetoacetate concentrations; higher brain concentrations of bound glucose, glucose 6-phosphate, pyruvate, lactate, beta-hydroxybutyrate, citrate, alpha-ketoglutarate, alanine, and adenosine triphosphate (ATP); lower brain concentrations of fructose 1,6-diphosphate, aspartate, adenosine diphosphate (ADP), creatine, cyclic nucleotides, succinyl coenzyme A (CoA), acid-insoluble CoA, and total CoA; and similar brain concentrations of glucose, malate, calculated oxaloacetate, glutamate, glutamine, adenosine monophosphate, phosphocreatine, reduced CoA, acetyl CoA, sodium, potassium, chloride, and water content. The metabolite data in the chronically ketotic rats demonstrate an increase in the cerebral energy reserve and energy charge. These data also suggest negative modification of the enzymes phosphofructokinase, pyruvic dehydrogenase, and alpha-ketoglutaric dehydrogenase; positive modification of glycogen synthase; and possible augmentation of the hexose transport system. There was no demonstrable difference in brain pH, water content, or electrolytes in the two groups of animals. We speculate that the increased brain ATP/ADP ratio is central to most, if not all, the observed metabolic perturbations and may account for the increased neuronal stability that accompanies chronic ketosis.

Acidosis↗
PubMed1979

Roles for insulin and glucagon in the development of ruminant ketosis -- a review.

Ketonemia can be a physiological response to a reduction in dietary intake. It also may occur when energy demands exceed the energy intake. Normally, alimentary ketogenesis is the major source of ketone bodies in ruminants. During ketonemia there is increased hepatic ketone body production. During physiological ketosis, the mobilization of free fatty acids is inadequate to support a high rate of hepatic ketogenesis. However, during clinical ketosis, the hormonal status (low insulin, high glucagon/insulin ratio) in combination with hypoglycemia promotes excessive lipid mobilization and a greater hepatic removal of fatty acids and switches the liver to a higher rate of ketogenesis. The low insulin, furthermore, can impair maximal ketone body utilization, thus exacerbating the hyperketonemia.

Acidosis↗
PubMed1977

[Blood sugar and ketone body content in cows with clinical ketosis].

The investigation confirms hypoglycaemia and hyperketonaemia as typical for ketosis. A reverse correlation has been found between the level of blood sugar and that of ketone bodies. The changes observed in both blood sugars and ketones have not been shown to manifest any definite relation to the feeding regime, which may not have been perfectly balanced but has supplied metabolizable energy and digestible protein for maintenance and production in excess. Five-day starving of freshly calved, clinically normal cows may cause a dependable drop of the blood sugar level and rise of the ketone bodies to an extent that vary from that observed in ketosis-affected cows showing no clinical picture characteristic of the disease. The glycaemic reaction observed with the glucose-tolerance and the adrenaline tests shows that there is no apparent differences in the carbohydrate metabolism and the glycosynthetic capacity of the liver between diseased and clinically normal animals. The use of the two tests as auxiliary clinical methods has not been effective in registering the deviations in the status of the adrenal cortex and the pituitary gland.

Acidosis↗
PubMed1978

Metabolic effects of clofibrate in insulin-dependent ketosis-prone diabetic man.

This study examined the effects of clofibrate therapy on basal plasma substrate and hormone concentrations in ketosis-prone insulin-dependent diabetic man. A double-blind crossover design was utilized during a 3-mo period in which clofibrate treatment (1 g b.i.d.) was compared to that of a lactose placebo (1 g b.i.d.). Our results demonstrate that clofibrate treatment resulted in a significant reduction in the concentration of plasma glucose, ketone bodies, free fatty acids, triglyceride, and cholesterol in diabetic man. These beneficial effects were observed without demonstrable changes in circulating concentrations of insulin and glucagon. These observations suggest that in ketosis-prone diabetic man, clofibrate therapy may provide an adjunct to exogenous insulin administration.

Adult↗
PubMed1978

Blood amine acid levels in patients with insulin excess (functioning insulinoma) and insulin deficiency (diabetic ketosis).

Blood amino acid concentrations were determined in the postabsorptive state in nine patients with insulin excess (functioning insulinomas), nine juvenile-type diabetics with insulin deficiency (diabetic ketosis due to insulin withdrawal), six juvenile diabetics in moderate metabolic control, and five healthy control subjects. Blood branched-chain amino acid (BCAA) levels were elevated in diabetic ketosis and decreased in patients with insulinomas. Blood concentrations of BCAA were significantly correlated to blood glucose levels, and in diabetics they were also correlated to blood ketone bodies, serum free fatty acids, and glycerol levels. These data indicate an inverse relationship between circulating effective insulin levels and blood BCAA concentrations. It is suggested that blood levels of BCAA might represent an indicator of insulin-dependent alterations of protein metabolism.

Adenoma, Islet Cell↗
PubMed1979

Normalization of insulin and glucagon secretion in ketosis-resistant diabetes mellitus with prolonged diet therapy.

Glucose tolerance and insulin and glucagon secretion were examined sequentially during 6 months of calorie and carbohydrate restriction in an obese, recent-onset, ketosis-resistant diabetic adult. The subject was then followed for 9 additional months, during which some weight was regained. Fasting plasma glucose levels returned to normal after 6 week of calorie restriction and remained normal during periods of carbohydrate refeeding. Normalization of 2-h plasma glucose concentrations after a standard oral carbohydrate load required 5 months, and glucose disposal after an iv glucose load did not return to normal until the end of the study. Insulin secretion in response to oral glucose reached maximal levels during the first months of weight reduction and then decreased as glucose tolerance continued to improve. Acute phase insulin release in response to iv glucose gradually increased throughout the study. Glucagon stimulation by iv arginine and suppression by iv glucose also returned to normal levels slowly over several months. Abnormalities in glucose tolerance and glucoregulatory hormone secretion of ketosis-resistant diabetes are totally reversible with prolonged dietary therapy. Reduction in tissue resistance to the action of insulin also appeared to be of major importance in the recovery of normal glucose tolerance in this subject.

Adult↗
PubMed1977

Investigation of insulin sensitivity in treated subjects with ketosis-prone diabetes mellitus.

Two similar intravenous infucion techniques have been utilized to investigate insulin sensitivity in young subjects with recent-onset ketosis-prone diabetes mellitus. All subjects presented initially with mild to moderately severe ketoacidosis and had been treated with daily insulin therapy for two to eight weeks at the time of study. Six diabetics and 10 normal subjects (group A) received intravenous infusions of glucose (6 mg./kg./min), insulin (80 mU./min.) for 150 minutes. Steady-state plasma glucose (SSPG) and insulin levels (SSPI) were reached by 90 minutes and maintained through the end of the study. As all subjects achieve simolas SSPI while simultaneously receiving similar glucose loads, the SSPG can be used to measure individual insulin sensitivity. Under these conditions the diabetics in group A had a mean SSPG (+/-S.E.) of 99+/-26 mg./100ml., which was not different from the level of 98 +/-14mg./100 ml. for their control subjects. Six diabetics and six normal subjects (group B) received infusions of only glucose (6 mg./kg./min.) and insulin (80 mU./min.). Similar SSPI levels were attained in both the diabetic and control subjects, and their mean SSPG (+/-S.E.) levels were not significantly different (83+/- 13 vs. 61 +/-6 mg./100 ml.). One diabetic in group A and two diabetics in group B had SSPG levels above the highest values measured in their control groups. However, all three had markedly elevated fasting plasma glucose levels on the day of study. In contrast, nine well-controlled diabetics had normal insulin sensitivity. These results suggest that well-controlled subjects with ketosis-prone diabetes mellitus have normal sensitivity to insulin.

Adolescent↗
PubMed1978

The importance of adrenocortical steroids in the pathogenesis of ketosis in diabetic guinea pigs (Caviae porcellus)

The roles of adrenocortical steroids in the pathogenesis of diabetic ketosis were investigated in guinea pigs. Groups of normal and Streptozotocin-induced diabetic animals were either given saline as a control, methylprednisilone as an exogenous steroid, or adrenocorticotrophin to stimulate endogenous steroid production. Plasma and urine ketone determinations were made daily for six days at which time animals were necropsied. The qualitative procedure used failed to detect ketonemia, and ketonuria was only found in diabetic guinea pigs treated with steroids. The results support the hypothesis that the absence of ketosis in spontaneously diabetic guinea pigs may be the result of a relative glucocorticoid insufficiency secondary to fatty degeneration of the adrenal glands, a common lesion in spontaneously diabetic guinea pigs.

Adrenal Cortex Hormones↗
PubMed1977

Lactic acidosis complicating diabetic ketosis in a patient with hyperthyroidism.

The present report describes a patient with insulin-dependent diabetes who developed simultaneously lactic acidosis and ketoacidosis following insulin deprivation. Administration of insulin at low doses rapidly corrected both ketosis and lactic acidosis. There had been neither circulatory collapse, nor phenformin intake, and hepatic function was normal. The development of lactic acidosis in this case was possibly precipitated by hyperthyroidism. A review of the literature indicates that lactic acidosis is a very rare complication of diabetic ketosis per se.

Acidosis↗
PubMed1979

Oral nicotinic acid as a treatment for ketosis.

Changes in blood metabolites and milk production were measured in eight cows with subclinical or clinical ketosis following treatment with daily doses of 12 g nicotinic acid fed with the concentrate mixture. Ketotic cows displayed a positive milk ketone test, reduced milk production and feed intake, hypoglycemia, hyperketonemia, and elevated free fatty acids in plasma. The milk ketone test was negative in all cows 5 to 9 days following initiation of treatment. After 7 days of treatment, milk production and glucose in plasma were increased while there were decreases in plasma beta-hydroxybutyrate and free fatty acids. No relapses occurred.

Acidosis↗
PubMed1977

[Biochemical and histological studies of cows with ketosis].

Biochemical and histological investigations were carried out with cows affected with ketosis in a subclinical and clinical form. Parellel studies were performed with normal (control) cows originating from the herds with the ill animals and manifesting the same physiologic status. It was found that the blood level of glucose in the diseased cows was lowered more than 2.6 times, and the content of ketone bodies was higher-- it was increased 4.6 times, that of total lipids was 2.6 times higher, and that of free fatty acids was 3.5 times higher as compared to the same indices in the controls. The blood content of pyruvate in the affected cows was also increased. The liver glycogen in these animals was lowered from 2.1 to 4.1 times. The activity of glucose-6-phosphatase was lower, and that of glucose-6-phosphatedehydrogenase was higher as against the same indices shown by normal cows.

Acidosis↗
PubMed1979

A field survey of fat mobilization and liver function of dairy cows during early lactation. Relationship to energy balance, appetite and ketosis.

NEFA, total lipids, bilirubin, GOT, acetoacetate and glucose in blood plasma of cows were measured during early lactation. Feeding and yield were also recorded. NEFA and bilirubin values showed a gradual decrease with advancing lactation, while total lipids rose gradually during the first months of lactation. GOT showed no definite trend during early lactation. Acetoacetate values were at maximum 21--30 days post partum and glucose values were high at partus and low during the first weeks of lactation. NEFA were negatively correlated to energy balance during the first month of lactation. Total lipids, bilirubin and GOT seemed not to be dependent on energy balance in cows with normal appetite. NEFA, bilirubin and GOT were significantly elevated in cows with reduced appetite. NEFA were positively correlated to bilirubin, GOT and acetoacetate and negatively correlated to glucose. The correlation coefficients were higher during the first month of lactation than during the second and third month. Cows contracting clinical ketosis showed high values of NEFA a long time before any clinical symptoms appeared. Significantly increased values of acetoacetate occurred only the last days before treatment when plasma glucose had reached low values.

Acetoacetates↗