scholarly journals Ketone body supplement label claims: what supplement has been supplemented?

2019 ◽  
Vol 31 (1) ◽  
pp. 1-2
Author(s):  
D Da Costa ◽  
V Bangalee ◽  
K Subban ◽  
R Naidoo

Background: There is a keen interest in performance-enhancing supplementation and the associated benefits, despite reports of incorrect label claims made by manufacturers and the questionable efficacy of the supplements. The use of ketone body supplements as a source of fuel during exercise and sporting performance, in particular, is of interest to sportspeople. By increasing blood ketone body levels, with an accompanying decrease in blood glucose, may indicate a state of nutritional ketosis, whereby the body no longer relies on glucose metabolism but rather the metabolism of ketone bodies. This could be beneficial for long, slow steady-state endurance exercise. Discussion: There are numerous ketone body supplements on the market manufactured in South Africa and internationally. However, unlike medicines, the sports supplementation industry is poorly regulated. Furthermore, ketone body supplementation with regard to its effects on improving exercise and athletic performance is still unconvincing. Conclusion: Within the ever-changing sports supplementation industry, ketone body supplements are being used despite controversies regarding the accuracy and scientific merit of label claims. The ingredients and their quantities, as well as the performance benefits, need to be objectively validated.

Author(s):  
Minsoo Kang ◽  
Sun Kyoung Han ◽  
Suhyun Kim ◽  
Sungyeon Park ◽  
Yerin Jo ◽  
...  

Abstract Hepatic gluconeogenesis is the central pathway for glucose generation in the body. The imbalance between glucose synthesis and uptake leads to metabolic diseases such as obesity, diabetes, and cardiovascular diseases. Small leucine zipper protein (sLZIP) is an isoform of LZIP and it mainly functions as a transcription factor. Although sLZIP is known to regulate the transcription of genes involved in various cellular processes, the role of sLZIP in hepatic glucose metabolism is not known. In this study, we investigated the regulatory role of sLZIP in hepatic gluconeogenesis and its involvement in metabolic disorder. We found that sLZIP expression was elevated during glucose starvation, leading to the promotion of phosphoenolpyruvate carboxylase and glucose-6-phosphatase expression in hepatocytes. However, sLZIP knockdown suppressed the expression of the gluconeogenic enzymes under low glucose conditions. sLZIP also enhanced glucose production in the human liver cells and mouse primary hepatic cells. Fasting-induced cyclic adenosine monophosphate impeded sLZIP degradation. Results of glucose and pyruvate tolerance tests showed that sLZIP transgenic mice exhibited abnormal blood glucose metabolism. These findings suggest that sLZIP is a novel regulator of gluconeogenic enzyme expression and plays a role in blood glucose homeostasis during starvation.


1970 ◽  
Vol 116 (5) ◽  
pp. 865-874 ◽  
Author(s):  
G. D. Baird ◽  
R. J. Heitzman

1. The hepatic concentrations of the ketone bodies and of metabolites and activities of enzymes involved in gluconeogenesis were measured in healthy lactating and non-lactating cows 48h after administration of Voren, an ester of dexamethasone, and compared with those found in control animals given saline. Parallel measurements were also made of the blood concentrations of several of the metabolites. 2. Blood glucose concentrations were raised in the Voren-treated animals, whereas blood ketone body and free fatty acid concentrations were unaltered. Similarly there was no change in the hepatic concentrations of the ketone bodies. 3. Significant increases were found in the hepatic concentrations of citrate, 2-oxo-glutarate and malate in both groups of animals given Voren. 4. The hepatic concentrations of those glycolytic intermediates that were measured either decreased or did not change after Voren treatment. 5. The enzymes aspartate transaminase and fructose 1,6-diphosphatase were unchanged in activity after Voren administration, whereas phosphopyruvate carboxylase (EC 4.1.1.32) activity was depressed in the lactating group. However, glucose 6-phosphatase, tryptophan oxygenase and tyrosine aminotransferase increased in activity. 6. In several cases those hepatic metabolites that increased in concentration after Voren administration were present in lower concentration in normal lactating cows than in normal non-lactating cows. The same applied mutatis mutandis to those metabolites that were decreased by Voren. 7. These findings are discussed in relation to the use of glucocorticoids in the treatment of bovine ketosis.


Sports ◽  
2019 ◽  
Vol 7 (2) ◽  
pp. 40 ◽  
Author(s):  
Sihui Ma ◽  
Katsuhiko Suzuki

A ketogenic diet (KD) could induce nutritional ketosis. Over time, the body will acclimate to use ketone bodies as a primary fuel to achieve keto-adaptation. Keto-adaptation may provide a consistent and fast energy supply, thus improving exercise performance and capacity. With its anti-inflammatory and anti-oxidative properties, a KD may contribute to muscle health, thus preventing exercise-induced fatigue and damage. Given the solid basis of its potential to improve exercise capacity, numerous investigations into KD and exercise have been carried out in recent years. This narrative review aims to summarize recent research about the potential of a KD as a nutritional approach during endurance exercise, focusing on endurance capacity, recovery from fatigue, and the prevention of exhaustive exercise-induced muscle and organ damage.


1986 ◽  
Vol 233 (2) ◽  
pp. 485-491 ◽  
Author(s):  
A M Rofe ◽  
R Bais ◽  
R A Conyers

During starvation for 72 h, tumour-bearing rats showed accelerated ketonaemia and marked ketonuria. Total blood [ketone bodies] were 8.53 mM and 3.34 mM in tumour-bearing and control (non-tumour-bearing) rats respectively (P less than 0.001). The [3-hydroxybutyrate]/[acetoacetate] ratio was 1.3 in the tumour-bearing rats, compared with 3.2 in the controls at 72 h (P less than 0.001). Blood [glucose] and hepatic [glycogen] were lower at the start of starvation in tumour-bearing rats, whereas plasma [non-esterified fatty acids] were not increased above those in the control rats during starvation. After functional hepatectomy, blood [acetoacetate], but not [3-hydroxybutyrate], decreased rapidly in tumour-bearing rats, whereas both ketone bodies decreased, and at a slower rate, in the control rats. Blood [glucose] decreased more rapidly in the hepatectomized control rats. Hepatocytes prepared from 72 h-starved tumour-bearing and control rats showed similar rates of ketogenesis from palmitate, and the distribution of [1-14C] palmitate between oxidation (ketone bodies and CO2) and esterification was also unaffected by tumour-bearing, as was the rate of gluconeogenesis from lactate. The carcinoma itself showed rapid rates of glycolysis and a poor ability to metabolize ketone bodies in vitro. The results are consistent with the peripheral, normal, tissues in tumour-bearing rats having increased ketone-body and decreased glucose metabolic turnover rates.


Blood ◽  
2018 ◽  
Vol 132 (Supplement 1) ◽  
pp. 2350-2350
Author(s):  
Zeynep Karakas ◽  
Cihangir Sevimli ◽  
Nurdan Gul ◽  
Rana Comert ◽  
Memduh Dursun

Abstract The relationship between pancreatic iron overload and glucose dysregulation has not been well defined and need further investigation. Pancreas iron load measurements are also necessary to understand how hepatic, pancreatic, and cardiac iron burden prospectively modulate the evolution of diabetes in transfusion dependent thalassemia (TDT). Aim: This study aims to evaluate the presence of pancreatic iron overload among TDT patients in Turkey based on the MRI R2* and T2* results as well as to determine its association to Fasting blood glucose (FBG), insulin, fructosamine, Homa-IR, C-peptide, ferritin, liver, cardiac and hypophysis MRI R2* results. Material and Methods: This study was conducted at the Thalassemia Center in Istanbul University, Istanbul Medical Faculty. Forty-one TDT patients included the study with a mean age of 29.9±9,9 (median 29) years old, ranging from 11 to 45 years old. Pancreatic, liver, cardiac and hypophsis MRI's were conducted using 1.5 Tesla Philips MRI machine in the Department of Radiology. Pancreatic MRI R2* results < 30 Hz were considered normal, 30-100 Hz as mild, and > 100 Hz as moderate to severe pancreatic siderosis. Pancreatic MRI T2 results >26 ms were is normal, < 10 ms is severe iron overload as presented at literature. Correlations between pancreatic MRI R2* results and FBG, insulin, fructosamine, Homa-IR, C-peptide, ferritin, cardiac and hypophysis MRI R2* were evaluated using the Pearson correlation, Man Whitney U test. Results: Laboratory findings of glucose metabolism and MRI's of liver, pancreas, hypophsis and cardiac iron are shown at Table 1. There were no significant relationship between fasting blood glucose, insülin, C-peptid level, fructosamine, Homa-IR, ferritin and Pancreas T2* and R2* results (p>0.05). There was significant correlation between liver and pancreas MRI T2* and R2* results. (p<0.01). There was no significant correlation between hypophysis global R2, cardiac R2*, Pancreas T2* and, Pancreas R2* measurements (p>0.05). Fourteen patients were found to have normal pancreatic MRI R2* (34,1%) while 19 patients have normal pancreatic MRI T2 (46.3%). It is reported that T2 is irrelevant to age and sex, and R2 can be related to age-related fatty degeneration. There was significant pancreatic iron burden in 31.7% of patients (R2*>100 Hz), of whom only 1 patient was under 18 years of age.There were 22 (53.6%) patients with T2* <26 ms and had iron overload, 13 (31.7%) had T2 <10 ms and had significant iron overload. Almost three-quarters of patients (n:13, 31.7%) had moderate to severe pancreatic iron load on both T2* and R2* measurements. Thirteen patients with significant pancreatic iron overload had 3 severe hypophysis, 1 moderate, 2 severe cardiac siderosis. and had no serious liver iron burden. This shows that the treatment of chelation first led to liver, then heart and pituitary, respectively, and finally pancreatic iron burden and demonstrates the importance of pancreas MR in assessing the body iron load. Discussion:The lack of correlation between pancreatic and cardiac MRI R2* are in contrast to another demonstrating that pancreatic iron load are good predictors of cardiac iron load. This is due to the fact that our patients are followed up with cardiac MR and taken to the intensive chelation programs of the patients who detect iron in the heart. Previous studies also report that while pancreatic R2* may be sensitive for glucose dysregulation, most patients may still have no symptoms and normal blood glucose, indicating the presence of a preclinical iron burden. Pancreatic MRI R2* can detect pancreatic iron accumulation at a much earlier stage. Lack of excessive iron load in liver of our patient can be explain low glucose metabolism disorder despite high pancreatic iron overload. Disclosures No relevant conflicts of interest to declare.


1975 ◽  
Vol 146 (2) ◽  
pp. 447-456 ◽  
Author(s):  
P J Backshear ◽  
P A H Holloway ◽  
K G M M Alberti

1. The infusion of sodium dichloroacetate into rats with severe diabetic ketoacidosis over 4h caused a 2mM decrease in blood glucose, and small falls in blood lactate and pyruvate concentrations. Similar findings had been reported in normal rats (Blackshear et al., 1974). In contrast there was a marked decrease in blood ketone-body concentration in the diabetic ketoacidotic rats after dichloroacetate treatment. 2. The infusion of insulin alone rapidly decreased blood glucose and ketone bodies, but caused an increase in blood lactate and pyruvate. 3. Dichloroacetate did not affect the response to insulin of blood glucose and ketone bodies, but abolished the increase of lactate and pyruvate seen after insulin infusion. 4. Neither insulin nor dichloroacetate stimulated glucose disappearance after functional hepatectomy, but both agents decreased the accumulation in blood of lactate, pyruvate and alanine. 5. Dichloroacetate inhibited 3-hydroxybutyrate uptake by the extra-splachnic tissues; insulin reversed this effect. Ketone-body production must have decreased, as hepatic ketone-body content was unchanged by dicholoracetate yet blood concentrations decreased. 6. It was concluded that: (a) dichloroacetate had qualitatively similar effects on glucose metabolism in severely ketotic rats to those observed in non-diabetic starved animals; (b) insulin and dichloroacetate both separately and together, decreased the net release of lactate, pyruvate and alanine from the extra-splachnic tissues, possibly through a similar mechanism; (c) insulin reversed the inhibition of 3-hydroxybutyrate uptake caused by dichloroacetate; (d) dichloroacetate inhibited ketone-body production in severe ketoacidosis.


1985 ◽  
Vol 232 (1) ◽  
pp. 255-259 ◽  
Author(s):  
M J Holness ◽  
T N Palmer ◽  
M C Sugden

Effects of administration of tri-iodothyronine (T3) on activities of cardiac and renal pyruvate dehydrogenase complex (active form, PDHa) were investigated. In fed rats, T3 treatment did not affect cardiac or renal PDHa activity, although blood non-esterified fatty acid and ketone-body concentrations were increased. Starvation (48 h) of both control and T3-treated rats resulted in similar increases in the steady-state concentrations of fatty acids and ketone bodies, but inactivation of cardiac and renal pyruvate dehydrogenase complex activities was diminished by T3 treatment. Inhibition of lipolysis increased renal and cardiac PDHa in control but not in T3-treated 48 h-starved rats, despite decreased fatty acid and ketone-body concentrations in both groups. The results suggest that hyperthyroidism influences the response of cardiac and renal PDHa activities to starvation through changes in the metabolism of lipid fuels in these tissues.


Author(s):  
Juan Ramón Martínez-François ◽  
Nika N. Danial ◽  
Gary Yellen

On a ketogenic diet, ketone bodies provide an alternative fuel, replacing much of the glucose used ordinarily by the brain. This switch is thought to underlie its anticonvulsant effects. Brain fuel utilization can also be modified by a nondietary approach: genetic alteration of the protein BAD, which has known roles in regulating both apoptosis and glucose metabolism. When the metabolic function of BAD is genetically altered in mice, it produces reduced glucose and increased ketone body metabolism in neurons and astrocytes. This effect is related to regulation of BAD by phosphorylation and is independent of its apoptotic function. Mice with BAD modifications that produce decreased glucose metabolism exhibit a marked increase in the activity of neuronal ATP-sensitive potassium (KATP) channels and strong resistance to behavioral and electrographic seizures in vivo. This seizure resistance is lost upon genetic ablation of KATP channels, suggesting that KATP channels mediate BAD’s anticonvulsant effect.


1983 ◽  
Vol 245 (5) ◽  
pp. R624-R632 ◽  
Author(s):  
C. Cobelli ◽  
A. Ruggeri ◽  
G. Toffolo ◽  
A. Avogaro ◽  
R. Nosadini

Quantification of in vivo turnover of endogenous substances in nonsteady state is of fundamental importance for understanding a variety of physiological and clinical metabolic situations. Toward this end, a pool-fraction model has become a paradigm in the glucose and ketone body areas. We discuss the basic assumptions on which the pool-fraction model is based and the criteria on which it has been validated. Specific comments are then made on its current and potential use for quantifying the non-steady-state turnover of glucose, ketone bodies, and insulin. We conclude that the quantitative reliability of predictions provided by the pool-fraction model is quite poor and that new developments are needed for quantifying the non-steady-state situation.


2021 ◽  
Vol 14 ◽  
Author(s):  
Zsolt Kovács ◽  
Brigitta Brunner ◽  
Dominic P. D’Agostino ◽  
Csilla Ari

In certain disease states, such as epilepsy, the elevation of blood ketone levels with ketogenic diets (KDs) has beneficial effects, while exogenous ketone supplements (EKSs) were shown to increase the level of blood ketone bodies (such as β-hydroxybutyrate, βHB) and decrease blood glucose levels without dietary restrictions. It has been suggested that ketone body and glucose utilization of the body may be modified by age and gender resulting in changes in blood βHB and glucose levels, but it was not investigated through several months yet. Thus, we investigated whether the effect of an EKS on blood βHB and glucose level is modulated by age and sex in Wistar Albino Glaxo Rijswijk (WAG/Rij) rats, a model animal of human absence epilepsy. We used KEMCT (1:1 mix of ketone ester/KE and medium-chain triglyceride/MCT oil) by oral gavage in female and male WAG/Rij rats. Animals were fed with standard diet, which was supplemented by KEMCT (2.5 g/kg) once per month by oral gavage for 17 months. One hour after KEMCT treatment, changes in blood R-beta-hydroxybutyrate (R-βHB) and glucose levels were measured. KEMCT gavage significantly increased blood R-βHB and decreased blood glucose levels, in both male and female rats, compared with the controls. In male rats, the KEMCT-induced increase in blood R-βHB levels was lower at the 7th and 8th months and higher at the 16th and 17th months, compared with the results at the 1st month. KEMCT-generated increase in R-βHB levels was higher in female rats, compared with male rats between the 2nd and 11th months, but older (between the 14th and 17th months) female rats showed lower levels than males. KEMCT gavage induced significantly lower glucose levels at the 4th, 9th, 10th, 12th, and 13th months in both sexes, but between the 14th and 17th months, only males showed significantly lower levels, compared with the results at the 1st month. KEMCT treatment induced lower blood glucose levels in female than in male rats between the 1st and 8th months, but higher glucose levels were measured in female rats at the 17th month than in males. These findings suggest that age and sex can modify the EKS-evoked effects on blood R-βHB and glucose concentrations.


Sign in / Sign up

Export Citation Format

Share Document