This document provides an overview of ketone bodies including:
- Ketone bodies are acetone, acetoacetate, and β-hydroxybutyrate which are produced when fatty acids are broken down in the liver.
- Ketone bodies can be used as an energy source by other tissues when glucose is unavailable, as in starvation or untreated diabetes.
- Untreated diabetes and starvation can cause an overproduction of ketone bodies leading to dangerously high levels in the blood and urine.
- Jamaican vomiting sickness is caused by a toxin that inhibits fatty acid breakdown in the liver, causing ketone body and glucose dependence.
They are water soluble substances.
2. They are synthesized at a relatively low rate in well nourished individuals.
3. Plasma level of ketone bodies < 1mg/dl.
4. Urinary level of ketone bodies <3 mg/24 hour urine.
Triacylglycerol and compound lipid metabolismDipesh Tamrakar
Biosynthesis and metabolic regulation of triglyceride and other compound lipids: glycerophospholipids, sphingophospholipids, ether glycerolipids and glycolipids
Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids.
They are water soluble substances.
2. They are synthesized at a relatively low rate in well nourished individuals.
3. Plasma level of ketone bodies < 1mg/dl.
4. Urinary level of ketone bodies <3 mg/24 hour urine.
Triacylglycerol and compound lipid metabolismDipesh Tamrakar
Biosynthesis and metabolic regulation of triglyceride and other compound lipids: glycerophospholipids, sphingophospholipids, ether glycerolipids and glycolipids
Lipid metabolism entails the oxidation of fatty acids to either generate energy or synthesize new lipids from smaller constituent molecules. Lipid metabolism is associated with carbohydrate metabolism, as products of glucose (such as acetyl CoA) can be converted into lipids.
Formation and utilization of ketone bodies; ketoacidosisJinal Tandel
Formation and utilization of ketone bodies is part of lipid metabolism. After completion of this topic one can understand about Ketogenesis, utilization of Ketone bodies and ketoacidosis
Digestion and absorption of lipids ppt
what is lipid ppt
digestion of lipid ppt
phase of digestion and absorption ppt
phases of lipids ppt
digestion in mouth and stomach ppt
digestion in small intestine ppt
secretion of lipids ppt
enzyme involved in lipid digestion ppt
transportation phases of lipids ppt
principles of lipid digestion ppt
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
Formation and utilization of ketone bodies; ketoacidosisJinal Tandel
Formation and utilization of ketone bodies is part of lipid metabolism. After completion of this topic one can understand about Ketogenesis, utilization of Ketone bodies and ketoacidosis
Digestion and absorption of lipids ppt
what is lipid ppt
digestion of lipid ppt
phase of digestion and absorption ppt
phases of lipids ppt
digestion in mouth and stomach ppt
digestion in small intestine ppt
secretion of lipids ppt
enzyme involved in lipid digestion ppt
transportation phases of lipids ppt
principles of lipid digestion ppt
Lipid metabolism is the synthesis and degradation of lipids in cells.
It involves the breakdown or storage of fats for energy and the synthesis of structural and functional lipids, such as those involved in the construction of cell membranes.
In animals, these fats are obtained from food or synthesized by the liver.
KETONE BODY METABOLISM. FOR MBBS, BDS, LABORATORY MEDICINE pptxRajendra Dev Bhatt
Ketone bodies are produced from acetyl-CoA, mainly in the mitochondrial matrix of liver cells when carbohydrates are so scarce that energy must be obtained from breaking down of fatty acids.
Ketone bodies, or simply ketones are substances produced by the liver during gluconeogenesis, a process which creates glucose in times of fasting and starvation. There are three ketone bodies produced by the liver. They are acetoacetate, beta-hydroxybutyrate, and acetone. These compounds are used in healthy individuals to provide energy to the cells of the body when glucose is low or absent in the diet.
Ketone Bodies
Fatty acids undergo 𝛽-oxidation in the liver mitochondria to generate a high amount of energy and form three compounds, that are known as “ketone bodies”. These ketone bodies are water-soluble and do not require lipoproteins for transportation across the membrane. Ketone bodies are lipid molecules having a carbonyl group attached to two -R groups.
The three ketone bodies formed are –
1. Acetoacetate
2. D-3-hydroxybutyrate
3. Acetone
Ketogenesis – Definition
Ketogenesis is a catabolic pathway of metabolism. In this process, fatty acids and certain ketogenic amino acids are broken down to derive energy by alternative means. Ketone bodies are produced in the ketogenesis process.
Our body continuously produces ketone bodies in low amounts, but in certain cases like starving, when carbohydrates are present in less amount in diet, ketogenesis is preferred to compensate for the energy requirements.
Ketone bodies accumulated in an excess amount may lead to a condition called ketoacidosis, which may be fatal.
Ketogenesis Pathway
Our body normally derives energy from stored carbohydrate by the process of glycogenolysis (glycogen → glucose) or from non-carbohydrate sources such as lactate by the process of gluconeogenesis.
Ketogenesis occurs continuously in a healthy individual, but under certain conditions, when there is an increased concentration of fatty acids or carbohydrate reserves are decreased, ketogenesis happens at a higher rate:
• Under low blood glucose level, e.g. during fasting or starvation
• On exhaustion of carbohydrate reserve, e.g. glycogen
• When there is insufficient insulin, e.g. Type-1 diabetes
All the main body parts such as the brain, skeletal muscles, heart, etc. can utilise the energy formed by ketogenesis.
Insufficient gluconeogenesis results in hypoglycemia and excessive production of ketone bodies resulting in a fatal condition called ketoacidosis.
Ketogenesis Steps
The ketogenesis process occurs primarily in the mitochondria of liver cells. Below are the steps in the process of ketogenesis:
1. Transfer of fatty acids in mitochondria by carnitine palmitoyltransferase CPT-1
2. 𝛽-oxidation of fatty acid to form acetyl CoA
3. Acetoacetyl-CoA formation: 2 acetyl CoA form acetoacetyl CoA. The reaction is catalyzed by the enzyme thiolase
4. 3-hydroxy-3-methylglutaryl-CoA (HMG-CoA) synthesis: the step is catalyzed by HMG-CoA synthase
5. Acetoacetate formation: HMG-CoA is broken down to acetoacetate and acetyl-CoA by the action of HMG-CoA lyase
Acetoacetate thus produced forms other ketone bodies, acetone by decarboxylation and D-3-hydroxybutyrate by reduction.
Significance of Ketogenesis
• Ketogenesis is used to get energy by the brain, heart and skeletal muscles under fasting condition
• The ketogenic diet (low-carb, fat-rich diet) is used these days to lose weight.
Hello friends ,this presentation is all about ketone bodies .this will help you to understand what are ketone bodies and their functioning .it will benefit specially bpharmacy students.
Notes* for the subject 'Advanced Pharmaceutical Analysis'Sanathoiba Singha
As per the syllabus prescribed by Rajiv Gandhi University of Health Sciences, Karnataka, for M. Pharm (Pharmaceutical Analysis) 1st semester.
*not all topics have been included in this collection of notes.
As per the syllabus prescribed by Rajiv Gandhi University of Health Sciences, Karnataka, for M. Pharm (Pharmaceutical Analysis), 1st semester.
*not all topics have been covered in this file.
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Title: Sense of Taste
Presenter: Dr. Faiza, Assistant Professor of Physiology
Qualifications:
MBBS (Best Graduate, AIMC Lahore)
FCPS Physiology
ICMT, CHPE, DHPE (STMU)
MPH (GC University, Faisalabad)
MBA (Virtual University of Pakistan)
Learning Objectives:
Describe the structure and function of taste buds.
Describe the relationship between the taste threshold and taste index of common substances.
Explain the chemical basis and signal transduction of taste perception for each type of primary taste sensation.
Recognize different abnormalities of taste perception and their causes.
Key Topics:
Significance of Taste Sensation:
Differentiation between pleasant and harmful food
Influence on behavior
Selection of food based on metabolic needs
Receptors of Taste:
Taste buds on the tongue
Influence of sense of smell, texture of food, and pain stimulation (e.g., by pepper)
Primary and Secondary Taste Sensations:
Primary taste sensations: Sweet, Sour, Salty, Bitter, Umami
Chemical basis and signal transduction mechanisms for each taste
Taste Threshold and Index:
Taste threshold values for Sweet (sucrose), Salty (NaCl), Sour (HCl), and Bitter (Quinine)
Taste index relationship: Inversely proportional to taste threshold
Taste Blindness:
Inability to taste certain substances, particularly thiourea compounds
Example: Phenylthiocarbamide
Structure and Function of Taste Buds:
Composition: Epithelial cells, Sustentacular/Supporting cells, Taste cells, Basal cells
Features: Taste pores, Taste hairs/microvilli, and Taste nerve fibers
Location of Taste Buds:
Found in papillae of the tongue (Fungiform, Circumvallate, Foliate)
Also present on the palate, tonsillar pillars, epiglottis, and proximal esophagus
Mechanism of Taste Stimulation:
Interaction of taste substances with receptors on microvilli
Signal transduction pathways for Umami, Sweet, Bitter, Sour, and Salty tastes
Taste Sensitivity and Adaptation:
Decrease in sensitivity with age
Rapid adaptation of taste sensation
Role of Saliva in Taste:
Dissolution of tastants to reach receptors
Washing away the stimulus
Taste Preferences and Aversions:
Mechanisms behind taste preference and aversion
Influence of receptors and neural pathways
Impact of Sensory Nerve Damage:
Degeneration of taste buds if the sensory nerve fiber is cut
Abnormalities of Taste Detection:
Conditions: Ageusia, Hypogeusia, Dysgeusia (parageusia)
Causes: Nerve damage, neurological disorders, infections, poor oral hygiene, adverse drug effects, deficiencies, aging, tobacco use, altered neurotransmitter levels
Neurotransmitters and Taste Threshold:
Effects of serotonin (5-HT) and norepinephrine (NE) on taste sensitivity
Supertasters:
25% of the population with heightened sensitivity to taste, especially bitterness
Increased number of fungiform papillae
MANAGEMENT OF ATRIOVENTRICULAR CONDUCTION BLOCK.pdfJim Jacob Roy
Cardiac conduction defects can occur due to various causes.
Atrioventricular conduction blocks ( AV blocks ) are classified into 3 types.
This document describes the acute management of AV block.
Ozempic: Preoperative Management of Patients on GLP-1 Receptor Agonists Saeid Safari
Preoperative Management of Patients on GLP-1 Receptor Agonists like Ozempic and Semiglutide
ASA GUIDELINE
NYSORA Guideline
2 Case Reports of Gastric Ultrasound
New Drug Discovery and Development .....NEHA GUPTA
The "New Drug Discovery and Development" process involves the identification, design, testing, and manufacturing of novel pharmaceutical compounds with the aim of introducing new and improved treatments for various medical conditions. This comprehensive endeavor encompasses various stages, including target identification, preclinical studies, clinical trials, regulatory approval, and post-market surveillance. It involves multidisciplinary collaboration among scientists, researchers, clinicians, regulatory experts, and pharmaceutical companies to bring innovative therapies to market and address unmet medical needs.
Flu Vaccine Alert in Bangalore Karnatakaaddon Scans
As flu season approaches, health officials in Bangalore, Karnataka, are urging residents to get their flu vaccinations. The seasonal flu, while common, can lead to severe health complications, particularly for vulnerable populations such as young children, the elderly, and those with underlying health conditions.
Dr. Vidisha Kumari, a leading epidemiologist in Bangalore, emphasizes the importance of getting vaccinated. "The flu vaccine is our best defense against the influenza virus. It not only protects individuals but also helps prevent the spread of the virus in our communities," he says.
This year, the flu season is expected to coincide with a potential increase in other respiratory illnesses. The Karnataka Health Department has launched an awareness campaign highlighting the significance of flu vaccinations. They have set up multiple vaccination centers across Bangalore, making it convenient for residents to receive their shots.
To encourage widespread vaccination, the government is also collaborating with local schools, workplaces, and community centers to facilitate vaccination drives. Special attention is being given to ensuring that the vaccine is accessible to all, including marginalized communities who may have limited access to healthcare.
Residents are reminded that the flu vaccine is safe and effective. Common side effects are mild and may include soreness at the injection site, mild fever, or muscle aches. These side effects are generally short-lived and far less severe than the flu itself.
Healthcare providers are also stressing the importance of continuing COVID-19 precautions. Wearing masks, practicing good hand hygiene, and maintaining social distancing are still crucial, especially in crowded places.
Protect yourself and your loved ones by getting vaccinated. Together, we can help keep Bangalore healthy and safe this flu season. For more information on vaccination centers and schedules, residents can visit the Karnataka Health Department’s official website or follow their social media pages.
Stay informed, stay safe, and get your flu shot today!
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2. 2
CONTENTS
Topic Page no.
Introduction …………………………………………………………..... 1
Ketogenesis …………………………………………………………… 1-3
Utilisation of ketone bodies ………………………………………….... 3-4
Regulation of ketogenesis ……………………………………………. 4
General overview of ketone bodies ………………………………….. 5
Overproduction in diabetes mellitus and starvation………………….. 5-6
Jamaican vomiting sickness …………………………………………. 6-7
Rothera’s test ………………………………………………………… 7
References …………………………………………………………… 8
3. 3
Ketone bodies- Introduction
The compounds namely acetone, acetoacetate and β-hydroxybutyrate (or 3-Hydroxybutyrate)
are known as ketone bodies. Only the first two are true ketone* bodies while β-hydroxybutyrate
does not possess a keto (C=O) group. Ketone bodies are water soluble and energy yielding.
Acetone, however, is an exception, since it cannot be metabolized.
Fig.1 Ketone bodies.
In humans and most other mammals, acetyl-CoA formed in the liver during
oxidation of fatty acids can either enter the citric acid cycle or undergo conversion to the “ketone
bodies,” acetone, acetoacetate, and β-hydroxybutyrate, for export to other tissues. (The term
“bodies” is a historical artifact; the term is occasionally applied to insoluble particles, but these
compounds are quite soluble in blood and urine.) Acetone, produced in smaller quantities than the
other ketone bodies, is exhaled. Acetoacetate and β-hydroxybutyrate are transported by the blood
to tissues other than the liver (extrahepatic tissues), where they are converted to acetyl-CoA and
oxidized in the citric acid cycle, providing much of the energy required by tissues such as skeletal
and heart muscle and the renal cortex. The brain, which preferentially uses glucose as fuel, can
adapt to the use of acetoacetate or β-hydroxybutyrate under starvation conditions, when glucose is
unavailable. The production and export of ketone bodies from the liver to extrahepatic tissues
allows continued oxidation of fatty acids in the liver when acetyl-CoA is not being oxidized in the
citric acid cycle.
Ketogenesis
The synthesis of ketone bodies is termed as ‘ketogenesis’. Ketogenesis occurs only in the
mitochondria of liver cells. It occurs when there is a high rate of fatty acid oxidation in the liver.
The enzymes for ketone body synthesis are located in the mitochondrial
matrix. Acetyl CoA, formed by oxidation of fatty acids, pyruvate or some amino acids, is the
precursor for ketone bodies. Ketogenesis occurs through the following reactions:
i. Two moles of acetyl CoA condense to form acetoacetyl CoA. This reaction is catalyzed by
thiolase, an enzyme involved in the final step of β-oxidation. Hence, acetoacetate synthesis
is appropriately regarded as the reversal of thiolase reaction of fatty acid oxidation.
ii. Acetoacetyl CoA combines with another molecule of acetyl CoA to produce β-hydroxy β-
methyl glutaryl CoA (HMG CoA). HMG CoA synthase, catalysing this reaction, regulates
the synthesis of ketone bodies.
iii. HMG CoA lyase cleaves HMG CoA to produce acetoacetate and acetyl CoA.
iv.
v. Acetoacetate can undergo spontaneous decarboxylation to form acetone.
*The term ‘ketones’ should not be used because 3-hydroxybutyrate is not a ketone and
there are ketones in blood that are not ketone bodies e.g. pyruvate, fructose.
4. 4
iv. Acetoacetate can undergo spontaneous decarboxylation to form acetone.
vi. Acetoacetate can be reduced by a dehydrogenease to β-hydroxybutyrate.
Fig. 2 Ketogenesis.
β-Hydroxy-β-methylglutaryl CoA (HMG-CoA) is an intermediate in the pathway
of ketogenesis. Enzymes responsible for ketone body formation are associated mainly with the
mitochondria. Two acetyl-CoA moleccules formed in β-oxidation condense with another to form
acetoacetyl-CoA by a reversal of the thiolase reaction. Acetoacetyl-CoA, which is the starting
material for ketogenesis, also arises directly from the terminal four carbons of a fatty acid during
β-oxidation. Condensation of acetoacetyl-CoA with another molecule of acetyl-CoA by β-
hydroxy-β-methylglutaryl-CoA lyase then causes acetyl-CoA to split off from the HMG-CoA,
5. 5
leaving free acetoacetate. The carbon atoms split off in the acetyl-CoA, leaving free acetoacetate.
The carbon atoms split off in the acetyl-CoA molecule are derived from the original acetoacetyl-
CoA molecule. Both enzymes must be present in mitochondria for ketogenesis to take place.
This occurs solely in liver and rumen epithelium. β-Hydroxybutyrate
is quantitatively the predominant ketone body present in the blood and urine in ketosis.
Utilisation of ketone bodies (Catabolism)
The utilization of ketone bodies by the extrahepatic tissues requires the
activity of the enzyme thiolase. The catabolism of ketone bodies can be summarized by the
following steps:
i. Conversion of β-hydroxybutyrate to acetoacetate is necessary as a first step.
ii. Thiophorase then catalyzes transfer of CoA to acetoacetate to produce acetoacetyl
CoA.
a. Succinyl CoA is the donor for this transesterification reaction.
b. Acetoacetyl CoA is then split into two molecules of acetyl CoA, which can
enter the TCA cycle for fuel.
c. The liver does not contain thiophorase, so it cannot use ketone bodies as fuel.
Therefore, only those organs that express thiophorase can utilize ketone bodies
for energy.
Fig. 3 Catabolism of ketone bodies.
The acetyl CoA thus formed is oxidized in the citric acid cycle. If the blood level is
raised, oxidation of ketone bodies increases until, at a concentration of approximately
12 millimole/litre, they saturate the oxidative machinery.
The ketone bodies, being water soluble, are easily
transported from the liver to various tissues. The two ketone bodies- acetoacetate and
β-hydroxybutyrate serve as important sources of energy for the peripheral muscles such
as skeletal muscles, cardiac muscle, renal cortex, etc. The tissues which lack
mitochondria (e.g. erythrocytes) however, cannot utilize ketone bodies.
6. 6
Fig. 4 Transport of ketone bodies from the liver and pathways of utilization and oxidation in
extrahepatic tissues.
Regulation of ketogenesis
Ketogenesis is regulated at the following three crucial steps:
1. Control of free fatty acid (FFA) mobilization from adipose tissues.
2. The activity of carnitine palmitoyltransferase-I (CPT-I) in liver, which determines the
proportion of fatty acid flux that is oxidized rather than esterified.
3. Partition of acetyl-CoA between the pathway of ketogenesis and the citric acid cycle.
7. 7
Fig. 5 Regulation of ketogenesis.
General overview of ketone bodies
The general overview of ketone bodies can be better understood from the
chart given below:
Fig. 6 Formation, utilization, and excretion of ketone bodies (The main pathway is indicated by
the solid arrows).
Overproduction of ketone bodies during diabetes mellitus and starvation
In healthy people, acetone is formed in very small amounts from acetoacetate, which is easily
decarboxylated, either spontaneously or by the action of acetoacetate decarboxylase. Because
individuals with untreated diabetes produce large quantities of acetoacetate, their blood contains
significant amounts of acetone, which is toxic. Acetone is volatile and imparts a characteristic odor
to the breath, which is sometimes useful in diagnosing diabetes.
In untreated diabetes, when the insulin level is insufficient,
extrahepatic tissues cannot take up glucose efficiently from the blood, either for fuel or for
conversion to fat. Under these conditions, levels of malonyl-CoA (the starting material for fatty
acid synthesis) fall, inhibition of carnitine acyltransferase I is relieved, and fatty acids enter
mitochondria to be degraded to acetyl-CoA—which cannot pass through the citric acid cycle
because cycle intermediates have been drawn off for use as substrates in gluconeogenesis. The
8. 8
resulting accumulation of acetyl-CoA accelerates the formation of ketone bodies beyond the
capacity of extrahepatic tissues to oxidize them. The increased blood levels of acetoacetate and β-
hydroxybutyrate lower the blood pH, causing the condition known as acidosis. Extreme acidosis
can lead to coma and in some cases death. Ketone bodies in the blood and urine of individuals with
untreated diabetes can reach extraordinary levels—a blood concentration of 90 mg/100 mL
(compared with a normal level of <3 mg/100 mL) and urinary excretion of 5,000 mg/24 hr
(compared with a normal rate of ≤125 mg/24 hr). This condition is called ketosis. Ketosis is mild
in starvation but severe in diabetes mellitus.
Individuals on very low-calorie diets, using the fats stored in adipose tissue as their
major energy source, also have increased levels of ketone bodies in their blood and urine. These
levels must be monitored to avoid the dangers of acidosis and ketosis (ketoacidosis).
These effects lead to major clinical manifestations, including nausea, vomiting,
dehydration, electrolyte imbalance, loss of consciousness and, potentially, coma and death.
A characteristic sign of this condition is a fruity odor on the breath due to expiration of large
amounts of acetone.
Jamaican vomiting sickness
Jamaican vomiting sickness is an acute illness caused by the toxin hypoglycin A,
which is present in unripened fruit of the ackee tree. Hypogylcin A is present in the unripe aril
(external covering of seeds that develops after fertilization as an outgrowth from the ovule stalk)
at levels of over 1000ppm, which falls to less than 0.1ppm in the fully ripened aril.
When ingested, hypoglycin A is metabolized to produce
methylenecyclopropylacetic acid (MCPA). MCPA acts to inhibit the beta-oxidation of fatty acids
in two ways. First, it interferes with the transport of long-chain fatty acids into mitochondria. Also,
it inhibits acyl-CoA dehydrogenase, so that only unsaturated fatty acids can be fully oxidized.
Fatty acids accumulate in the liver. In absence of fatty acid metabolism, the body becomes
dependent on glucose and glycogen for energy.
Once the liver glycogen stores are depleted, the body cannot synthesize
glucose and severe hypoglycemia occurs.
Abdominal discomfort begins two to six hours after eating unripe ackee fruit,
followed by sudden onset vomiting. In severe cases, profound dehydration, seizures, coma and
death may occur. Children and those who are malnourished are more susceptible to the disease.
9. 9
Fig. 7 Fruit of Blighia sapida (Ackee fruit)
The ackee fruit (Blighia sapida) is native to West Africa. Although native to West Africa, the use
of ackee in food is especially prominent in Jamaican cuisine. Ackee is the national fruit of
Jamaica. Ackee pods should be allowed to ripen on the tree before picking. Prior to cooking, the
ackee arils are cleaned and washed. The arils are then boiled for approximately 5 minutes and the
water discarded.
Rothera’s test
It is a test for ketone bodies. 5ml of fresh urine is saturated with solid ammonium
sulphate and mixed with 10 drops of freshly prepared 2% sodium nitroprusside solution, which is
then mixed with 10 drops of concentrated ammonia water and allowed to stand for 15 minutes; the
presence of acetoacetic acid or of larger concentrations of acetone is indicated by the development
of a purple-blue color.
10. 10
Fig. 8 Rothera’s test.
REFERENCES:
Satyanarayana, U & Chakrapani, U (2013). Biochemistry 4th
Edition. New Delhi, India:
Reed Elsevier India Private Limited. 293-295.
Nelson, DL & Cox, MM (2008). Lehninger Principles of Biochemistry 5th
Edition. New
York: W.H. Freeman and Company. 666-668.
Murray, RK, Granner, DK, Mayes, PK & Rodwell, VK (2003). Harper’s Illustrated
Biochemistry 26th
Edition. USA: The McGraw-Hill Companies. 183-189.
11. 11
MacDonald, RG & Chaney, WG (2007). USML Road Map Biochemistry. USA: The
McGraw-Hill Companies. 113-115.