Plasma Ketone Body Concentrations Research Articles

Dietary supplementing phytosterols improves the metabolic status of perinatal cows revealed by plasma metabolomics and faecal microbial metabolism.

Previous research reported that dietary addition with phytosterols improved the energy utilisation of the rumen microbiome, suggesting its potential to alleviate the negative energy balance of perinatal cows. This experiment aimed to explore the effects of feeding phytosterols on the metabolic status of perinatal cows through plasma metabolomics and faecal bacteria metabolism. Ten perinatal Holstein cows (multiparous, 2 parities) with a similar calving date were selected four weeks before calving. After 7 days for adaptation, cows were allocated to two groups (n=5), which respectively received the basal rations supplementing commercial phytosterols at 0 and 200 mg/d during a 42-day experiment. The milk yield of each cow was recorded daily after calving. On days 1 and 42, blood and faeces samples were all collected from perinatal cows before morning feeding for analysing plasma biochemicals and metabolome, and faecal bacteria metabolism. Dietary addition with phytosterols at 200 mg/d had no effects on plasma cholesterol and numerically increased milk yield by 1.82 kg/d (p>0.10) but attenuated their negative energy balance in perinatal cows as observed from the significantly decreased plasma level of β-hydroxybutyric acid (p=0.002). Dietary addition with phytosterols significantly altered 12 and 15 metabolites (p<0.05) within the plasma and faeces of perinatal cows, respectively. Of these metabolites, 5 upregulated plasma fatty acids indicated an improved energy status (i.e., C18:1T, C14:0, C17:0, C18:0, and C16:0). Milk yield negatively correlated with plasma concentrations of ketone bodies (p=0.035) and 5-methoxytryptamine (p=0.039). Furthermore, dietary addition with phytosterols at 200 mg/d had no effects on fermentation characteristics and bacterial diversity of cow faeces (p>0.10) but improved potentially beneficial bacteria such as Christensenellaceae family (p<0.05) that positively correlated with feed efficiency. Dietary addition with phytosterols at 200 mg/d could effectively improve the energy status in perinatal cows by attenuating their negative energy balance.

Complex Positive Effects of SGLT-2 Inhibitor Empagliflozin in the Liver, Kidney and Adipose Tissue of Hereditary Hypertriglyceridemic Rats: Possible Contribution of Attenuation of Cell Senescence and Oxidative Stress.

(1) Background: empagliflozin, sodium-glucose co-transporter 2 (SGLT-2) inhibitor, is an effective antidiabetic agent with strong cardio- and nephroprotective properties. The mechanisms behind its cardio- and nephroprotection are still not fully clarified. (2) Methods: we used male hereditary hypertriglyceridemic (hHTG) rats, a non-obese model of dyslipidaemia, insulin resistance, and endothelial dysfunction fed standard diet with or without empagliflozin for six weeks to explore the molecular mechanisms of empagliflozin effects. Nuclear magnetic resonance (NMR)-based metabolomics; quantitative PCR of relevant genes involved in lipid and glucose metabolism, or senescence; glucose and palmitic acid oxidation in isolated tissues and cell lines of adipocytes and hepatocytes were used. (3) Results: empagliflozin inhibited weight gain and decreased adipose tissue weight, fasting blood glucose, and triglycerides and increased HDL-cholesterol. It also improved insulin sensitivity in white fat. NMR spectroscopy identified higher plasma concentrations of ketone bodies, ketogenic amino acid leucine and decreased levels of pyruvate and alanine. In the liver, adipose tissue and kidney, empagliflozin up-regulated expression of genes involved in gluconeogenesis and down-regulated expression of genes involved in lipogenesis along with reduction of markers of inflammation, oxidative stress and cell senescence. (4) Conclusion: multiple positive effects of empagliflozin, including reduced cell senescence and oxidative stress, could contribute to its long-term cardio- and nephroprotective actions.

Association of Circulating Ketone Bodies With Functional Outcomes After ST-Segment Elevation Myocardial Infarction

BackgroundCirculating ketone bodies (KBs) are increased in patients with heart failure (HF), corresponding with increased cardiac KB metabolism and HF severity. However, the role of circulating KBs in ischemia/reperfusion remains unknown. ObjectivesThis study sought to investigate longitudinal changes of KBs and their associations with functional outcomes in patients presenting with ST-segment elevation myocardial infarction (STEMI). MethodsKBs were measured in 369 participants from a randomized trial on early metformin therapy after STEMI. Nonfasting plasma concentrations of KBs (β-hydroxybutyrate, acetoacetate, and acetone) were measured by nuclear magnetic resonance spectroscopy at presentation, at 24 hours, and after 4 months. Myocardial infarct size and left ventricular ejection fraction (LVEF) were determined by cardiac magnetic resonance imaging at 4 months. Associations of circulating KBs with infarct size and LVEF were determined using multivariable linear regression analyses. ResultsCirculating KBs were high at presentation with STEMI (median total KBs: 520 μmol/L; interquartile range [IQR]: 315-997 μmol/L). At 24 hours after reperfusion, KBs were still high compared with levels at 4-month follow-up (206 μmol/L [IQR: 174-246] vs 166 μmol/L [IQR: 143-201], respectively; P < 0.001). Increased KB concentrations at 24 hours were independently associated with larger myocardial infarct size (total KBs, per 100 μmol/L: β = 1.56; 95% confidence interval: 0.29-2.83; P = 0.016) and lower LVEF (β = −1.78; 95% CI: (−3.17 to −0.39; P = 0.012). ConclusionsCirculating KBs are increased in patients presenting with STEMI. Higher KBs at 24 hours are associated with functional outcomes after STEMI, which suggests a potential role for ketone metabolism in response to myocardial ischemia. (Metabolic Modulation With Metformin to Reduce Heart Failure After Acute Myocardial Infarction: Glycometabolic Intervention as Adjunct to Primary Coronary Intervention in ST Elevation Myocardial Infarction (GIPS-III): a Randomized Controlled Trial; NCT01217307)

Homeostatic versus hedonic control of carbohydrate selection.

Macronutrient intake is associated with cardiometabolic health, ageing and longevity, but the mechanisms underlying its regulation have remained unclear. Most rodents increase carbohydrate selection under certain physiological and pathological conditions such as fasting. When presented with a choice between a basally preferable high-fat diet (HFD) and a high-carbohydrate diet (HCD) such as a high-sucrose diet, fasted mice first eat the HFD and then switch to the HCD during the first few hours of refeeding and continue to eat the HCD up to 24h in the two-diet choice approach. Such consumption of an HCD after fasting reverses the fasting-induced increase in the plasma concentration of ketone bodies more rapidly than does refeeding with an HFD alone. 5'-AMP-activated protein kinase (AMPK)-regulated neurons in the paraventricular nucleus of the hypothalamus (PVH) that express corticotropin-releasing hormone (CRH) are necessary and sufficient for the fasting-induced selection of carbohydrate over an HFD in mice. These neurons appear to contribute to a fasting-induced increase in the positive valence of carbohydrate without affecting the preference for more palatable and energy-dense diets such as an HFD. Identification of the neural circuits in which AMPK-regulated CRH neurons in the PVH of mice are embedded should shed new light on the physiological and molecular mechanisms responsible for macronutrient selection.

Sleep profile during fasting in PPAR-alpha knockout mice

Peroxisome proliferator-activated receptor alpha (PPARα) is a transcription factor that belongs to the nuclear receptor family and plays an important role in regulating gene expression associated with lipid metabolism. PPARα promotes hepatic fatty acid oxidation and ketogenesis in response to fasting. Because energy metabolism is known to affect sleep regulation, manipulations that change PPARα are likely to affect sleep and other physiological phenotypes. In this study, we examined the role of PPARα in sleep/wake regulation using PPARα knockout (KO) mice. Sleep, body temperature (BT), locomotor activity, arterial pressure (AP) and heart rate (HR) were recorded in KO mice and wild-type (WT) controls under ad libitum-fed conditions and 24-hour food deprivation (FD). KO and WT mice were identical in basal sleep amount, BT, mean AP and HR, although KO mice showed enhanced sleepiness (enhanced EEG slow-wave activity). In response to FD, KO mice showed a large drop in wakefulness and locomotor activity at the end of the dark phase, whereas WT mice did not. Similarly, AP and HR, which were suppressed by FD, decreased more in KO than in WT mice. Compared to WT mice, KO mice showed a reduced concentration of plasma ketone bodies and decreased mRNA expression of the ketogenic enzyme gene Hmgcs2 in the liver and brain under FD conditions. These results suggest that PPARα and/or lipid metabolism is involved in the maintenance of wakefulness and locomotor activity during fasting in mice.

Ketogenic diet in pyruvate dehydrogenase complex deficiency: short- and long-term outcomes

ObjectivesOur aime was to study the short- and long-term effects of ketogenic diet on the disease course and disease-related outcomes in patients with pyruvate dehydrogenase complex deficiency, the metabolic factors implicated in treatment outcomes, and potential safety and compliance issues.MethodsPediatric patients diagnosed with pyruvate dehydrogenase complex deficiency in Sweden and treated with ketogenic diet were evaluated. Study assessments at specific time points included developmental and neurocognitive testing, patient log books, and investigator and parental questionnaires. A systematic literature review was also performed.ResultsNineteen patients were assessed, the majority having prenatal disease onset. Patients were treated with ketogenic diet for a median of 2.9 years. All patients alive at the time of data registration at a median age of 6 years. The treatment had a positive effect mainly in the areas of epilepsy, ataxia, sleep disturbance, speech/language development, social functioning, and frequency of hospitalizations. It was also safe—except in one patient who discontinued because of acute pancreatitis. The median plasma concentration of ketone bodies (3-hydroxybutyric acid) was 3.3 mmol/l. Poor dietary compliance was associated with relapsing ataxia and stagnation of motor and neurocognitive development. Results of neurocognitive testing are reported for 12 of 19 patients.ConclusionKetogenic diet was an effective and safe treatment for the majority of patients. Treatment effect was mainly determined by disease phenotype and attainment and maintenance of ketosis.

Ketogenic Diet and Cancer-a Perspective.

Research of the last two decades showed that chronic low-grade inflammation, elevated blood glucose and insulin levels may play role in the onset of a number of non-communicable diseases such as type 2 diabetes and some forms of cancer. Regular exercise and fasting can ameliorate high blood glucose and insulin levels as well as increase the concentration of plasma ketone bodies. These, in consequence, may lead to reduction of inflammation. Exercise or severe restriction of caloric intake is not always advisable for patients, in particular those suffering from cancer. The ketogenic diet (KD), characterized by high fat, moderate protein and very low carbohydrate composition can evoke a physiological state similar to that triggered by exercise or fasting. These attributes of KD prompted its possible use in treatment of a number of metabolic diseases, including several types of malignancies. Although results from clinical studies employing KD in the treatment of cancer are still limited, the results obtained from animal models are encouraging and show that KD presents a viable option as an adjunct therapy for cancer.

Effect of Glucose Administration on the Metabolism during Surgery

Background and aim: Glucose is stored mainly in the liver and muscles as glycogen. However, the total calories are less than basal energy expenditure for one day. Overnight fast before surgery may be stressful for patients. Therefore, we investigated the effect of glucose administration on the metabolic state during anesthesia. Methods: After getting written informed consent, patients undergoing maxillofacial surgery were randomly assigned to two groups throughout the surgical procedure, G group receiving acetated Ringer solution with 1.5% glucose (n=12) and R group receiving acetated Ringer solution without glucose (n=11). Anesthesia was maintained with remifentanil and sevoflurane. Blood glucose level was monitored continuously using the STG-22TM from after the induction of anesthesia. Plasma ketone bodies were evaluated before and after surgery. Respiratory quotient (RQ) was monitored continuously during anesthesia using the indirect calorimetry V-Max. Results: In G group (n=12), patients received 0.17 ± 0.03 g/kg/hr of glucose. But hyperglycemia did not observed during surgery. The mean blood glucose levels were maintained stably <150 mg/dL during surgery. The plasma concentration of ketone bodies was significantly higher at T4 in R group than in G group (p=0.027). However, it decreased from T1 to T3, T4 in G group. RQ decreased significantly from 0.93 ± 0.14 to 0.78 ± 0.11 in the R group (p=0.037), while it was kept at 0.88 ± 0.09 in the G group. There is no significant difference between group R and group G in REE during operation. Conclusion: Intraoperative 0.17 ± 0.03 g/kg/hr of glucose administration may suppress ketogenesis and can maintain glucose metabolism successfully without causing hyperglycemia.

Lauric Acid Stimulates Ketone Body Production in the KT-5 Astrocyte Cell Line.

Coconut oil has recently attracted considerable attention as a potential Alzheimer's disease therapy because it contains large amounts of medium-chain fatty acids (MCFAs) and its consumption is thought to stimulate hepatic ketogenesis, supplying an alternative energy source for brains with impaired glucose metabolism. In this study, we first reevaluated the responses of plasma ketone bodies to oral administration of coconut oil to rats. We found that the coconut oil-induced increase in plasma ketone body concentration was negligible and did not significantly differ from that observed after high-oleic sunflower oil administration. In contrast, the administration of coconut oil substantially increased the plasma free fatty acid concentration and lauric acid content, which is the major MCFA in coconut oil. Next, to elucidate whether lauric acid can activate ketogenesis in astrocytes with the capacity to generate ketone bodies from fatty acids, we treated the KT-5 astrocyte cell line with 50 and 100 μM lauric acid for 4 h. The lauric acid treatments increased the total ketone body concentration in the cell culture supernatant to a greater extent than oleic acid, suggesting that lauric acid can directly and potently activate ketogenesis in KT-5 astrocytes. These results suggest that coconut oil intake may improve brain health by directly activating ketogenesis in astrocytes and thereby by providing fuel to neighboring neurons.

Contribution of PPARα and Ketone Body to Sleep Homeostasis in Mice

Sleep and energy metabolism have been known to share common regulatory mechanisms. Sleep restriction leads to metabolic disorders such as obesity and diabetes. However, the mechanisms of the relationships between sleep restriction and metabolic disorders have remained elusive. We have recently found that peroxisome proliferator‐activated receptors alpha (PPARα), a transcriptional factors belonging to the nuclear receptor, is involved in the regulation of sleep homeostasis. Chronic treatment of bezafibrate, a PPARs agonist enhanced the slow‐wave activity (SWA) in non‐rapid eye movement (NREM) sleep in mice. In the bezafibrate‐treated mice, plasma concentration of acetoacetate (AcAc) was increased while β‐hydroxybutyrate (BHB) was decreased. Ketogenesis is modulated by the activity of PPARα under the condition of low glucose availability. To investigate the specific effects of ketone bodies on sleep homeostasis, plasma concentration of ketone bodies were measured after sleep deprivation for 6 hours. Sleep deprivation increased plasma ketone bodies (both AcAc and BHB) and increased mRNA expression of PPARα and mitochondrial 3‐hydroxy‐3‐methylglutaryl CoA synthase 2 (Hmgcs2), a rate‐limiting enzymes of ketogenesis, in the hypothalamus and cortex. In addition, central injection of AcAc, but not BHB, increased SWA during NREM sleep and suppressed glutamate release. These results suggest that central PPARα and ketone body metabolism play a significant role in the interaction of lipid metabolism and sleep homeostasis.

Exercise enhances following sleep in mice

Increasing evidence suggests that acute or chronic exercise has significant effects on insomnia. However, the mechanisms underlying neural function of physical activity on the sleep functions are still unclear. The present study was designed to verify the effect of acute treadmill exercise on sleep in mice. Male ICR mice (10 weeks old) were subjected to a single bout of running (at the speed of 100 rpm/min) for 0, 5, 15, 30, or 60 minutes at the beginning of the light phase. In order to unify the duration of sleep deprivation, mice in each group were deprived sleep during non-running period (for up to 90 minutes). After the running, sleep was recorded for 14 hours. Mice running for 5 or 15 minutes showed no difference in following sleep. Mice with running for 30 minutes showed remarkable increase in the amount of non-rapid eye movement (NREM) sleep and enhanced slow-wave activity (SWA) during NREM sleep. Plasma concentration of ketone bodies (acetoacetate and β-hydroxybutyrate) in mice with running for 30 minutes were increased compared with that of 15-mitutes running or control (only sleep-deprived/non-treated) mice. These findings suggest that acute exercise induces longer and deeper sleep and enhance the ketone body production.

Retrospective case studies of the efficacy of caprylic triglyceride in mild-to-moderate Alzheimer's disease.

Under normal conditions, the adult human brain is fueled primarily by glucose. A prominent feature of Alzheimer’s disease (AD) is region-specific decreases in cerebral glucose metabolism. Ketone bodies are a group of compounds produced from fat stores during periods of low glucose availability that can provide an alternative to glucose for brain metabolism. Consumption of sufficient quantities of caprylic triglyceride (CT) increases plasma concentrations of ketone bodies and may be beneficial in conditions of compromised glucose metabolism, such as AD. The present study describes the use of CT in mild-to-moderate AD in routine clinical practice. Case records from eight patients with extensive monitoring of cognitive function using the Mini-Mental State Examination (MMSE) and who had received CT for ≥6 months were reviewed. All were outpatients aged ≥50 years, cared for in standard practice, had a diagnosis of probable AD of mild-to-moderate severity (MMSE 14–24), and had received CT for at least 6 months in addition to other approved pharmacotherapy for AD. Response to CT administration as measured by MMSE scores varied by patient. However, the rate of decline in MMSE scores appeared slower than previously published reports for patients treated with pharmacotherapy alone. Profiling of individual patients may provide insight regarding those most likely to benefit from addition of CT to currently approved AD pharmacotherapy.

Diet physical form, fatty acid chain length, and emulsification alter fat utilization and growth of newly weaned pigs1

An experiment was conducted to examine the interplay of diet physical form (liquid vs. dry), fatty acid chain length [medium- (MCT) vs. long-chain triglyceride (LCT)], and emulsification as determinants of fat utilization and growth of newly weaned pigs. Ninety-six pigs were weaned at 20.0 ± 0.3 d of age (6.80 ± 0.04 kg) and fed ad libitum 1 of 8 diets for 14 d according to a 2(3) factorial arrangement of treatments with 6 pens per diet and 2 pigs per pen. The MCT contained primarily C8:0 and C10:0 fatty acids, whereas the LCT mainly contained C16:0, C18:0, C18:1, and C18:2. Diet physical form greatly impacted piglet growth (P < 0.001), with liquid-fed pigs (486 g/d) growing faster than dry-fed pigs (332 g/d) by 46%. Pigs fed LCT grew 22% faster (P = 0.01) than MCT-fed pigs; however, effects of emulsifier were not detected (P > 0.1). Furthermore, feed intake and G:F were 15% and 29% greater for liquid-fed pigs, and intake also was 21% greater for pigs fed LCT (P = 0.01). Diet physical form had no effect on apparent ileal fatty acid digestibility, but as expected, digestibility was greater (P < 0.001) for the MCT than the LCT diet (98.5% vs. 93.4%). Emulsification improved digestibility of most fatty acids in pigs fed LCT but not MCT (interaction, P < 0.01). Both jejunal and ileal villi height increased from 7 to 14 d postweaning (P < 0.01). Liquid-fed pigs had greater jejunal crypt depth (P < 0.05) compared with pigs fed the dry diet; however, ileal morphology was not affected by diet physical form, fat chain length, or emulsification. Plasma ketone body concentrations were 6-fold greater in pigs fed MCT than LCT, and the difference was greater in pigs fed dry diets (interaction, P = 0.01). The bile salt concentration in jejunal digesta was 2.2-fold greater in pigs fed LCT than in pigs fed MCT (P < 0.001). Collectively, we conclude that feeding liquid diets containing emulsified LCT can improve fat utilization and markedly accentuate feed intake, growth, and G:F of weanling pigs.

Impact of feeding and post prandial time on plasma ketone bodies in sows during transition and lactation1

Two experiments were conducted with the aim of studying how dietary fat source, reproductive stage (Exp. 1), and diurnal variation (Exp. 2) affect plasma ketone bodies in sows. In Exp. 1, 40 second-parity sows were fed 1 of 5 lactation diets from 7 d prepartum until 28 d postpartum, with low or high levels (3% or 8%) of dietary fats with different proportions of medium- and long-chain fatty acids. Blood was obtained by jugular venipuncture on d 3 and 7 prepartum, and d 1, 10, 17, and 28 postpartum, and concentrations of plasma beta-hydroxy butyric acid (BHBA), acetoacetate + acetone (AcAc+Ac), glucose, NEFA, lactate, acetate, and butyrate were determined. For 4 out of 5 treatments, plasma BHBA decreased slightly, whereas plasma AcAc+Ac remained stable. However, plasma BHBA (P < 0.01) and AcAc+Ac (P < 0.001) doubled after d 10 of lactation in sows fed 4% octanoic acid and 4% fish oil diet (4+4% FO; P < 0.001), compared with earlier in lactation (P < 0.001). Plasma AcAc+Ac was positively related to BHBA (P < 0.01), glucose (P < 0.05), and butyrate (P < 0.001), and negatively related to the acetate:butyrate ratio (P < 0.001). In addition, plasma BHBA was positively related to lactate (P < 0.01), acetate, and butyrate (P < 0.05). In Exp. 2, diurnal variations of plasma metabolites were studied in 5 sows sampled every second hour from a jugular catheter throughout a 24-h period on d 5 and 17 of lactation and analyzed as in Exp. 1. In addition, milk and urine samples were collected and analyzed for BHBA and AcAc+Ac. No diurnal variations in plasma BHBA or AcAc+Ac were observed and plasma AcAc+Ac was unchanged from d 5 to 17 of lactation (3.7 μM), whereas BHBA declined from 58 μM on d 5 of lactation to 52 μM on d 17 of lactation (P < 0.05). Minor amounts of AcAc+Ac were found in urine (8.6 μM) and this was not affected by days in milk, whereas the content of AcAc+Ac in milk and BHBA in milk and urine were less than the detection limit in 4 of 5 sows. In conclusion, dietary fat source affected plasma concentrations of ketone bodies, but the concentrations were much less than normally observed in dairy cows and, therefore, primary ketosis does not appear to be a major problem in sows. In addition, this study indicates that the intermediary metabolism of sows was challenged when sows were exposed to high fat diets in late gestation.

Effect of a lucerne feeding strategy in the first week postpartum on feed intake and ketone body profiles in blood plasma, urine, and milk in Holstein cows

The objectives were to investigate the effects of a lucerne feeding strategy to postpartum transition dairy cows on feed intake and ketone body profiles in plasma, urine, and milk. At calving, 13 Holstein cows were assigned to one of two treatments: a control lactation diet or a lucerne haylage lactation diet (lucerne) in the first week postpartum. From week 2 to 4 postpartum, all cows were fed the control lactation diet. In the first week postpartum, dry matter intake (DMI) was unaffected by treatment, but during week 2–4 postpartum, DMI was lower for lucerne as compared with control. The concentrations of ketone bodies in plasma, urine, and milk tended to be greater at 4 days in milk for lucerne as compared with control. Plasma concentrations of ketone bodies correlated stronger to urinary concentrations than to milk concentrations.

Breast-v.formula-feeding: impacts on the digestive tract and immediate and long-term health effects

The health benefits of breast-feeding have been recognised for a long time. In particular, breast-feeding is associated with lower incidence of necrotising enterocolitis and diarrhoea during the early period of life and with lower incidence of inflammatory bowel diseases, type 2 diabetes and obesity later in life. The higher nutritional and protective degree of human milk is related to its nutritional composition that changes over the lactation period and to the biological activities of specific components while lower growth rate of breast-fed infants may be attributed to their self-regulation of milk intake at a lower level than formula-fed infants. Many results now suggest that the developmental changes in intestinal and pancreatic function that occur postnatally are modulated by the diet. Indeed, formula-feeding induces intestinal hypertrophy and accelerates maturation of hydrolysis capacities; it increases intestinal permeability and bacterial translocation, but does not induce evident differences in microbiota composition. Whether these changes would be beneficial for enhancing absorptive capacities and for educating the gut-associated immune system remains to be further studied. Moreover, it is evident that formula-feeding increases basal blood glucose and decreases plasma ketone body concentrations, while discrepancies on postprandial glycaemia, insulin and incretin responses in both human studies and experimental studies are inconclusive. Manipulating the composition of formula, by reducing protein content, adding prebiotics, growth factors or secretory IgA can modulate intestinal and pancreatic function development, and thereby may reduce the differential responses between breast-fed and formula-fed neonates. However, the developmental responses of the digestive tract to different feeding strategies must be elucidated in terms of sensitivity to developing diseases, taking into account the major role of the intestinal microbiota.

Effect of intraoperative acetated Ringer’s solution with 1% glucose on glucose and protein metabolism

To investigate the effects of the intraoperative administration of Ringer's solution with 1% glucose on the metabolism of glucose, lipid and muscle protein during surgery. Thirty-one adult patients, American Society of Anesthesiologists physical status I or II, undergoing elective otorhinolaryngeal, head and neck surgeries were randomly assigned to one of two patient groups: those receiving acetated Ringer's solution with 1% glucose (Group G) or those receiving acetated Ringer's solution without glucose (Group R) throughout the surgical procedure. Plasma glucose was measured at anesthetic induction (T0), artery 1 h (T1), 2 h (T2), 3 h after anesthetic induction (T3) and at the end of surgery (T4). Plasma ketone bodies, insulin and 3-methylhistidine were measured at T0 and T4. The intravenous infusion for patients in Group G and R was 6.1 + or - 0.8 and 6.3 + or - 1.7 ml/kg/h, respectively, with Group G patients receiving a dose of 4.1 g/h glucose. Plasma glucose levels were significantly higher in Group G than in Group R patients at T1, T2, T3 and T4; however, plasma glucose remained <150 mg/dl in both groups. The plasma concentration of ketone bodies was significantly higher (P < 0.05) in Group R than in Group G patients at T4. Changes in plasma 3-methylhistidine concentration was significantly lower in Group G than in Group R patients. These results indicate that acetated Ringer's solution with 1% glucose decreased protein catabolism without hyperglycemia among the Group G patients. The infusion of a small dose of glucose (1%) during minor otorhinolaryngeal, head and neck surgeries may suppress protein catabolism without hyperglycemia and hypoglycemia.

Plasma concentration of anti‐diuretic hormone and urine volume in response to intraruminal administration of acetate, propinata and butyrate in suckling calves

Acetate, propionate, and butyrate were intraruminally administered to dry feed-fed suckling calves to evaluate their effects on plasma ketone bodies, anti-diuretic hormone (ADH) concentrations, and urine volume. Four male Holstein calves (5-7 weeks old) were given 1.0 L of warm water or 0.5 mole of one of the acids in 1.0 L of warm water. A 4 x 4 Latin square design was adopted for the experiment. The acetate group showed significantly higher plasma acetate concentrations than the other three groups between 0.25 h and 2.0 h after administration (P < 0.01). Plasma glucose concentrations did not differ markedly among the groups. The butyrate group showed significantly higher plasma ketone body concentrations than the other three groups until the end of the experiment (P < 0.01). Plasma ADH concentrations quickly rose in the butyrate group and remained significantly higher than in the other three groups from 0.25 h to 2.5 h after administration (P < 0.05). In accordance with the elevation of plasma ADH levels, the butyrate group showed decreases in urine volume and increases in urine osmolarity (P < 0.05). Plasma osmolarity and hematocrit values (Ht) were not different among the groups. These results suggest that the administration of acetate and propionate had little effect on ADH secretion.

Changes in Insulin, Glucose and Ketone Bodies, But Not Leptin or Body Fat Content Precede Restoration of Luteinising Hormone Secretion in Ewes

The reproductive system, including pulsatile luteinising hormone (LH) secretion, is inhibited by deficits in energy availability and restored by energy surfeits. Plasma LH, insulin, leptin, ghrelin, glucose, ketone body, and nonesterified fatty acid concentrations were measured in ovariectomised, food-restricted ewes before and after return to ad libitum feeding to determine the factors that change in time to account for the restoration of pulsatile LH secretion. At 07.00 h, blood was sampled every 10 min for 5 h from ovariectomised, hypogonadotrophic, chronically food-restricted and ad libitum-fed ewes (Fed). At 12.00 h, four of the food-restricted sheep were given ad libitum access to food (Re-Fed), while three ewes continued to be food restricted (Restricted). Sampling continued for 5 h and resumed again on the mornings of days 2, 4, and 9. A pulse of LH was seen within 1 h of re-feeding in all Re-Fed ewes, and interpulse interval (IPI) was significantly shorter in Re-Fed compared to Restricted ewes and longer than in Fed ewes during the period after re-feeding. Re-Fed LH IPI was not restored to that of Fed ewes until sometime between days 4 and 9. The first pulse occurred within minutes, whereas restoration of IPI occurred after 4-8 days. Prior to the initial LH pulses seen in Re-Fed ewes, plasma ketone bodies first fell and then rose to levels significantly above those in Restricted ewes. Significant changes in circulating insulin, ghrelin, glucose, and total ketone body concentrations, daily food intake and lean body mass preceded restoration of Re-Fed LH IPI some time between days 4 and 9, but there were no significant changes in adiposity or circulating leptin concentrations, consistent with the hypothesis that LH pulses are reinitiated by changes in the availability of oxidisable metabolic fuels and possibly insulin, but not leptin concentrations.

Plasma concentration of antidiuretic hormone in response to intraruminal administration of butyrate in suckling calves

Our previous study has revealed that providing dry feeds increased the plasma concentration of antidiuretic hormone (ADH) in suckling calves, leading to altered water balance. To examine whether ketone bodies formed from ruminal fermentation-derived butyrate induced ADH secretion in suckling calves, the effects of intraruminal administration of butyrate on plasma concentration of ADH and ketone bodies, plasma and urine osmolality, and urine volume were examined. Six male Holstein calves aged 4 wk were used. Three levels of butyrate (0 g, 22 g and 44 g) were intraruminally administrated in a 3 × 3 Latin square design, and blood plasma and urine were analyzed. Plasma concentration of ketone bodies was increased by intraruminal administration of butyrate within 15 min in a dose-dependent manner, and the elevation of plasma levels continued until 4 h. Plasma concentration of ADH was also increased by the butyrate treatment, and it was higher in the 44 g butyrate group than in the 22 g butyrate group from 15 min to 2 h. The duration of the elevated plasma concentration of ADH was shorter than that of plasma concentration of ketone bodies. The relationship between plasma concentrations of ADH and those of ketone bodies was statistically significant, although the relationship was weaker. In accordance with the elevation of plasma ADH levels, the butyrate treatment resulted in the decreases in urine volume and increases in urine osmolality. Plasma osmolality was not different among the groups. The present results suggest that ruminal butyrate-derived ketone bodies are at least partly responsible for ADH secretion in suckling calves fed with dry feeds, and that the secreted ADH decreases urine volume through the increase in urine osmolality.