c) Peptide YY
2. Brown adipose tissue (BAT), plays an important role in energy metabolism in many mammals. The false statement about BAT,out of the followings is –
a) Storage of energy in the form of lipids
b) Expenditure of stored energy as heat
c) Increased Metabolic activity of BAT by leptin
d) BAT dissipates the hydrogen ion gradient in the oxidative respiration chain
3) Body Mass Index(BMI) gives a measure of relative weight adjusted for height. The healthy range for BMI is between-
a) 15- 19.5
b) 19.5- 25.0
c) 25- 29.9
d) Equal to 30 or > 30.
4) Which statement is false about ‘Upper abdominal obesity’?
a) Increased abdominal circumference (> 102 cm in men and 88 cm in women
b) High waist–hip ratios (> 1.0 in women and > 0.85 in men)
c) Risk of diabetes mellitus, stroke, coronary artery disease, and early death
d) Visceral fat within the abdominal cavity is more hazardous to health than subcutaneous fat around the abdomen.
5) Choose the true statement about ‘lower abdominal obesity’
a) Also called, ‘Apple shaped obesity’
b) Waist to hip ratio (< 1.0 for women and <0.8 for men)
c) Relatively common in females
d) Associated with increased risk for coronary heart disease stroke and diabetes mellitus.
6) Although the adipocyte has generally been regarded as a storage depot for fat, it is also an endocrine cell that releases numerous molecules in a regulated fashion. Which of the followings is not an adipose derived chemical ?
7) The major role of leptin in body-weight regulation is-
a) to signal satiety to the hypothalamus
b) to reduce dietary intake and fat storage
c) modulation of energy expenditure and carbohydrate metabolism
d) All of the above.
8) Which of the followings is not a secondary cause of obesity ?
a) Cushing syndrome
d) Diabetes mellitus
9) Which of the following adipose derived hormones promotes insulin sensitivity in peripheral tissues ?
10) Which of the followings statement is true about metabolic syndrome ?
a) Associated with lower body obesity
b) Associated with type 1 diabetes mellitus
c) Associated with metabolic diseases
d) Associated with increased risk for diabetes mellitus and cardiovascular diseases
11) Orlistat is the only FDA approved drug for treatment of obesity, the mechanism of action involves-
a) Increasing BMR
b) Inhibition of appetite centre
c) Promotes satiety
d) Inhibition of gastric and pancreatic lipases
12)- Dieting is the most commonly practiced approach to weight control. One can estimate the effect of calorie restriction on the reduction in adipose tissue. Since one pound of adipose tissue corresponds to ———— kilo calories.
13) Bariatric surgery is an increasingly prevalent treatment option for patients with obesity. Choose the incorrect statement about it-
a) Most popular is the roux-en-Y gastric bypass (RYGB)
b) The operation can be done laparoscopically
c) Can be the treatment of choice for any grade of obesity
d) results in substantial amounts of weight loss—close to 50% of initial body weight
Key to answers- 1)- d, 2)- a, 3)-b, 4)- b, 5)-c , 6)-b, 7)- d, 8)- d, 9)- a, 10)-d, 11)-d, 12)-d, 13)-cPlease help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
To simplify BMR
- The energy required by an individual during physical, emotional and digestive rest.
- It is the minimum energy required to sustain vital functions like working of heart, brain, circulation, respiration, ion transport and maintenance of cellular integrity
1) Person should be awake but at complete physical and mental rest
2) Person should be without food for 12-18 hours- Post absorptive state. This is to avoid the effect of digestion and absorption, the SDA of food stuffs and to prevent any chances of starvation.
3) He should be in recumbent or reclining position in bed.
4) There should be normal conditions of environment- temperature, pressure and humidity. The temperature should be between 200– 250 C. Under above conditions, energy expended by the individual is to maintain respiration, circulations, muscle tone, functions of viscera like kidney, heart, liver and brain and for the maintenance of body temperature.
Energy Expenditure in basal metabolism– Usually 50- 70% of the daily expenditure in sedentary individuals, BMR can be responsible for burning 70% of the total calories but the figure varies due to different factors. The factors that affect BMR are as follows-
Factors affecting BMR
1) Age- BMR decreases with advancing age. In children it is high due to more surface area.
2) Sex-Males have more muscle mass and lower body weight. Thus they have high BMR. Females have lower muscle mass more body fat thus have lower BMR.
3) Hereditary factors– Some people are born with faster metabolism and some with slower metabolism
4) Body Surface area- Surface area depends on weight and height. Greater the surface area, higher is the BMR and vice versa. Tall, thin people have a higher BMR than short persons. Since much of the basal metabolism is for the maintenance of body temperature and the heat loss is proportional to body surface area. Thus BMR is proportional to surface area.
5) Environmental conditions- Temperature outside body also affects BMR. Exposure to cold causes an increase in BMR so as to create the extra need for heat for the maintenance of body temperature. A short exposure to heat has little or no effect on BMR but upon prolonged exposure to high temperature there is compensatory heat loss, this results in increase in BMR. In colder regions of the world, BMR is higher and in tropical regions the BMR is lower.
6) Body Temperature-For every 0.5 degree rise in body temperature there is 7% increase in BMR. With the rise in temperature, there is increase in the rate of chemical reactions causing increased BMR.
7) Exercise- Physical exercise not only influences body weight by burning calories. It also helps to raise BMR by building extra lean tissues. Lean tissue is metabolically more demanding than fat tissue. The increase in BMR due to exercise is also due to increased cardiac output.
8) Drugs- Caffeine, Benzedine, alcohol, epinephrine and nicotine increase BMR. Reverse is seen with certain anesthetics.
9) Pregnancy- The BMR of pregnant mother rises after 6 months of gestation. BMR of mother is a sum total of her own BMR as in the non pregnant state and of that of fetal metabolism.
10) Racial variations- BMR varies with different racial groups. Higher values of > 33 % above normal have been reported in Eskimos.
11) Barometric pressure- Moderate decrease in pressure causes no effect on BMR, but a fall of pressure to half an atmosphere as occurs in mountain climbing increases BMR.
12) State of nutrition- BMR is lowered in states of starvation, malnutrition and wasting diseases.
13) Hormones-Thyroid hormone increases BMR. In thyrotoxicosis BMR rises 50-100% above normal, while in Myxoedema, BMR falls 35-45% below normal. Adrenaline, catecholamines, growth hormone, all of them increase BMR, Male sex hormone increases BMR to 10% or more. Anterior pituitary through its effect on TSH also affects BMR.
Short term factors affecting BMR
Illnesses such as fever, high level of stress hormones in the body and either an increase or decrease in environmental temperature result in an increase in BMR. Fasting, starvation or malnutrition all result in a lowering of BMR.
Measurement of BMR
BMR can be determined by the following methods-
1) Open Circuit system- In this system both O2 consumption and CO2 output are measured. Although it is very accurate but due to high degree of skills involved, it is less commonly used.
2) Closed circuit method-In clinical practice, the BMR is estimated by measuring O2 consumption of the patient for 2-6 minutes period under basal conditions. The O2 consumption is measured under closed circuit system. The apparatus commonly used is Benedict’s Roth metabolism apparatus. The test is usually run for 6 minutes and the volume of O2 consumed in that period is measured and corrected to standard conditions of temperature and pressure.
The average O2 consumption for 6 minutes is multiplied by 10 to convert into hourly basis and then multiplied by 4.825oC. The heat production is represented by each litre of O2 consumed. This gives the heat production in C/hour. Since the BMR is expressed as C/Sq.met/Hour, the energy output per hour has to be divided by the surface area of the individual.
Calculation of surface area of an individual
The surface area of an individual adult is about 1.8 square meter.
1) Du- Bois Surface area formula- A simple formula for calculating the surface area is as follows
BSA = (W 0.425 x H 0.725) x 0.007184
where the weight is in kilograms and the height is in centimeters and body surface area is in square meters.
2) By using normograms– Most conveniently the surface area is calculated from the normograms if the height and weight are known. Height is measured in feet/cm ; weight is measured in pounds/kg and surface area is calculated in square meters.
3) Harris–Benedict equations
BMR calculation for men (metric)
BMR = 66.47 + (13.75 x weight in kg ) + ( 5.003 x height in cm ) – ( 6.755 x age in years )
BMR calculation for women (metric)
BMR = 655.1 + (9.563 x weight in kg ) + ( 1.850 x height in cm ) – ( 4.676 x age in years )
4) Read’s formula
BMR = 0.75 (PR +0.74 x PP)
PR is pulse rate
PP is pulse pressure.
The result is expressed as percentage of the normal and is corrected within a range of ± 10%
Normal range of BMR
A healthy adult male has a BMR of about 40C/sq.m/hour and adult female has about 37 C/Sq.m/hour
Example of calculation of BMR
1) The normal BMR for an individual of the patient’s age and sex is obtained from the standard tables.
2) The patient’s actual rate is expressed as + or – % of the normal.
3) In a male aged 35 years with height-170 cm , weight- 70 kg and O2 consumption 1.2 liters in a 6 minutes time, the BMR can be calculated as follows-
O2 consumption/hour = 1.2 x10 = 12 liters
- or 12 x 4.825 = 58 Kcal/hour
Surface area from normogram = 1.8 sq.m.
Therefore BMR= 58/1.8 = 32 C/Sq.m/hour
The normal BMR for this patient by reference to standard table is 39.5 C/Sq.m/hour.
Hence the patient is having surface area of
= – 18.98 % below normal.
Significance of BMR
1) Diagnostic Aid
It is used for the diagnosis of various pathological conditions specially assessing the thyroid functions. The pathological variations in BMR are as follows-
a) Fever- Infections and febrile diseases elevate BMR, usually in proportion to increase in body temperature.
b) Diseases- BMR is increased in-
- Some types of anemia
- Cardiac failure
- Perforation of ear drum(False increase)
- Cushing syndrome
BMR is deceased in-
- Addison’s disease
2) Calculation of Caloric requirement- It is essential in the calculation of caloric requirement of an individual for prescribing a diet of adequate calorific value and planning nutrition.
3) To know the effect of food and drugs- BMR is calculated to know the effect of special food stuffs and drugs.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
1) Fructose excess can cause gouty arthritis and renal stones
Fructose is mainly metabolized through Fructose-1-P pathway. Unlike phosphofructokinase, which is involved in glucose metabolism, fructokinase has no negative feedback system to prevent it from continuing to phosphorylate its substrate, i.e. Fructose to form fructose -1-phosphate, and as a consequence ATP can be depleted,(Figure-1) causing intracellular phosphate depletion, and activation of AMP deaminase (Figure -2).
AMP deaminase enzyme causes conversion of AMP to IMP (Inosine monophosphate) and is inhibited by inorganic phosphate. Phosphate depletion causes loss of inhibition and thus it is activated, IMP is subsequently degraded to Inosine, Hypoxanthine , Xanthine and finally to Uric acid (Figure-1). Excessive uric acid generation leads to gout or renal stones (Urate stones). Thus excessive fruit consumption should be avoided by such patients.
Figure-1- Showing metabolism of fructose. The uninhibited fructokinase causes ATP depletion. The resulting metabolites are finally converted to uric acid.
Figure-2- Showing degradation of AMP, the key enzyme AMP deaminase is inhibited by inorganic phosphate. ATP depletion caused by active Fructokinase causes loss of inhibition of AMP deaminase by inorganic phosphate resulting in over activity of enzyme and overproduction of IMP and thus excess Uric acid.
2) Reasons to discourage fructose to treat hypoglycemia
Fructose has often been suggested as a treatment for hypoglycemia. It does contribute towards formation of Glucose and glycogen but there are several good reasons to discourage it as a treatment of hypoglycemia
The mechanism of glucose production is as follows-
Increased concentrations of Dihroxyacetone phosphate (DAP) and glyceraldehyde- 3-phosphate (GAP) produced from the metabolism of fructose in the liver drive the pathway toward glucose and subsequent glycogen synthesis (See figure-3).
Figure-3- Dihydroxyacetone phosphate(DAP) and glyceraldehyde -3-P produced from fructose metabolism condense together in the presence of Aldolase to form Fructose 1,6 bisphosphate, that is cleaved by fructose 1,6 bisphosphatase (FD pase) to form fructose-6-P. Glucose-6-P produced from Fructose-6-P by the action of Phospho hexose isomerase is converted to free glucose by the action of glucose-6-phosphatase. Hence by these reactions, Glucose is produced from fructose, blood glucose level rises. Surplus glucose-6-P can enter pentose phosphate pathway or can be converted to Glucose-1-P under the effect of Phosphoglucomutase and can be used up for the formation of Glycogen.
There are several good reasons to discourage the use of fructose to treat hypoglycemia
1) The process of formation of glucose from fructose is not an immediate process.
2) Secondly the conversion of fructose to glucose uses 2 ATPs. One ATP is spent at the first step for the formation of fructose-1-P and the second ATP is spent for the conversion of glyceraldehyde to Glyceraldehyde-3-P (Figure-3).Normal hepatic activity alone utilizes all of the liver’s ATP-synthesizing capacity.There is no good reason to increase hepatic ATP utilization for fructose metabolism. Glucose metabolism on the other hand produces ATP instead of utilizing.
3) Moreover fructose is not a direct energy source for brain and muscle as these tissue lack fructokinase and fructose transporters while Glucose is a preferred fuel for brain and can be utilized in almost all the cells of the body. Hence Glucose (also called dextrose) instead of fructose can be given orally or intravenously depending upon the situation to treat hypoglycemia.
3) What is the reason that even after consumption of lots of fruits or a large amount of fructose rich drink appetite is not suppressed?
1) Fructose does not stimulate release of insulin. One of insulin’s important functions is central regulation of hunger.Fructose does not affect the hypothalamus directly or through insulin.Fructose does not appear to dampen the sense of hunger.
Insulin release can modulate food intake by at least two mechanisms. First, insulin concentration in the central nervous system has a direct inhibitory effect on food intake. In addition, insulin may modify food intake by its effect on leptin secretion, which is mainly regulated by insulin-induced changes in glucose metabolism in fat cells.. Thus, a low insulin concentration after ingestion of fructose would be associated with lower average leptin concentrations than would be seen after ingestion of glucose. Because leptin inhibits food intake, the lower leptin concentrations induced by fructose would tend to enhance food intake and thus the appetite is not suppressed.
2) Ghrelin, a hormone produced by endocrine cells in the stomach, increases food intake and decreases fat oxidation and appears to have an anabolic role in long-term regulation of energy balance. Ghrelin secretion is normally suppressed after meals, but it is not suppressed by fructose consumption.
Thus this is another reason for non suppression of appetite even upon excessive consumption of fruits and also the reason for fructose related obesity and the obesity related complications.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
The mean annual consumption of sucrose plus fructose in developed countries is approximately 25% of the caloric intake. Because of the differences in the hepatic metabolism of fructose and glucose ,fructose is more lipogenic than glucose and is therefore more readily converted in the liver to triglyceride, which can be exported and stored in adipose tissue.
Metabolism of fructose
Much of the ingested fructose is metabolized by the liver, using the fructose 1-phosphate pathway (See figure-1) .
1) The first step is the phosphorylation of fructose to fructose 1-phosphate by fructokinase.
2) Fructose-1-phosphate is then split into glyceraldehyde and Dihydroxyacetone phosphate, an intermediate in glycolysis. Since there is only one phosphate attached to Fructose, it goes to only one of the trioses, the other is subsequently phosphorylated. This aldol cleavage is catalyzed by a specific fructose 1-phosphate aldolase.
3) Glyceraldehyde is then phosphorylated to glyceraldehyde -3-phosphate, a glycolytic intermediate, by triose kinase.
4) Alternatively, fructose can be phosphorylated to fructose 6-phosphate by hexokinase. The two triose phosphates, Dihydroxyacetone phosphate and glyceraldehyde 3-phosphate, may be degraded by glycolysis or may be substrates for aldolase and hence gluconeogenesis, which is the fate of much of the fructose metabolized in the liver. (See figure-1 and follow the steps)
Figure-1-showing the metabolism of fructose. Excess fructose consumption can lead to increase in adipose mass as well as increase in glycogen stores
Biochemical Basis of fructose induced metabolic alterations
Fructose undergoes more rapid glycolysis in the liver than does glucose, because it bypasses the regulatory step catalyzed by phosphofructokinase (Figure-1). This allows fructose to flood the pathways in the liver. High fructose consumption can lead to excess pyruvate production, causing a buildup of acetyl CoA which is directed toward fatty acid synthesis. Additionally, DHAP can be converted to glycerol3-phosphate providing the glycerol backbone for the triglyceride molecule. Triglycerides are incorporated into very low density lipoproteins (VLDL), the carriers for transportation of endogenously synthesized lipids , which are released from the liver destined toward peripheral tissues for storage in both fat and muscle cells.causing obesity (Figure-2).
Figure- 2 showing the fructose related metabolic complications.
Excessive fructose consumption is also believed to contribute to the development of non-alcoholic fatty liver disease (hepatic steatosis) In addition, several studies have demonstrated that fructose increases circulating triglyceride levels in the postprandial period and evidence indicates that this effect is more pronounced in persons with existing hyperlipidemia or insulin resistance .Thus, long-term consumption a diet high in fructose may increase the risk of atherosclerosis or other cardiovascular disease.
In addition, recent data indicate that compared with glucose, consuming fructose with meals, which does not stimulate insulin secretion, results in a reduction of circulating leptin concentrations and an attenuated postprandial suppression of ghrelin, a hormone produced by the stomach that stimulates hunger and increases food intake .
Insulin and leptin are important long-term regulators of food intake and energy balance. Both insulin and leptin act in the central nervous system to inhibit food intake and to increase energy expenditure, most likely by activating the sympathetic nervous system (SNS). Insulin is secreted from the β-cells in the endocrine pancreas in response to circulating nutrients (glucose and amino acids) and to the incretin hormones, glucose-dependent insulinotropic polypeptide (GIP) and glucagon-like peptide-1 (GLP-1), which are released during meal ingestion and absorption. Insulin can also act indirectly by stimulating leptin production from adipose tissue via increased glucose metabolism.
In contrast, dietary fat and fructose do not stimulate insulin secretion and therefore do not increase leptin production. Ghrelin, a hormone produced by endocrine cells in the stomach, increases food intake and decreases fat oxidation and appears to have an anabolic role in long-term regulation of energy balance. Ghrelin secretion is normally suppressed after meals, but it is not suppressed by fructose consumption. Thus, with respect to the hormones insulin, leptin, and ghrelin that are involved in the long-term endocrine regulation of food intake, energy balance, and body adiposity ,dietary fructose behaves more like dietary fat than do other types of carbohydrate that are composed of glucose . The lack of effect of fructose on these hormones suggests that chronic consumption of a diet high in fructose could contribute, along with dietary fat and inactivity, to increased energy intake, weight gain, and obesity. Obesity eventually leads to insulin resistance, diabetes mellitus and metabolic syndrome.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
2) What is the normal RDA for protein in a balanced diet for a normal adult?
a) 1G/Kg body weight
b) 10 G/Kg body weight
c) 100G/Kg body weight
d) 50 G/Kg body weight
3) Which of the following nutrients is rich in cholesterol?
b) Egg yolk
4) A balanced diet should have the ratio of Carbohydrate: Protein: Fats as-
5) The recommended ratio of Mono unsaturated: Saturated: Poly unsaturated fatty acids in a balanced diet should be-
6) The recommended intake of fats in a balance diet should be—% of the total calories
7) What is the caloric requirement of a 60 kg person with sedentary life style?
8) What should be the optimum ratio of cereals and pulses in a normal diet?
9) Which out of the following is not a polyunsaturated fatty acid?
a) α- Linolenic acid
b) Y- Linolenic acid
c) Caproic acid
d) Arachidonic acid
10) Which out of the following is present in animal fat ?
a) Erucic acid
b) Palmitoleic acid
c) Palmitic acid
d) Linoleic acid
11) A respiratory quotient of 0.82 signifies a—- diet
12) Which of the following is incorrect about BMR?
a) BMR increases in hyperthyroidism
b) BMR is directly proportional to the surface area
c) BMR decreases with the increasing temperature
d) BMR increases during starvation.
13) Which of the following has the maximum specific dynamic action?
b) Green peas
14) Mediterranean diet rich in olive oil (rich in oleic acid) lowers the incidence of Ischemic heart disease. Oleic acid is a-
a) Polyunsaturated fatty acid
b) Mono unsaturated fatty acid
c) Type of plant cholesterol
d) Saturated fatty acid
15) Hypoalbuminemia, hypokalemia, Hypomagnesemia and fatty liver are hallmarks of-
a) Electrolyte imbalance
d) Viral hepatitis
16) High fiber diet-
a) Lowers cholesterol
b) Improves glycemic control
c) Promotes peristalsis
d) All of the above.
17) The daily fiber content in a balanced diet should be-
a) 10 G/day
b) 50 G/day
c) 20 G/day
18) Which out of the following nutrients has the lowest glycemic index?
d) Ice cream
19) Choose the incorrect statement about iron out of the followings?
a)Jaggery is a good source
b) Milk is a poor source
c) Papaya is a rich source
d) Liver is a rich source.
20) All except one are conditions causing negative nitrogen balance–
d) Surgical trauma.
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a) 1 pound of water by 1°F
b) 1 pound of water by 1°C
c) 1 gram of water by 1°F
d) 1 gram of water by 1°C
2) The average adult requirement of calories per day is:
3) The caloric yield of fats is:
a) 4 calories per gram
b) 5 calories per gram
c) 7 calories per gram
d) 9 calories per gram
4) Lack of fiber in tube feedings can result in:
b) Nausea and vomiting
5) Which of the following compounds can be synthesized in humans?
b) Linoleic acid
6) In which of the following tissues, is glucose the major fuel in prolonged fasting?
d) Red blood cells
7) Which of the following vitamins is required for the synthesis of NAD+?
b) Pantothenic acid
d) Vitamin B6
8) Which of the following would be observed after 1 week of starvation?
a) The brain uses glucose and ketone bodies as fuel sources
b) Liver glycogen stores are only partially depleted due to an increase in gluconeogenesis
c) Nitrogen balance is maintained due to release of amino acids from muscle
d) Fatty acids from adipose stores are the major source of fuel for red blood cells.
9) Which of the following would be observed in a person who is resting after an overnight fast?
a) Liver glycogen stores are completely depleted
b) Liver gluconeogenesis is not an important process
c) Muscle glycogen stores are used up for maintenance of blood glucose
d) Fatty acids are released from adipose Triacyl glycerol store.
10) Which of the following vitamins is required for the synthesis of Coenzyme A ?
b) Pantothenic acid
11) The energy expended by an individual in a resting, post absorptive state is called-
a) Specific dynamic action
b) Basal metabolic rate
c) Diet induced thermogenesis
d) Respiratory quotient
12) Choose the incorrect statement about saturated fatty acids?
a) Fatty acids without any double bond in the side chain are called saturated fatty acids
b) Consumption of saturated fatty acids lowers plasma cholesterol and raises plasma HDL
c) Main sources of saturated fatty acids are dairy and meat products
d) Palmitic and Stearic acids are the chief saturated fatty acids of the body
13) All except one are true about essential fatty acids-
a) Deficiency is characterized by dermatitis, hair loss and poor wound healing
b) Lower Plasma LDL but raise HDL, thus they are cardio protective
c) All of them are polyunsaturated fatty acids
d) Cheese, butter and most of the animal fats are chief sources.
14) Which of the following proteins has low biological value?
15) The RDA for carbohydrates is-
a) 130 G/Day
b) 45-65 % of the total calories
c) Any of the above
d) None of the above
16) Which of the following corresponds to negative nitrogen balance?
d) Recovery from illness.
17) Which of the followings correspond to positive nitrogen balance?
18) Choose the incorrect statement about Kwashiorkor –
a) Primary energy deficit
b) Associated with edema
c) Skin is hypo pigmented and peels of easily
d) Flag sign is a characteristic finding
19) Basal metabolic rate is low in which of the following conditions-
b) Hot climate
c) Old age
d) All of the above
20) Which one of the followings contains the highest percentage of mono unsaturated fatty acids?
a) Corn oil
b) Soybean oil
c) Coconut oil
d) Olive oil
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b) Febrile conditions
c) Diabetes mellitus
2- Choose the incorrect statement about BMR out of the following-
a) BMR is directly related to the surface area
b) BMR is inversely proportional to the age
c) BMR is increased in warm climate
d) Males have higher BMR than age matched females.
3- The percentage of total calories obtained from carbohydrates should be between-
a) 15- 20%
4- All are true about milk as a diet except-
a) It is low in iron content but rich in calcium, sodium and potassium
b ) The major carbohydrate is lactose
c) The chief proteins are caseinogens and lactalbumin
d) It is rich in vitamin C and D but poor in Vitamin A and Riboflavin.
5- In a child suffering from marasmus which of the following clinical manifestation is not observed?
a) Watery diarrhea with acid stools
b) Subnormal temperature
c) Visible peristalsis from thin abdominal wall
d) Generalized edema.
6- The chemical score of gelatin is –
7- Which of the following has the best chemical score?
8- In a person on hunger strike from the past three days which of the following urinary tests would give a positive reaction?
9- A child has presented with growth retardation, inability to walk and bruises all over the body. Which of the following nutrients should be recommended as a supplement to the diet?
b) Egg yolk
c) Citrus fruits
10- Which of the following has the highest glycemic index?
a) Ice cream
11- All except one are true about the significance of dietary fiber ?
a) It promotes peristalsis
b) Reduces Cholesterol absorption
c) Increases glycemic index
d) Acts as an anti oxidant
12- Which of the following has the highest Specific dynamic action (SDA) ?
c) Corn oil
13- An 8 months-old-child has been brought to the pediatric OPD. The examination reveals a thin lean emaciated child. There is history of diarrhea and refusal to feeds from the last few days. The child has been diagnosed with ‘marasmus’. What could have been the source of energy to the brain cells during the period of food deprivation?
b) Fatty acids
c) Ketone bodies
d) Branched chain amino acids.
14- A 34- year-old female has reported with a history of forgetfulness, loss of hair and cold intolerance. She has been diagnosed with hypothyroidism. What would be the effect of this disease on BMR?
a) BMR remains unaltered
b) BMR increases
c) BMR goes down
d) There is initial rise with a subsequent fall.
15- A 68- year- old male has been brought to the emergency in a state of coma. The patient is a known alcoholic from the past 10 years. A diagnosis of hepatic encephalopathy has been made. Which of the following nutrient should be avoided so as to reduce the ammonia formation in the body?
d) Minerals and vitamins
16- An adequate amount of tyrosine can reduce the requirement of Phenyl alanine in the diet, this effect is said to be-
a) Mutual supplementation of nutrients
b) Sparing effect
c) Specific dynamic action
d) None of the above.
17- Which of the following is a correct statement to justify the cause of fatty liver in Kwashiorkor?
a) There is more mobilization of lipids from adipose mass
b) There is more synthesis of lipids in the liver
c) There is deficiency of apo B100 protein
d) All of the above.
18- In diabetes mellitus there is reduced oxidation of carbohydrates; what will the effect of insulin administration on RQ ?
a) It will increase
b) It will decrease
c) No effect
d) Initial rise and then fall
19- Which of the following is not a component of dietary fiber?
20- Which of the following nutrients is rich in short and medium chain fatty acids ?
b) Peanut oil
c) Sunflower oil
d) Almond oil
21- Human most easily tolerate a lack of which of the following nutrient ?
Key to answers-1)- a, 2)- c, 3)- c, 4)-d, 5)- d, 6)- a, 7)- b, 8)-c, 9)- c, 10)- d, 11)- c, 12)- a, 13)- c, 14)- c, 15)- a, 16)- b, 17)- c, 18)- a, 19)- d, 20)-a, 21)-bPlease help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
It consists of all of the components of the cell walls of plants that are not broken down by the body’s digestive enzymes.
Dietary Fiber and Total Fiber
“Dietary fiber” as noted on the “Nutrition Facts Label” of commercial foods, is fiber originally present in the food. “Total fiber” consists of dietary fiber and added fiber – substances that are adding to original food to increase their fiber content or to change their physical properties. Pectin, for example, is added to jam to give it a gel form.
Dietary fiber can be grouped into two main categories, those that are soluble and those that are insoluble in water.
Soluble fiber (viscous fiber) partly dissolves in water and forms gel with it. Foods rich in soluble fiber include beans and other legumes (peas, soy, and lentils), oats, barley, citrus fruits (oranges, grapefruit), psyllium husk and flax seed. Substances found in soluble fiber are gum, pectin, some hemicelluloses, mucilage and storage polysaccharides (starch and glycogen).
Beneficial Effects of Soluble Fiber
- Soluble fiber may prevent both diarrhea and constipation. It absorbs water from the gut and thus makes stool soft, but not bulky.
- Soluble fiber may help in weight loss. It slows down the speed of the passage of food through the gut thus giving a feeling of fullness.
- Soluble fiber may help to prevent and treat diabetes type 2. It slows down absorption of glucose from the intestine into the blood thus preventing high spikes of glucose in the blood after a meal.
- Soluble fiber may lower total and LDL cholesterol and thus helps to prevent ischemic heart disease and stroke. It binds bile acids in the bowel and removes them from the body and thus reduces their absorption into the blood. Lost bile acids are replaced by synthesis from blood cholesterol. This is one theory about how soluble fiber lowers blood cholesterol levels.
- Soluble fiber may prevent bile salt diarrhea after a gallbladder removal.
Unwanted Effects of Soluble Fiber
Soluble fiber, if ingested in excess may cause:
- Abdominal bloating and flatulence
- Dehydration, if ingested without water
- Pectin may reduce absorption of cholesterol-lowering drugs, like Lovastatin
Soluble Fiber Supplements
Examples of soluble fiber supplements:
- Metamucil (psyllium – isphagula)
- Citrucel (methylcellulose)
- Benefiber (wheat dextrin)
- FiberChoise (Inulin)
The soluble fibers such as pectin and true plant gums are mucilaginous and are digestible.
Pectins are predominantly polygalacturonic acids with varying amounts of other hexose or pentose residues.
True plant gums are complex poly saccharides composed of primarily arabinose, fucose, galactose, mannose, rhamnose, and xylose. The gums are soluble in water and are digestible by the enzymes in the intestinal tract. Both pectins and gums are mucilaginous; they absorb water to form viscous gels in the stomach that decrease the rate of gastric emptying. The mucilaginous nature of the soluble fibers, pectins, and gums tends to decrease the rate at which carbohydrates are digested and absorbed, thus decreasing both the rise in blood glucose levels and the ensuing increase in insulin concentration.
Insoluble fiber can not be dissolved in water. Foods rich in insoluble fiber include whole wheat and other whole grains and most dark green leafy vegetables, like cabbage and cauliflower. Substances found in insoluble fiber include cellulose, hemicellulose and lignin.
Beneficial Effects of Insoluble Fiber
- Insoluble fiber may help to prevent constipation, hemorrhoids and diverticulosis. It binds water and thus makes stool soft and bulky; it also speeds up the passage of food through the intestine.
Unwanted Effects of Insoluble Fiber
- Ingesting foods with insoluble fiber containing sulphur (garlic, onions) may result in excessive gas.
- Insoluble fiber eaten on an empty stomach may aggravate symptoms of irritable bowel syndrome.
- Insoluble fiber ingested without water may result in severe constipation or even intestinal obstruction.
- Certain types of insoluble fiber may trigger diarrhea in sensitive people.
- Excessive ingestion of supplements containing insoluble fiber, especially in small children, may reduce absorption of calcium, magnesium, iron, copper and zinc.
1) Cellulose is a major structural component of plant cell walls. Cellulose is a long, linear polymer of glucose (β-D-glucopyranose) units that are joined by β(1→4) glycosidic bonds . Cellulose molecules have an extended, rigid structure that is stabilized by interchain hydrogen bonds.
Starch, the plant storage polysaccharide, which is also a polymer of glucose, differs in its structure in that the glucose monomer units are joined by α(1→4) glycosidic bonds .Starch is composed of two types of polymers, amylose, which has a nonbranched helical structure, and amylopectin, which is branched with α(1→6) glycosidic bonds joining the branches to the main polymer chain. Although starch is easily digested by salivary and pancreatic amylase and the disaccharidases present on the brush border of intestinal mucosal cells, cellulose cannot be hydrolyzed. The β(1→4) glycosidic bonds of the cellulose chain cannot be cleaved by the amylases present in the digestive tract.
Figure -1- Showing the molecular structure of cellulose, indicating the repeating disaccharide unit, cellobiose.
Figure- 2-The molecular structure of starch, indicating the repeating disaccharide unit, maltose, as well as the α-1,6-glycosidic bond present in the branch points of amylopectin.
2) Hemicelluloses are also polysaccharides that are structural components of plant cell walls. However, unlike what their name implies, they are unrelated to cellulose. They are polymers that are made up of a variety of sugar monomers that include glucose, galactose, mannose, arabinose, and xylose, as well as acidic forms of these monosaccharides. Xylose is the monosaccharide that is most abundant. Hemicelluloses have a random, amorphous structure that is suitable for their location in the plant cell wall matrix. Depending on their molecular structure, hemicelluloses are partially digestible.
3) Lignins are formed by the irreversible dehydration of sugars that result in aromatic structures. The remaining alcohol or phenol OH groups can react with each other and with aldehyde and ketone groups to form polymers. These polymers cannot be broken down by the digestive enzymes and, like cellulose and the indigestible portion of hemicelluloses, form the stool bulk.
Figure-3- A lignin molecule in an early stage of condensation. The aromatic rings are a result of irreversible dehydration of sugar residues.
Although cellulose and hemicellulose are insoluble, they absorb water to swell and increase the stool bulk. This results in larger, softer stools. It has been shown that diets plentiful in insoluble fiber also increase the transit time of food in the digestive tract and decrease intracolonic pressure. Lignins, in addition to increasing stool bulk, also bind organic molecules such as cholesterol and many potential carcinogens.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
Analysis of a plasma sample indicated elevated levels of Alanine, Acetoacetate, β hydroxy butyrate, and blood urea nitrogen(BUN). However her plasma glucose concentration was low (55mg/dL) . She was hospitalized, given intravenous feeding, antidepressant medications and subsequently shifted to an 1800 Cal (7500 kJ) diet. Her recovery was uneventful.
How was the patient obtaining energy during the time when she was not eating?
How could patient maintain her plasma glucose within normal limits even though she was not eating?
What is the significance of elevated plasma Alanine level?
Why is BUN elevated?
What is indicated by the fact that the plasma Acetoacetate and β– hydroxy butyrate levels are elevated?
It is a case of starvation. The high blood Alanine level signifies the catabolic state. Alanine in excess is released during starvation from muscle to serve as a substrate for glucose production in liver. Acetoacetate and β hydroxy butyrate are ketone bodies which are used as alternative fuel during conditions of glucose deprivation . High BUN signifies protein degradation; the carbon skeletons of amino acids are utilized for glucose production while amino groups are converted to urea.
Prolonged fasting may result from an inability to obtain food, from the desire to lose weight rapidly, or in clinical situations in which an individual can not eat because of trauma,surgery, neoplasms, burns etc or even in depression (As in the given case) . In the absence of food the plasma levels of glucose, amino acids and triacylglycerols fall, triggering a decline in insulin secretion and an increase in glucagon release. The decreased insulin to glucagon ratio, and the decreased availability of circulating substrates, make this period of nutritional deprivation a catabolic state, characterized by degradation of glycogen, triacylglycerol and protein. This sets in to motion an exchange of substrates between liver,adipose tissue, muscle and brain that is guided by two priorities (i) the need to maintain glucose level to sustain the energy metabolism of brain ,red blood cells and other glucose requiring cells and (ii) to supply energy to other tissues by mobilizing fatty acids from adipose tissues and converting them to ketone bodies to supply energy to other cells of the body.
A typical well-nourished 70-kg man has fuel reserves totaling about 161,000 kcal (670,000 kJ). The energy need for a 24-hour period ranges from about 1600 kcal (6700 kJ) to 6000 kcal (25,000 kJ), depending on the extent of activity. Thus, stored fuels suffice to meet caloric needs in starvation for 1 to 3 months. However, the carbohydrate reserves are exhausted in only a day.
Energy supply during starvation
During starvation the energy needs are fulfilled by three types of fuels, glucose, fatty acids and ketone bodies.
a) Glucose supply during starvation (Gluconeogenesis)
Energy needs of brain and RBCs
Even under conditions of starvation, the blood-glucose level has been maintained above 2.2 mM (40 mg/dl). The first priority of metabolism in starvation is to provide sufficient glucose to the brain and other tissues(such as red blood cells) that are absolutely dependent on this fuel.However, precursors of glucose are not abundant. Most energy is stored in the fatty acyl moieties of triacylglycerols. Fatty acids cannot be converted into glucose, because acetyl CoA cannot be transformed into pyruvate. The glycerol moiety of triacylglycerol can be converted into glucose, but only a limited amount is available. The only other potential source of glucose is amino acids derived from the breakdown of proteins. However, proteins are not stored,and so any breakdown will necessitate a loss of function.
Thus, the second priority of metabolism in starvation is to preserve protein,which is accomplished by shifting the fuel being used from glucose to fatty acids and ketone bodies by cells other than brain cells and the cells lacking mitochondria.
It is a biological compromise to provide glucose to these cells as a priority. During prolonged starvation , when the gluconeogenic precursors are not available, proteins are however broken down to use carbon skeleton of glucogenic amino acids for glucose production.
b) Fatty acid oxidation
Energy need of liver
The low blood-sugar level leads to decreased secretion of insulin and increased secretion of glucagon. Glucagon stimulates the mobilization of triacylglycerols in adipose tissue and gluconeogenesis in the liver. The liver obtains energy for its own needs by oxidizing fatty acids released from adipose tissue. The concentrations of acetyl Co A and citrate consequently increase, which switch off glycolysis. Thus glucose utilization is stopped in liver cells to preserve glucose for priority cells
Energy need of muscles
The uptake of glucose by muscle is markedly diminished because of the low insulin level, whereas fatty acids enter freely.Consequently, muscle shifts almost entirely from glucose to fatty acids for fuel.The beta-oxidation of fatty acids by muscle halts the conversion of pyruvate into acetyl CoA, because acetyl CoA stimulates the phosphorylation of the pyruvate dehydrogenase complex, which renders it inactive. Most of the pyruvate is transaminated to alanine, at the expense of amino acids arising from breakdown of “labile” protein reserves synthesized in the fed state. The alanine, lactate and much of the keto-acids resulting from this transamination are exported from muscle, and taken up by the liver, where the alanine is transaminated to yield pyruvate. Pyruvate is a major substrate for gluconeogenesis in the liver.(Figure-1)
Figure- 1-showing Glucose Alanine and Cori’s cycle
In adipose tissue the decrease in insulin and increase in glucagon results in activation of intracellular hormone-sensitive lipase.This leads to release from adipose tissue of increased amounts of glycerol(which is a substrate for gluconeogenesis in the liver) and free fatty acids,which are used by liver, heart, and skeletal muscle as their preferred metabolic fuel, therefore sparing glucose.
Loss of muscle mass
During starvation, degraded proteins are not replenished and serve as carbon sources for glucose synthesis. Initial sources of protein are those that turn over rapidly, such as proteins of the intestinal epithelium and the secretions of the pancreas. Proteolysis of muscle protein provides some of three-carbon precursors of glucose. The nitrogen part of the amino acids is converted to urea (BUN)
Energy need of peripheral tissues
After about 3 days of starvation, the liver forms large amounts of acetoacetate and beta- hydroxybutyrate. Their synthesis from acetyl CoA increases markedly because the citric acid cycle is unable to oxidize all the acetyl units generated by the degradation of fatty acids. Gluconeogenesis depletes the supply of oxaloacetate, which is essential for the entry of acetyl CoA into the citric acid cycle. (Figure-2) Consequently, the liver produces large quantities of ketone bodies, which are released into the blood. At this time, the brain begins to consume appreciable amounts of acetoacetate in place of glucose. After 3 days of starvation, about a third of the energy needs of the brain are met by ketone bodies. The heart also uses ketone bodies as fuel. After several weeks of starvation, ketone bodies become the major fuel of the brain.
Figure- 2-fatty acid oxidation and ketosis during starvation.
In essence, ketone bodies are equivalents of fatty acids that can pass through the blood-brain barrier. Only 40 g of glucose is then needed per day for the brain, compared with about 120 g in the first day of starvation. The effective conversion of fatty acids into ketone bodies by the liver and their use by the brain markedly diminishes the need for glucose. Hence, less muscle is degraded than in the first days of starvation. The breakdown of 20 g of muscle daily compared with 75 g early in starvation is most important for survival.
A person’s survival time is mainly determined by the size of the triacylglycerol depot.
What happens after depletion of the triacylglycerol stores? The only source of fuel that remains is proteins. Protein degradation accelerates, and death inevitably results from a loss of heart, liver, or kidney function.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!
Case details –
The patient is obese and is also suffering from “Metabolic syndrome”. She has a history of obesity dating to early child hood and also has a positive family history. Her symptoms are suggestive of metabolic syndrome, a common complication of Obesity. Some of her features can be discussed as –
1) Obesity –She has an apple (android) pattern of fat distribution. Her waist to hip ratio is 41/39=1.05. Apple shape is defined as a waist to hip ratio of more than 0.8 in women, and more than 1.0 in men. She has therefore apple pattern of fat distribution which is common in males. Compared with other women of same body weight who have gynoid fat pattern, the presence of increased visceral or intra abdominal adipose tissue places her at greater risk for diabetes, hypertension,dyslipidemia and coronary heart disease. (The gynoid, “pear- shaped” or lower body obesity is defined as a waist to hip ratio of less than 0.8 for women and less than 1.0 for men. The pear shape is relatively benign health wise and is commonly found in females).
2) BMI (Body Mass Index)
BMI=Weight (kg)/height (m2).
For this patient
188 Pounds=85.5 kg (Approximately)
5 feet 1 inch height=1.55 meters (154.94 cm)
= 35.6 kg/ m2
World Health Organization (WHO) criteria based on BMI
Under this convention for adults,
Grade 1 overweight (commonly and simply called overweight) is a BMI of 25-29.9 kg/m2.
Grade 2 overweight (commonly called obesity) is a BMI of 30-39.9 kg/m2.
Grade 3 overweight (commonly called severe or morbid obesity) is a BMI greater than or equal to 40 kg/m2.
From the result calculated for the given patient, it is indicated that the patient is obese (Grade 2 overweight).
3) Metabolic syndrome The patient is also suffering from ‘Insulin resistance syndrome’.She has hypertension, dyslipidemia, Hyperinsulinemia and impaired glucose tolerance.
Metabolic syndrome also referred to as Syndrome X or insulin resistance syndrome consists of a number of metabolic risk factors that increase the risk for atherosclerotic cardiovascular disease (CVD) and other cardiovascular complications such as cardiac arrhythmias, heart failure, and thrombotic events.
a) Criteria for diagnosis According to the National Cholesterol Education Program (NCEP) Adult Treatment Panel III (ATP III) report, there are six major components of metabolic syndrome relating to the development of CVD:
1) abdominal obesity
2) atherogenic dyslipidemia
3) elevated blood pressure
4) insulin resistance (with or without the presence of glucose intolerance)
5) proinflammatory state, and
6) prothrombotic state.
Note- A prothrombotic state is characterized by abnormalities,specifically elevations, in procoagulant factors, anti fibrinolytic factors,platelet alterations, and endothelial dysfunction. A proinflammatory state is characterized by elevations of circulating inflammatory molecules such as C-reactive protein (CRP), tumor necrosis factor-alpha, plasma resistin, interleukin (IL)-6, and IL-18. CRP is a general marker of inflammation that has been linked to CVD in patients with metabolic syndrome.
b)Associated diseases– Cardiovascular diseases and type 2 diabetes mellitus can be present in association with metabolic syndrome. The relative risk for new-onset CVD in patients with the metabolic syndrome, in the absence of diabetes, averages between 1.5- and threefold. Overall, the risk for type 2 diabetes in patients with the metabolic syndrome is increased three to fivefold. Patients with metabolic syndrome are also at increased risk for peripheral vascular disease. In addition to the features specifically associated with metabolic syndrome,insulin resistance is accompanied by other metabolic alterations. These include increases in uric acid,microalbuminuria, nonalcoholic fatty liver disease (NAFLD) and/or polycystic ovarian disease (PCOS), and obstructive sleep apnea (OSA).
A person suspected of having this syndrome should have a through history taken especially with regard to family history and presence of other cardiovascular risk factors.
c) An examination should include:-
a) Recording the body weight
b) Calculating the BMI
c) Measurement of the waist circumference in inches
d) Calculating the hip-waist ratio
e) Measurement of the subcutaneous fat at 4 sites-biceps, triceps, sub scapular and supra-iliac
f) Blood pressure measurement.
d) Laboratory Tests
1) Fasting lipids and glucose estimations are needed to determine if the metabolic syndrome is present.
2) The measurement of additional biomarkers associated with insulin resistance must be individualized. Such tests might include apo B, high-sensitivity CRP,fibrinogen, uric acid, urinary microalbumin, and liver function tests.
3) A sleep study should be performed if symptoms of OSA are present.
4) If PCOS is suspected based on clinical features and an ovulation, testosterone, luteinizing hormone, and follicle-stimulating hormone should be measured.
e) Management of metabolic syndrome – is highly dependent on the control of all of the contributing factors. This includes both underlying risk factors as well as metabolic risk factors. Lifestyle modifications should be implemented immediately for all patients diagnosed with metabolic syndrome. Lifestyle modifications include weight reduction, increased physical activity and nutritional therapy. Additional risk assessments should be performed in patients to assure appropriate goals of therapy throughout the course of the syndrome.
A 40 –year- old woman, 5 feet 1 inch tall and weighing 188 pounds came for consultation to a physician complaining of frequent episodes of dizziness and numbness in her legs. She was too worried for her weight. Her waist measured 41 inches and hip measured 39 inches. Her only child who was 15-year-old, her sister and both of the parents were overweight. The patient recalled that she had been obese throughout her childhood and adolescence. Over the past 6 years she had been on seven different diets for periods of two weeks to three months, losing from 5 to 25 pounds. On discontinuation of each diet, she regained weight returning to 185 to 190 pounds.
During routine physical examination the patient was observed to be hypertensive (blood pressure of 200/120 mm Hg) but no abnormality was detected upon examination of Chest, CNS and Abdomen .
The patient was asked to return to the clinic a week later in the fasting state,during which time a blood specimen was obtained. Blood Biochemistry revealed fasting hyperglycemia, hyperinsulinemia, dyslipidemia, and glucose intolerance.
What is the probable diagnosis?
What other investigations should be carried out to confirm the diagnosis?
Calculate the BMI for this woman and comment on the grade of obesity.Please help "Biochemistry for Medics" by CLICKING ON THE ADVERTISEMENTS above!