Ketone Bodies

Ketone Bodies

Q. 1

Acetyl coA can be directly converted to all except

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Q. 1

Acetyl coA can be directly converted to all except

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Ans. A

Explanation:

Glucose [Ref: Harper 28/e p132,133]Repeat from May 10

Acetyl CoA has a special central role. It’s a common product of Carbohydrates. Fats and Protein. Acetyl CoA thus formed can then undergo multiple fates:

– Oxidized to produce energy via Citric acid cycle (TCA cycle)

– Synthesized into

– Fatty acids

– Cholesterol and other steroids

– Ketone bodies

Acetyl CoA cannot be converted into Glucose. It is not a substrate of gluconeogenesis. Substrates for Gluconeogenesis

–     Glucogenic amino acids

–     Lactate

– Glycerol

– Propionate


Q. 2

Acetyl coA can be directly converted to all except 

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Q. 2

Acetyl coA can be directly converted to all except 

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Ans. A

Explanation:

Glucose [Ref: Harper 28/e p132,133] Repeat from May 11


Q. 3

Acetyl CoA, which cordinates carbohydrate, ketone and fat pathways can be directly converted to all of the following, except:

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Q. 3

Acetyl CoA, which cordinates carbohydrate, ketone and fat pathways can be directly converted to all of the following, except:

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Ans. A

Explanation:

Acetyl CoA cannot be converted to glucose. Acetyl CoA cannot be directly converted to pyruvate on a net basis since the two carbon backbone of acetyl CoA cannot be converted to oxaloacetate via the TCA cycle because two carbons are lost as carbon dioxide. 

Acetyl CoA has a special central role. It cordinates carbohydrates, ketone and fat pathways.

Acetyl CoA formed can then undergo multiple fates:

It can be oxidized to produce energy via Citric acid cycle (TCA cycle).

In fed state it is directed toward synthesis of cholesterol and/ or fats/ triacylglycerols in the liver.

Excess acetyl-CoA generated can be used for the synthesis of ketone bodies.

Q. 4

Ketone bodies are by products of metabolism of?

 A

Carbohydrate

 B

Protein

 C

Fat

 D

All of the above

Q. 4

Ketone bodies are by products of metabolism of?

 A

Carbohydrate

 B

Protein

 C

Fat

 D

All of the above

Ans. C

Explanation:

Free fatty acids are the precursors of ketone bodies in the liver. While an active enzymatic mechanism produces acetoacetate from acetoacetyl-CoA in the liver, acetoacetate once formed cannot be reactivated directly except in the cytosol, where it is used in a much less active pathway as a precursor in cholesterol synthesis. This accounts for the net production of ketone bodies by the liver.

Ref: Botham K.M., Mayes P.A. (2011). Chapter 22. Oxidation of Fatty Acids: Ketogenesis. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e. 

 


Q. 5

Acetyl CoA is produced from various reactions in the body. Acetyl coA can be directly converted to all, EXCEPT:

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Q. 5

Acetyl CoA is produced from various reactions in the body. Acetyl coA can be directly converted to all, EXCEPT:

 A

Glucose

 B

Fatty acids

 C

Cholesterol

 D

Ketone bodies

Ans. A

Explanation:

Acetyl CoA is formed from glucose. Following are the fate of Acetyl CoA after its formation:

  • Oxidation in TCA cycle to form CO2 AND H2O
  • Cholesterol biosynthesis
  • Ketogenesis
  • Fatty acid synthesis
  • Acetylation reactions (Detoxication)
  • Formation of acetyl choline
  • Melatonin synthesis
 
Ref: Textbook of Medical Biochemistry By Chatterjea, 2011, Page 442.

Q. 6

Which of the following will be elevated in the bloodstream about 4 hours after a fat-rich meal?

 A

Chylomicrons

 B

Ketone bodies

 C

VLDL

 D

LDL

Q. 6

Which of the following will be elevated in the bloodstream about 4 hours after a fat-rich meal?

 A

Chylomicrons

 B

Ketone bodies

 C

VLDL

 D

LDL

Ans. C

Explanation:

The clearance of chylomicrons from the blood is rapid, the half-time of disappearance being under 1 h in humans. The residual triacylglycerol, plus triacylglycerol newly synthesized in the liver are secreted in very low-density lipoprotein as a source of fuel for peripheral tissues. Ketone bodies and non-esterified fatty acids are elevated in fasting, not after a meal.

Ref: Botham K.M., Mayes P.A. (2011). Chapter 25. Lipid Transport & Storage. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

 


Q. 7

A 26-year-woman undertakes a prolonged fast for religious reasons. Which of the following metabolites will be most elevated in his blood plasma after 3 days?

 A

Glucose

 B

Glycogen

 C

Ketone bodies

 D

Non-esterified fatty acids

Q. 7

A 26-year-woman undertakes a prolonged fast for religious reasons. Which of the following metabolites will be most elevated in his blood plasma after 3 days?

 A

Glucose

 B

Glycogen

 C

Ketone bodies

 D

Non-esterified fatty acids

Ans. C

Explanation:

As he becomes progressively more starved, his liver will synthesize ketone bodies as an additional fuel for muscle, which cannot meet all of its energy needs from fatty acid metabolism. This spares glucose for the brain and red blood cells.

Higher than normal quantities of ketone bodies present in the blood or urine constitute ketonemia (hyperketonemia) or ketonuria, respectively. The overall condition is called ketosis.
The basic form of ketosis occurs in starvation and involves depletion of available carbohydrate coupled with mobilization of free fatty acids .
 
Ref: Botham K.M., Mayes P.A. (2011). Chapter 22. Oxidation of Fatty Acids: Ketogenesis. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e

 


Q. 8

All of the following are ketone bodies produced in fatty acid oxidation, EXCEPT:

 A

Acetone

 B

Acetoacetate

 C

a-Ketoglutarate

 D

b-hydroxybutyrate

Q. 8

All of the following are ketone bodies produced in fatty acid oxidation, EXCEPT:

 A

Acetone

 B

Acetoacetate

 C

a-Ketoglutarate

 D

b-hydroxybutyrate

Ans. C

Explanation:

Increased fatty acid oxidation is a characteristic of starvation and of diabetes mellitus, and leads to ketone body production by the liver (ketosis). 
 
Under metabolic conditions associated with a high rate of fatty acid oxidation, the liver produces considerable quantities of acetoacetate and beta-hydroxybutyrate.
Acetoacetate continually undergoes spontaneous decarboxylation to yield acetone.
These three substances are collectively known as the ketone bodies. Acetoacetate and 3-hydroxybutyrate are interconverted by the mitochondrial enzyme D(–)-3-hydroxybutyrate dehydrogenase.
 
Ref: Botham K.M., Mayes P.A. (2011). Chapter 22. Oxidation of Fatty Acids: Ketogenesis. In D.A. Bender, K.M. Botham, P.A. Weil, P.J. Kennelly, R.K. Murray, V.W. Rodwell (Eds), Harper’s Illustrated Biochemistry, 29e.

Q. 9

Acetyl CoA is used for synthesis of following, except :

 A

Carbohydrates

 B

Ketone bodies

 C

Cholesterol

 D

Non-ketogenic amino acids only

Q. 9

Acetyl CoA is used for synthesis of following, except :

 A

Carbohydrates

 B

Ketone bodies

 C

Cholesterol

 D

Non-ketogenic amino acids only

Ans. D

Explanation:

Acetyl-CoA is the third branch point of primary metabolic control, and coordinates carbohydrate, ketone, and fat/lipid pathways.Acetyl-CoA is the product of carbohydrate, protein, and lipid catabolism.Acetyl-CoA is a substrate for the citric acid cycle and can be oxidized to generate energy. It is not used for the synthesis of non ketogenic amino acids only.

 
Ref:Valencik M.L., Mastick C.C. (2012). Chapter 10. Metabolism and Vitamins/Minerals. In L.W. Janson, M.E. Tischler (Eds), The Big Picture: Medical Biochemistry.

Q. 10

A 45-year old woman presents with complaints of increased appetite, thirst and increased frequency of urination. On examination, she had gangrene of the feet and diminished peripheral pulses in the leg. Oral glucose tolerance test done shows the following value:

Parameters

Fasting

lhr

2hr

Blood glucose (mg/dL)

155

270

205

Urine glucose

-ve

+++

++

Ketone bodies

-ve

-ve

-ve

 

All of the following statements are correct for the above mentioned case except:

 A

She is suffering from insulin dependent diabetes mellitus

 B

She is suffering from non-insulin dependent diabetes mellitus

 C

She can be treated with oral hypoglycemic drugs only when diet and exercise could not control the pathological situation

 D

Knowledge of family history of diabetes mellitus is useful in predicting the nature of the diabetes

Q. 10

A 45-year old woman presents with complaints of increased appetite, thirst and increased frequency of urination. On examination, she had gangrene of the feet and diminished peripheral pulses in the leg. Oral glucose tolerance test done shows the following value:

Parameters

Fasting

lhr

2hr

Blood glucose (mg/dL)

155

270

205

Urine glucose

-ve

+++

++

Ketone bodies

-ve

-ve

-ve

 

All of the following statements are correct for the above mentioned case except:

 A

She is suffering from insulin dependent diabetes mellitus

 B

She is suffering from non-insulin dependent diabetes mellitus

 C

She can be treated with oral hypoglycemic drugs only when diet and exercise could not control the pathological situation

 D

Knowledge of family history of diabetes mellitus is useful in predicting the nature of the diabetes

Ans. A

Explanation:

Oral glucose tolerance test in this patient is consistent with the diagnosis of non-insulin dependent diabetes mellitus. Fasting glucose of 126 mg/dL, and a glucose of 200 mg/dL 2 hour after an oral glucose challenge, confirms the diagnosis of DM. Along with this ketones are absent which indicate non insulin dependent diabetes.

Ref: Harrison’s Internal Medicine, 18th Edition, Chapter 344

 


Q. 11

True about Acetyl CoA:

 A

Precursor for synthesis of cholesterol and other steroids.

 B

Form ketone bodies

 C

Starting material for synthesis of fatty acid and Arise from glycolysis both

 D

All

Q. 11

True about Acetyl CoA:

 A

Precursor for synthesis of cholesterol and other steroids.

 B

Form ketone bodies

 C

Starting material for synthesis of fatty acid and Arise from glycolysis both

 D

All

Ans. D

Explanation:

ALL i.e. (Precursor for synthesis of cholesterol and other steroids, Form ketone bodies, Starting material for synthesis of fatty acid, Arise from glycolysis)


Q. 12

Acetyl CoA can be converted into all of the following, Except

 A

Glucose

 B

Fatty Acids

 C

Cholesterol

 D

Ketone bodies

Q. 12

Acetyl CoA can be converted into all of the following, Except

 A

Glucose

 B

Fatty Acids

 C

Cholesterol

 D

Ketone bodies

Ans. A

Explanation:

A i.e. Glucose

Acetyl coenzyme A arises from pyruvate (the end product of aerobic glycolysis) by irreversible oxidative decarboxylation catalyzed by pyruvate dehydrogenase (PDH) complexQ

–                   Acetyl CoA is not a substrate for gluconeogenesis and cannot be converted back to glucoseQ. This is because acetyl CoA cannot be converted back to pyruvateQ since its carbon backbone is lost in citric acid cycle as CO2. Hence fatty acids cannot be converted into glucose

–                   Substrates for gluconeogenesis are : proprionic acid (in ruminants), g,lucogenic amino acids, glycerol, pyruvate and lactate (Mn- “Proper GPL”)

– Acetyl CoA is used in oxidative phosphorylation (in TCA cycle) for energy production; in acetylation reaction (coenzyme pantothenic acid) for detoxification & acetyl choline formation. It is also used in cholesterol synthesis, steroidogenesis (steroid hormone & vitamin D3 synthesis), lipogenesis (fatty acid synthesis and elongation, synthesis of ether lipids like plasmalogens & PAF) and ketogenesis (ketone body formation).

–                   Acetyl CoA is a precursor or starting material (& substrate for enzymes) for synthesis of cholesterol & ketone bodies (= substrate for HMG CoA synthetase) and fatty acid synthesis (= substrate for fatty acid synthase, acetyl CoA carboxylase or malonyl CoA synthetase and malonyl transaceylase)

–                                     Malic enzyme forms malic acid from pyruvic acidQ in presence of CO2 & NADPH.


Q. 13

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

 A

HMG -Co-A Reductase

 B

HMG-Co-A Lyase

 C

HMG-Co-A Synthase

 D

Thiokinase

Q. 13

Which of the following enzymes is common to the synthesis of cholesterol and ketone bodies:

 A

HMG -Co-A Reductase

 B

HMG-Co-A Lyase

 C

HMG-Co-A Synthase

 D

Thiokinase

Ans. C

Explanation:

C i.e. HMG-Co-A Synthase


Q. 14

Which organ does not utilise ketone bodies:

 A

Liver

 B

Brain

 C

Skeletal muscles

 D

Cardiac muscles

Q. 14

Which organ does not utilise ketone bodies:

 A

Liver

 B

Brain

 C

Skeletal muscles

 D

Cardiac muscles

Ans. A

Explanation:

A i.e. Liver


Q. 15

Energy source used by brain in later days of Starvation is

 A

Glucose

 B

Ketone bodies

 C

Glycogen

 D

Fatty acids

Q. 15

Energy source used by brain in later days of Starvation is

 A

Glucose

 B

Ketone bodies

 C

Glycogen

 D

Fatty acids

Ans. B

Explanation:

B i.e. Ketone bodies


Q. 16

Which of the following metabolic events will not occur following 12-24 hour of fasting

 A

Increase in free fatty acids

 B

Increase in ketone bodies

 C

Decrease in Glycogen

 D

Decrease in Serum Proteins

Q. 16

Which of the following metabolic events will not occur following 12-24 hour of fasting

 A

Increase in free fatty acids

 B

Increase in ketone bodies

 C

Decrease in Glycogen

 D

Decrease in Serum Proteins

Ans. D

Explanation:

D i.e. Decrease in serum Proteins

Glycogenolysis and liver gluconeogenesis (initially by degradation of glucogenic aminoacids of muscle proteins followed by glycerol & lactate) are sources of energy in brief (1st stage) of starvation (ie 12 to 72 hours of fasting). Gluconeogenesis the main process, increases during brief fasting but decreases on prolonged fasting.

–  During starvation serum proteins are not utilized as a source of energyQ. Brief fasting is associated with increased proteolysis (break down) of muscle proteins (not serum proteins) thereby decreasing total muscle proteins, whereas the serum protein levels are unaltered (ie not decreased)Q. Proteolysis of muscles provide glucogenic aminoacids (alanine & glutamine increasing liver gluconeogenesis

–  On prolonged fasting (starvation), adipose tissue breakdown (beta-oxidation) becomes the main source of energy; thereby increasing production of ketone bodies. However it is important to note that this over produced ketone bodies are utilized mainly by brain not by muscles as the utilization of glucose by brain and utilization of ketone bodies by by-muscle decreases during prolonged starvation. In the same way, decreased gluconeogenesis in prolonged starvation is responsible for decreased muscle protein degradation and decreased production of urea.


Q. 17

A 45-year old woman visited her physician with complaints of increased appetite and thirst with increased frequency of urination. She also had the symptoms of diminished or impalpable pulses in the feet, besides gangrene of the feet. Her laboratory findings on the oral glucose tolerance test are as follows:      (AI 2004)

Parameters

Fasting

1 hr

2 hr

Blood glucose

(mg/dL)

155

270

205

Urine glucose

-ve

+++

++

Ketone bodies

-ve

-ve

-ve

Which of the following statements is not correct for the above mentioned case:

 A

She was suffering from insulin dependent diabetes mellitus

 B

She was suffering from non-insulin dependent diabetes mellitus

 C

She was treated with oral hypoglycemic drugs only when diet and exercise could not control the pathological situation

 D

Knowledge of family history of diabetes mellitus is useful in predicting the nature of the diabetes

Q. 17

A 45-year old woman visited her physician with complaints of increased appetite and thirst with increased frequency of urination. She also had the symptoms of diminished or impalpable pulses in the feet, besides gangrene of the feet. Her laboratory findings on the oral glucose tolerance test are as follows:      (AI 2004)

Parameters

Fasting

1 hr

2 hr

Blood glucose

(mg/dL)

155

270

205

Urine glucose

-ve

+++

++

Ketone bodies

-ve

-ve

-ve

Which of the following statements is not correct for the above mentioned case:

 A

She was suffering from insulin dependent diabetes mellitus

 B

She was suffering from non-insulin dependent diabetes mellitus

 C

She was treated with oral hypoglycemic drugs only when diet and exercise could not control the pathological situation

 D

Knowledge of family history of diabetes mellitus is useful in predicting the nature of the diabetes

Ans. A

Explanation:

Answer is A (She was suffering from insulin dependent diabetes mellitus) :

The patient in question is suffering from non insulin dependent diabetes mellitus i.e. type H DM.

Before proceeding with the explanation to this question you need to be clear with the distinguishing characteristics between type I & type II DM. Reread explanation to the previous questions on DM.

Points which favour a diagnosis of non insulin dependant diabetes mellitus (type 2) in this question:

  1. Age > 40 yrs (45 yrs)
  2. Complication in the form of impalpable pulses in feet, gangrene at presentation hint to the possibility of occult disease which is likely to have been present for some time prior to diagnosis.

Note: This type of diabetes goes unrecognised for many years because the hyperglycemia develops gradually and in the early stages it is often not severe enough for the patient to notice any feature of developing complications. The presence of the microvascular complications of diabetes at presentation e.g. peripheral neuropathy hypertension, atherosclerosis dyslipidemia points in favour of a diagnosis of long standing undetected type II D.M.

Absence of Ketonuria: Ketonuria is a feature of type — I diabetes.

As depicted in the comparative analysis:

  • Family history (genetic tendency) is more important in type II disease and is useful in predicting the nature of diabetes.
  • Protocol for management of type II diabetes involves diet control and exercise as the primary management, followed by oral hypoglycemics and still further by insulin if pathological situations can not be controlled.

Q. 18

An obese lady aged 45 years, was brought to emergency in a semi comatose condition. The laboratory investigations showed K+ (5.8 mmol/L); Na+ (136 mmol/L); blood pH (7.1), HCO3 (12 mmol/L),’ ketone bodies (350 mg/dl). The expected level of blood glucose for this lady is:

 A

< 45 mg/dl

 B

< 120 mg/dl

 C

>180 mg/dl

 D

< 75 mg/dl

Q. 18

An obese lady aged 45 years, was brought to emergency in a semi comatose condition. The laboratory investigations showed K+ (5.8 mmol/L); Na+ (136 mmol/L); blood pH (7.1), HCO3 (12 mmol/L),’ ketone bodies (350 mg/dl). The expected level of blood glucose for this lady is:

 A

< 45 mg/dl

 B

< 120 mg/dl

 C

>180 mg/dl

 D

< 75 mg/dl

Ans. C

Explanation:

Answer is C (> 180 mg/dL);

`The patient in question is a case of diabetic Ketoacidosis.

Diabetic Ketoacidosis is associated with serum glucose levels between 250-300 mg/dl’


Q. 19

Ketone bodies are synthesised in:          

 A

Muscle

 B

Liver

 C

Kidney

 D

Brain

Q. 19

Ketone bodies are synthesised in:          

 A

Muscle

 B

Liver

 C

Kidney

 D

Brain

Ans. B

Explanation:

 

Ketone bodies are two molecules, acetoacetate and hydroxybutyrate.

The term “ketone body” is historical: only acetoacetate is an actual ketone.

Ketone bodies are synthesized in the liver from acetyl-CoA.


Q. 20

Which of the following is true about ketone bodies:

 A

Synthesized in intestine

 B

Normally used by brain in preference to glucose

 C

In peripheral tissues, they are converted to HMG CoA

 D

Ketone bodies are produced during diabetes and starvation

Q. 20

Which of the following is true about ketone bodies:

 A

Synthesized in intestine

 B

Normally used by brain in preference to glucose

 C

In peripheral tissues, they are converted to HMG CoA

 D

Ketone bodies are produced during diabetes and starvation

Ans. D

Explanation:

 

The production of ketone bodies and their utilization become more significant when glucose is in short supply to the tissues, as observed in starvation, and diabetes mellitus

Ketone bodies

  • They are three water-soluble compounds
  • They are produced as by-products when fatty acids are broken down for energy in the liver and kidney.
  • They are used as a source of energy in the heart and brain.
  • In the brain, they are a vital source of energy during fasting.
  • The three endogenous ketone bodies are acetone, acetoacetic acid, and beta-hydroxybutyric acid
  • Although beta-hydroxybutyric acid is not technically a ketone but a carboxylic acid.
  • Other ketone bodies such as beta-ketopentanoate and beta-hydroxypentanoate may be created as a result of the metabolism of synthetic triglycerides such as triheptanoin
  • Ketone bodies can be used for energy.
  • Ketone bodies are transported from the liver to other tissues, where acetoacetate and beta-hydroxybutyrate can be reconverted to acetyl-CoA to produce energy, via the citric acid cycle.
  • The heart gets little energy from ketone bodies except under special circumstances; it uses mainly fatty acids.
  • The brain gets a portion of its energy from ketone bodies when glucose is less available (e.g., during fasting, strenuous exercise, low carbohydrate, ketogenic diet and in neonates).
  • In the event of low blood glucose, most other tissues have additional energy sources besides ketone bodies (such as fatty acids), but the brain does not.
  • After the diet has been changed to lower blood glucose for 3 days, the brain gets 25% of its energy from ketone bodies.
  • After about 4 days, this goes up to 70% (during the initial stages the brain does not burn ketones, since they are an important substrate for lipid synthesis in the brain).

Ketone bodies are produced from acetyl-CoA mainly in the mitochondrial matrix of hepatocytes when carbohydrates are so scarce that energy must be obtained from breaking down fatty acids.

Because of the high level of acetyl CoA present in the cell, the pyruvate dehydrogenase complex is inhibited, whereas pyruvate carboxylase becomes activated.

  • Thus, the oxaloacetate produced will enter gluconeogenesis rather than the citric acid cycle, as the latter is also inhibited by the elevated level of NADH resulting from beta-oxidation of fatty acids.
  • The excess acetyl-CoA is therefore rerouted to ketogenesis.
  • Such a state in humans is referred to as the fasted state.
  • Acetone is produced by spontaneous decarboxylation of acetoacetate, yielding levels of acetone much lower than those of other ketone bodies.
  • Acetone cannot be converted back to acetyl-CoA, so it is excreted in the urine, or (as a consequence of its high vapor pressure) exhaled.
  • Acetone is responsible for the characteristic “fruity” odor of the breath of persons in ketoacidosis
  • When even larger amounts of ketone bodies accumulate such that the blood’s pH is lowered to dangerously acidic levels, this state is called ketoacidosis.
  • Both acetoacetic acid and beta-hydroxybutyric acid are acidic, and, if levels of these ketone bodies are too high, the pH of the blood drops, resulting in ketoacidosis.
  • This happens most often in untreated Type I diabetes, and somewhat less often in Type II.

Q. 21

In starvation, which is seen:       

 A

Increased supply of glucose

 B

Decreased rate of lipolysis

 C

Ketone bodies formation

 D

Low glucagon levels

Q. 21

In starvation, which is seen:       

 A

Increased supply of glucose

 B

Decreased rate of lipolysis

 C

Ketone bodies formation

 D

Low glucagon levels

Ans. C

Explanation:

 

Starvation biochemistry

  • When food intake ceases, the body enters the starvation response.
  • Initially, the body’s glycogen stores are used up in about 24 hours.
  • The level of insulin in circulation is low and the level of glucagon is very high.
  • The main means of energy production is lipolysis.
  • Gluconeogenesis converts glycerol into glucose and the Cori cycle converts lactate into usable glucose.
  • Two systems of energy enter the gluconeogenesis: proteolysis provides alanine and lactate produced from pyruvate, while acetyl CoA produces dissolved nutrients (Ketone bodies), which can be detected in urine and are used by the brain as a source of energy.
  • In terms of insulin resistance, starvation conditions make more glucose available to the brain.

Q. 22

Ketone bodies are formed in:        

 A

Liver

 B

Pancreas

 C

Kidneys

 D

Lungs

Q. 22

Ketone bodies are formed in:        

 A

Liver

 B

Pancreas

 C

Kidneys

 D

Lungs

Ans. A

Explanation:

 

Ketone bodies

  • They are three different water-soluble biochemicals that are produced as by-products when fatty acids are broken down for energy in the liver.
  • Two of the three are used as a source of energy in the heart and brain while the third (acetone) is a waste product excreted from the body.
  • In the brain, they are a vital source of energy during fasting.
  • The three endogenous ketone bodies are

– Acetone,

Acetoacetic acid, and

–  Beta-hydroxybutyric acid


Q. 23

Brain in starvation uses:  

TN 11; UP 12

 A

Amino acids

 B

Cellulose

 C

Ketone bodies

 D

Glycerol

Q. 23

Brain in starvation uses:  

TN 11; UP 12

 A

Amino acids

 B

Cellulose

 C

Ketone bodies

 D

Glycerol

Ans. C

Explanation:

Ans. Ketone bodies


Q. 24

Major source of energy for brain in fasting/ starvation ‑

 A

Glucose

 B

Glycogen

 C

Fatty acids

 D

Ketone bodies

Q. 24

Major source of energy for brain in fasting/ starvation ‑

 A

Glucose

 B

Glycogen

 C

Fatty acids

 D

Ketone bodies

Ans. C

Explanation:

Q. 25

A sectioned slice of liver is shown in the image.From the following given options,which is true regarding pathogenesis of this condition of liver?

 A

Increased entry of free fatty acids into the liver

 B

Decreased conversion of fatty acids into ketone bodies

 C

Block in the excretion of lipoprotein from the liver into plasma.

 D

All of the above

Q. 25

A sectioned slice of liver is shown in the image.From the following given options,which is true regarding pathogenesis of this condition of liver?

 A

Increased entry of free fatty acids into the liver

 B

Decreased conversion of fatty acids into ketone bodies

 C

Block in the excretion of lipoprotein from the liver into plasma.

 D

All of the above

Ans. D

Explanation:

Ans:D.)All of the above.

Fatty liver is shown in the image.

FATTY LIVER

MORPHOLOGIC FEATURES:

  • Grossly, the liver in fatty change is enlarged with a tense, glistening capsule and rounded margins.
  • The cut surface bulges slightly and is pale-yellow to yellow and is greasy to touch .

Microscopically, characteristic feature is the presence of numerous lipid vacuoles in the cytoplasm of hepatocytes.

Fat in H & E stained section prepared by paraffin embedding technique appear non-staining vauloes because it is dissolved in alcohol :

  • i) The vacuoles are initially small and are present around the nucleus (microvesicular).
  • ii) But with progression of the process, the vacuoles become larger pushing the nucleus to the periphery of the cells (macrovesicular).
  • iii) At times, the hepatocytes laden with large lipid vacuoles may rupture and lipid vacuoles coalesce to form fatty cysts.
  • iv) Infrequently, lipogranulomas may appear consisting of collections of lymphocytes, macrophages, and some multinucleated giant cells.
  • v) Fat can be demonstrated in fresh unfixed tissue by frozen section followed by fat stains such as Sudan dyes (Sudan III, IV, Sudan black) and oil red O. Alternatively, osmic acid which is a fixative as well as a stain can be used to demonstrate fat in the tissue.

PATHOGENESIS:

In fatty liver, intracellular accumulation of triglycerides can occur due to defect at one or more of the following 6 steps in the normal fat metabolism :

  • 1. Increased entry of free fatty acids into the liver.
  • 2. Increased synthesis of fatty acids by the liver.
  • 3. Decreased conversion of fatty acids into ketone bodies resulting in increased esterification of fatty acids to triglycerides.
  • 4. Increased α-glycerophosphate causing increased esterification of fatty acids to triglycerides.
  • 5. Decreased synthesis of ‘lipid acceptor protein’ resulting in decreased formation of lipoprotein from triglycerides.
  • 6. Block in the excretion of lipoprotein from the liver into plasma

Even a severe form of liver cell dysfunction may be reversible; e.g. an alcoholic who has not developed progressive fibrosis in the form of cirrhosis, the enlarged fatty liver may return to normal if the person becomes teetotaller.


Q. 26

All are true about ketone bodies except ‑

 A

Acetoacetate is primary ketone body

 B

Synthesized in mitochondria

 C

Synthesized in liver

 D

HMG CoA reductase is the rate-limiting enzyme

Q. 26

All are true about ketone bodies except ‑

 A

Acetoacetate is primary ketone body

 B

Synthesized in mitochondria

 C

Synthesized in liver

 D

HMG CoA reductase is the rate-limiting enzyme

Ans. D

Explanation:

Ans. is ‘d’ i.e., HMG CoA reductase is the rate-limiting enzyme 


Q. 27

Ketone bodies are used by all except ‑

 A

Brain

 B

RBCs

 C

Skeletal muscles

 D

Hepatocytes

Q. 27

Ketone bodies are used by all except ‑

 A

Brain

 B

RBCs

 C

Skeletal muscles

 D

Hepatocytes

Ans. D

Explanation:

Ans. is ‘d’ i.e., Hepatocytes

  • Ketone bodies are synthesized by liver and are utilized by extrahepatic tissues like heart, muscles, renal cortex and brain (in starvation).
  • Liver cannot utilize ketone bodies because it lacks enzyme succinyl-CoA-acetoacetate CoA transferase, which is required for the activation of ketone bodies.
  • The first reaction in use of ketone bodies is activation of acetoacetate.

                                              CoA-transferase

Succinyl CoA + acetoacetate ___________________  Acetoacetyl CoA + succinate


Q. 28

During starvation, muscle uses ‑

 A

Fatty acids

 B

Ketone bodies

 C

Glucose

 D

Proteins

Q. 28

During starvation, muscle uses ‑

 A

Fatty acids

 B

Ketone bodies

 C

Glucose

 D

Proteins

Ans. A

Explanation:

Ans. is ‘a’ i.e., Fatty acids 


Q. 29

Ketone bodies are not used by ‑

 A

Muscle

 B

Brain

 C

RBC

 D

Renal cortex

Q. 29

Ketone bodies are not used by ‑

 A

Muscle

 B

Brain

 C

RBC

 D

Renal cortex

Ans. C

Explanation:

Ans. is ‘c’ i.e., RBC 

  • Only glucose is the sole fuel for RBCs.
  • As RBCs have no mitochondria, they oxidize glucose anaerobically to lactate.
  • Liver also cannot use ketone bodies because of lack of succinyl-CoA-acetoacetate-CoA transferase, which is required for activation of ketone bodies.


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