View clinical trials related to Ketosis.
Filter by:The purpose of this study is to help us better understand how plasma ketones respond to a low-carb diet when combined with an SGLT2 inhibitor.
This study aims to investigate the early metabolic effects and acute phase response of an oral clear supplement containing whey protein plus carbohydrates in young healthy volunteers during fasting-induced organic response
The goal of this clinical trial is to evaluate the safety and tolerability of free beta-hydroxybutyrate induced ketosis in healthy individuals. The main question it aims to answer is: - Is free beta-hydroxybutyrate safe and well tolerated by adults? Participants will be asked to ingest 10 grams of beta-hydroxybutyrate, diluted in water and sweetened with Stevia, every morning between 9:00 and 11:00 for four weeks.
What is the effect of a ketone drink on liver glucose production, and postprandial glycemia, in people with type 2 diabetes.
One important difference between KE compounds is the ketone-promoting components, which determines the circulating ratio of blood ketone bodies, BHB and AcAc, and may in turn lead to important metabolic and signaling differences. Whereas some actions of the ketone bodies BHB and AcAc are shared, R-BHB has a broad range of signaling functions that are distinct from AcAc, some of which are shared by the non-circulating, non-oxidizable enantiomer, S-BHB. AcAc also has metabolic and signaling actions that are independent of BHB and is selectively oxidized in some cells that cannot oxidize BHB. Furthermore, responses to different ketone bodies vary between tissue types. A second difference between KE arises from the balance between direct delivery of ketones compared to indirectly elevating ketone concentration via metabolism of non-classical or classical ketogenic precursors. Classical ketogenesis itself may drive adaptation and some of the functional benefits associated with ketosis. BDO is included in all of the KE compounds, but it is currently unknown how consumption of BDO alone, and its metabolism via non-classical ketogenesis acutely affects metabolism. Additionally, ketogenesis is now understood to occur in certain cells outside the liver with important local biological effects, for example ketogenesis driven by medium chain fatty acids has been reported in astrocytes in vitro. Provision of systemic BHB by a KE may elicit different biological effects in some tissues such as the brain versus promoting in situ ketogenesis in that tissue. Overall, not only are functional effects of KE incompletely defined, but also it is unknown which effects are common to all KE versus which are specific to an individual KE compound (i.e., BHB Monoester vs AcAc Diester) or which may be attributable to the BDO precursor common to all of the KE. This study will be the first comparative full crossover study of all available KE and the precursor BDO at two serving sizes. Outcomes will focus on established effects of the BHB Monoester (including the effects on ketones, glucose and acid-base balance) and compare these with the effects of the AcAc Diester, C8 Ketonef Diester and BDO.
Diabetic ketoacidosis (DKA), a frequent complication of diabetes, is the consequence of a profound insulin deficiency responsible for osmotic polyuria and thus major losses of water, glucose, sodium and potassium as well as a metabolic acidosis due to the uncontrolled production of ketonic acids. Management includes fluid replacement, insulin therapy and correction of metabolic disorders (including potassium loss). Initially described in patients with type 1 diabetes (T1D), it is now often observed in patients with type 2 diabetes (T2D) in whom it is more a matter of insulin resistance than an absolute deficiency. However, international guidelines recommend a similar dose of intravenous insulin (0.10 IU/kg/hour) regardless of the type of diabetes. During treatment, metabolic complications are frequent and potentially serious, especially in T2D due to cardiovascular comorbidities. The research hypothesis is that decreasing the insulin dose will reduce metabolic complications without influencing time to resolution in adult patients, regardless of diabetes type.
Sodium glucose co-transporter 2 (SGLT2) inhibitors have revolutionized care for people living with type 2 diabetes mellitus (T2DM). They reduce a person's risk of heart failure, renal failure, myocardial infarction, stroke, cardiovascular mortality, and potentially all-cause mortality. Remarkably, some of these benefits also extend to people who do not have T2DM. While the benefits of SGLT2 inhibitors are impressive, there is one life-threatening side effect associated with their use: diabetic ketoacidosis (DKA). The ability to predict which patients are at highest risk of DKA is needed to sufficiently mitigate this risk. Moreover, considering the impressive benefits of SGLT2 inhibitors, identifying patients at the lowest risk of SGLT2 inhibitor-associated DKA is also important so that providers do not overestimate risk in those who stand to benefit most. Advances in genomic technologies and related analyses have provided unprecedented opportunities to bring genomics-driven precision medicine initiatives to the forefront of clinical research. Leading these developments has been the progress made by genome-wide association studies (GWAS) due to decreasing genotyping costs, and consequently, the ability to routinely study large numbers of patients. These approaches allow for systematic screening of the genome in an unbiased manner and have accelerated the discovery of genetic variants and novel biological processes that contribute to the development of adverse treatment outcomes. By using innovative approaches, which harness large cohorts of population controls, sample size limitations that are associated with rare adverse drug reactions such as SGLT2 inhibitor-associated DKA can be overcome. The DANGER study represents a highly innovative new direction wherein partnership among basic science researchers and computational biologists will lead to the application of genomic techniques to identify genetic variants that may be associated with SGLT2 inhibitor-associated DKA.
Diabetic ketoacidosis (DKA) is a common acute complication of type 1 diabetes mellitus (T1DM). DKA is characterized by hyperglycemia, metabolic acidosis, increased levels of ketone bodies in blood and urine. This leads to osmotic diuresis and severe depletion of water and electrolytes from both the intra- and extracellular fluid (ECF) compartments. Estimation of the degree of dehydration for children admitted with DKA is of great clinical importance. The calculation of the amount of deficit therapy depends on the estimated degree of dehydration. However, the degree of dehydration present during DKA is difficult to be clinically assessed. Hyperosmolality tends to preserve intravascular volume with maintenance of peripheral pulses, blood pressure, and urine output until extreme volume depletion occurs. Metabolic acidosis leads to hyperventilation and dry oral mucosa as well as decreased peripheral vascular resistance and cardiac function . consequently, hyper-osmolality may lead to an underestimation of the degree of dehydration, whereas metabolic acidosis may lead to an overestimation of the degree of dehydration. This makes the physical findings unreliable in this setting. Several clinical and biochemical markers were suggested to assess and stage the degree of dehydration at hospital admission. The blood urea nitrogen , hematocrit , plasma albumin are useful markers of the degree of ECF contraction.However, Several previous studies demonstrated that there was no agreement between assessed and measured degree of dehydration which is calculated according to change in body weight at admission and after correction of dehydration. there were tendencies to overestimated or underestimate the degree of dehydration between different physicians. The assessment of the magnitude of dehydration in DKA is of major interest and continues to be a subject of research. This study aims to assess the association between different clinical and laboratory parameters in children with diabetic ketoacidosis and the degree of dehydration at hospital admission among those children.
Ketone bodies are a fuel source and signaling molecule that are produced by your body during prolonged fasting or if you consistently eat at low-carbohydrate diet. Blood ketones can be used as a source of energy during fasting and are used by your brain as an alternative source of fuel to glucose. Previous studies have found that ketones, when consumed in form of a supplement drink, can increase blood ketone levels and lower blood glucose, the amount of sugar in your blood. This is of potential interest for individuals with high blood sugar, such as people living with type 2 diabetes. However, there are different types of ketone supplements that differ in how they are metabolized in the body. Little is known about how these supplements affect blood ketone and blood glucose levels. The main objective of this study is to determine the effect of three different ketone supplements on blood ketones and blood glucose. The results of this pilot study will be used to guide future research for larger and more extensive studies on ketone supplements.
Ketogenic dietary therapies (KDTs) are well-established, safe, non-pharmacologic treatments used for children and adults with drug-resistant epilepsy and other neurological disorders. Ketone bodies levels undergo a significant inter-individual and intra-individual variability and can be affected by several factors. This evidence suggests the need for personalized monitoring for diet optimization, especially at the beginning of the treatment but during whole follow-up. Possible variations in glycemia and ketone bodies' blood level according to different phases of menstrual cycle have not been systematically assessed yet, but this time window deserves special attention because of hormonal and metabolic related changes. We present the methodological protocol for a longitudinal, multicentric study aimed at searching for subtle changes in ketone bodies blood level during menstrual cycle in epileptic female patients undergoing a stable ketogenic diet. The study will be divided into two phases. The first one will be purely observational, aiming at the assessment of ketonemia during menstrual cycle. Whether this finding will be confirmed, a second phase of ketogenic diet therapy adjustment will be scheduled.