Nutrition

Chapter 4 Nutrition

I. Key Dietary Terminology

A. Overview

1. The dietary reference intake (DRI) is a set of several reference values, including the recommended dietary allowance related to adequate intakes and upper levels of intakes.

2. The recommended dietary allowance (RDA) refers to intakes needed for optimal health; it is not a minimum daily requirement.

3. Daily energy expenditure depends most importantly on the basal metabolic rate (BMR) and on postprandial thermogenesis and the degree of physical activity.

4. The respiratory exchange rate (RER), also called the respiratory quotient, is the rate of oxygen consumption for different carbon sources.

1. RDA represents an optimal dietary intake of nutrients that under ordinary conditions can maintain a healthy general population.

2. RDA varies with sex, age, body weight, diet, and physiologic status.

a. Example: RDAs for nutrients increase in childhood, in pregnancy, and during lactation.

D. Basal metabolic rate (BMR)

2. Postprandial thermogenesis

a. Energy used in digestion, absorption, and distribution of nutrients

b. Accounts for about 10% of daily energy expenditure

Daily energy expenditure: BMR + postprandial thermogenesis + physical activity

3. Physical activity is variable and is expressed as an activity factor, which when multiplied by the BMR equals the daily energy expenditure.

a. The activity factor is 1.3 for a sedentary person, 1.5 for a moderately active person, and 1.7 for a very active person (e.g., marathon runner).

1. The BMI is used to determine obesity, defined as a BMI greater than 30 (normal is 20 to 25).

2. BMI = weight in kg/height in m²

BMI: weight in kg/height in m²

3. To improve BMI, the total calories expended must be greater than the total intake of calories.

a. When primarily drawing on adipose tissue to meet energy needs, to lose about 1 lb, a person must expend 3500 calories more than are consumed.

4. Sample calculations using two patients, A and B:

II. Dietary Fuels

A. Overview

1. Dietary carbohydrates with α-1,4 glycosidic linkages are digested to monosaccharides and transported directly to the liver through the hepatic portal vein.

2. Dietary carbohydrates with β-1,4 glycosidic linkages are not digested but serve other functions in the gut such as reducing cholesterol absorption and softening the stool.

3. Triacylglycerols are the major dietary lipids, although phospholipids and cholesterol are also consumed in the diet.

4. Long-chain triacylglycerols and cholesterol are packaged in chylomicrons and bypass the liver by transport through the lymphatics to the subclavian vein.

Short- and medium-chain triacylglycerols are transported as free fatty acids directly through the portal to the liver.

5. Dietary proteins are digested to free amino acids for the synthesis of proteins and to supply carbon skeletons for the synthesis of glucose for energy.

6. Nitrogen balance is an indication of net synthesis (growth), loss (breakdown), or stability in bodily proteins.

B. Dietary carbohydrates (see Chapter 1)

2. α-Amylase, which is found in saliva in the mouth and in pancreatic secretions in the small intestine, cleaves the α-1,4 linkages in starch, producing smaller molecules (e.g., oligosaccharides and disaccharides).

Starch digestion by α-amylase

3. Intestinal brush border enzymes (e.g., lactase, sucrase, maltase) hydrolyze dietary disaccharides into the monosaccharides glucose, galactose, and fructose, which are reabsorbed into the portal circulation by carrier proteins in intestinal epithelial cells (see Chapter 3).

a. Glucose is the predominant sugar in human blood.

b. Glucose is stored as glycogen, which is primarily located in liver and muscle.

c. Complete oxidation of carbohydrates to CO₂ and H₂O in the body produces 4 kcal/g.

Lactose intolerance: inability to digest lactose provides growth medium for intestinal bacteria; converted into lactic acid and hydrogen gas; osmotic diarrhea

d. Lactose intolerance due to lactase deficiency is discussed in Box 4-1.

BOX 4-1 Lactose Intolerance

Lactose intolerance, the most common type of digestive enzyme deficiency, is caused by insufficient lactase activity. It may result from an inherited decrease in lactase production or from damage to mucosal cells by drugs, diarrhea, or protein deficiency (e.g., kwashiorkor). The incidence of lactose intolerance is much higher (up to 90%) in those of Asian and African descent than in those of northern European descent (<10%).

The signs and symptoms of lactose intolerance result from the inability to digest lactose, a disaccharide that is present in dairy products. Unabsorbed lactose is osmotically active, causing retention of water in the gastrointestinal tract and production of a watery diarrhea. Bacterial degradation of lactose produces lactic acid and hydrogen gas, which causes abdominal bloating, cramps, and flatulence. The stool has an acid pH. Elimination of dairy products from the diet is the most effective treatment.

Carbohydrate: 4 kcal/g

4. Insoluble and soluble dietary fiber has β-1,4 glycosidic linkages which cannot be hydrolyzed by amylase and supply no energy, but they serve several important functions in the body.

a. Fiber increases intestinal motility, which results in less contact of bowel mucosa with potential carcinogens (e.g., lithocholic acid).

b. Fiber reduces the risk for colorectal cancer by absorbing carcinogens and reducing transit time.

c. Fiber softens the stool, which alleviates constipation and reduces the incidence of diverticulosis of the sigmoid colon.

Insoluble fiber: increases transit time; decreases exposure to carcinogens

Soluble fiber: increases favorable bacteria; decreases serum cholesterol level

Fiber: softens stool; prevents sigmoid diverticulosis

d. Fiber reduces absorption of cholesterol (decreasing blood cholesterol), fat-soluble vitamins, and some minerals (e.g., zinc).

e. Soluble fiber (e.g., oat bran, psyllium seeds) has a greater cholesterol-lowering effect than insoluble fiber (e.g., wheat bran).

f. β-Glucan from oat bran fosters growth of beneficial bacteria; prebiotic effect (bacteria are probiotic).

C. Dietary lipids

1. Long-chain free fatty acids from triacylglycerols provide the major source of energy to cells, with the exception of RBCs and the brain.

2. Dietary fats also contain essential fatty acids and are required for the absorption of fat-soluble vitamins.

3. The composition of dietary triacylglycerols varies in plants and animals.

5. Dietary triacylglycerols are digested primarily in the small intestine (Fig. 4-1).

a. Pancreatic lipase (aided by colipase) degrades triacylglycerol into 2-monoacylglycerol and free fatty acids.

4-1 Digestion of dietary lipids and assembly of nascent chylomicrons. Pancreatic lipase acts on triacylglycerol to produce 2-monoacylglycerol and free fatty acids, and pancreatic cholesterol esterase hydrolyzes cholesteryl esters to free cholesterol. These degradation products, as well as phospholipids and fat-soluble vitamins, are micellarized by bile salts and absorbed into intestinal cells by passive diffusion. Triacylglycerols are resynthesized, cholesterol is re-esterified, and all components are packaged into nascent chylomicrons with apolipoprotein B-48 on their surfaces. ApoB-48 is required for secretion of chylomicrons into the lymphatics and bloodstream.

Pancreatic lipase: converts triacylglycerols into 2-monoacylglycerol and free fatty acids

b. Pancreatic cholesterol esterase hydrolyzes cholesteryl esters and releases free cholesterol.

d. Nascent chylomicrons are assembled in mucosal cells and contain triacylglycerols (≈85%), cholesteryl esters (≈3%), phospholipids, the fat-soluble vitamins (i.e., A, D, E, and K), and apolipoprotein B-48, which is necessary for secretion of chylomicrons into the lymphatics.

ApoB-48: important in formation of chylomicrons and secretion into lymphatics

e. When discharged into the lymphatic vessels, lipoproteins rich in triacylglycerols ultimately enter the bloodstream and circulate to deliver fatty acids to tissues (see Chapter 7).

f. Complete oxidation of fats to CO₂ and H₂O in the body produces 9 kcal/g.

Dietary triacylglycerol: 9 kcal/g

6. The pathophysiology of lipid malabsorption is discussed in Box 4-2.

D. Dietary proteins

1. The biologic value of a dietary protein is determined by its content of essential amino acids (see Chapter 1).

a. Plant proteins (e.g., rice, wheat, corn, beans) are of low biologic value unless they are combined to provide all of the essential amino acids.

(1) Combining rice and beans or corn and beans provides higher biologic value than any one source.

b. Animal proteins (e.g., eggs, meat, poultry, fish, and dairy products) are of high biologic value because they contain all of the essential amino acids.

c. The dietary RDA for high-quality protein is 0.8 g/kg for men and women, which equals about 60 g/day for men and about 50 g/day for women.

BOX 4-2 Pathogenesis of Malabsorption

Malabsorption is a general term referring to increased fecal excretion of fat, called steatorrhea, with concurrent deficiencies of vitamins (particularly fat-soluble vitamins), minerals, carbohydrates, and proteins. The pathophysiology of malabsorption is classified as pancreatic insufficiency, bile salt deficiency, and small bowel disease.

Pancreatic insufficiency causes a maldigestion of fats due to diminished lipase activity, resulting in the presence of undigested neutral fats and fat droplets in stool. There is also maldigestion of proteins due to diminished trypsin, leading to undigested meat fibers in stool. Carbohydrate digestion is not affected because of the presence of amylase in salivary glands and disaccharidases in brush border enzymes. Chronic pancreatitis due to alcoholism is the most common cause of pancreatic insufficiency in adults; chronic pancreatitis due to cystic fibrosis is the most common cause in children.

Bile salt deficiency results in defective emulsification of fats, which is necessary for their absorption by small intestinal villi. Causes of bile salt deficiency include cirrhosis (i.e., inadequate production of bile salts and acids from cholesterol); intrahepatic or extrahepatic blockage of bile (e.g., calculus in common bile duct); bacterial overgrowth in the small bowel with destruction of bile salts; excess binding of bile salts (e.g., use of cholestyramine); and terminal ileal disease (i.e., inability to recycle bile salts and acids).

Small bowel disease associated with a loss of the villous surface leads to a malassimilation of fats, proteins, and carbohydrates. Celiac disease, or sprue, an autoimmune disease caused by antibodies directed against gluten in wheat, and Crohn’s disease, an inflammatory bowel disease involving the terminal ileum, commonly produce malabsorption.

Characteristic clinical findings for malabsorption include weight loss, anemia, chronic diarrhea, and malnutrition. The signs and symptoms associated with multiple fat-soluble vitamin deficiencies are usually present. Night blindness (i.e., vitamin A deficiency), rickets (i.e., vitamin D deficiency), and a hemorrhagic diathesis with ecchymoses and gastrointestinal bleeding (i.e., vitamin K deficiency) are the usual findings.

Biologic value of protein: determined by degree of representation by essential amino acids

Biologic value for animal protein: higher than for plant protein

2. Digestion of dietary proteins begins in the stomach, where the low pH denatures proteins, making them more susceptible to enzymatic hydrolysis.

3. Proteins are in a constant state of degradation and resynthesis.

a. When amino acids are oxidized, their nitrogen atoms are fed into the urea cycle in the liver and excreted as urea in the urine (primary route), feces, and sweat (see Chapter 8).

(1) Other nitrogenous excretory products include uric acid, creatinine, and ammonia.

b. Nitrogen balance is the difference in the amount of nitrogen (protein) consumed and the amount of nitrogen excreted in the urine, sweat, and feces.

4. Carbohydrates have a protein-sparing effect.

a. An adequate intake of carbohydrate provides the glucose that is necessary for maintaining normal blood sugar levels.

b. An inadequate intake of carbohydrate (<150 g/day) causes degradation of skeletal muscle to provide carbon skeletons (e.g., pyruvate) for gluconeogenesis (see Chapter 9).

5. Protein-energy malnutrition results from inadequate intake of protein or calories.

Carbohydrates are protein sparing.

Marasmus: total calorie deprivation

a. Marasmus is caused by a diet deficient in protein and calories (e.g., total calorie deprivation).

(1) Marasmus is marked by extreme muscle wasting (i.e., broomstick extremities) due to breakdown of muscle protein for energy and by growth retardation.

(2) It occurs primarily during the first year of life.

b. Kwashiorkor is caused by a diet inadequate in protein in the presence of an adequate carbohydrate intake.

(1) Marked by pitting edema and ascites (i.e., loss of the oncotic effect of albumin), enlarged fatty liver (i.e., decreased apolipoproteins), anemia, diarrhea (i.e., loss of brush border enzymes), and defects in cellular immunity

(2) Less extreme muscle wasting than occurs in marasmus due to the protein-sparing effect of carbohydrates

Kwashiorkor: inadequate protein intake; protein sparing due to increased carbohydrates

III. Water-Soluble Vitamins

A. Overview (Fig. 4-2 and Table 4-1)

1. Thiamine functions in oxidative decarboxylation and pentose phosphate pathway; deficiency produces beriberi.

2. Riboflavin functions primarily in electron transport; deficiency produces glossitis, stomatitis.

3. Niacin functions in NAD⁺ and NADP⁺ as cofactors for redox reactions; deficiency produces pellagra.

4. Pantothenic acid functions in fat and carbohydrate metabolism as a component of acetyl CoA and fatty acid synthase; deficiency symptoms are unknown.

5. Pyridoxine functions in transamination reactions, heme synthesis, glycogenolysis, and various other amino acid conversions; deficiency produces sideroblastic anemia and peripheral neuropathy.

6. Cobalamin functions in single carbon metabolism; deficiency produces macrocytic anemia and pernicious anemia.

7. Folic acid functions in single carbon metabolism; deficiency produces macrocytic anemia.

8. Biotin functions in carboxylase reactions; deficiency produces dermatitis, alopecia, glossitis.

9. Ascorbic acid (vitamin C) functions in hydroxylation reactions; deficiency produces scurvy.

4-2 Classification and functions of the vitamins.

TABLE 4-1 Water-Soluble Vitamins: Signs and Symptoms of Deficiency

Vitamin	Signs and Symptoms of Deficiency
Thiamine (vitamin B₁)	Wernicke-Korsakoff syndrome (confusion, ataxia, nystagmus, ophthalmoplegia, antegrade and retrograde amnesia, precipitated by giving thiamine with glucose in intravenous solution); peripheral neuropathy (dry beriberi); dilated cardiomyopathy (wet beriberi)
Riboflavin (vitamin B₂)	Corneal neovascularization; glossitis; cheilosis; angular stomatitis
Niacin (vitamin B₃)	Pellagra, with diarrhea, dermatitis, dementia
Pantothenic acid (vitamin B₅)	None identified
Pyridoxine (vitamin B₆)	Sideroblastic anemia; peripheral neuropathy; convulsions
Cobalamin (vitamin B₁₂)	Macrocytic (megaloblastic) anemia; neutropenia and thrombocytopenia; hypersegmented neutrophils; glossitis; subacute combined degeneration (posterior column and lateral corticospinal tract demyelination); dementia; achlorhydria, atrophic gastritis body and fundus, increased serum gastrin (only in pernicious anemia); increased plasma homocysteine; increased urine methylmalonic acid
Folic acid	Same as vitamin B₁₂ deficiency with the following exceptions: no neurologic dysfunction and normal urine methylmalonic acid level
Biotin	Dermatitis, alopecia, glossitis, lactic acidosis
Ascorbic acid (vitamin C)	Bleeding diathesis (ecchymoses, hemarthroses, bleeding gums, perifollicular hemorrhages, corkscrew hairs); loosened teeth; poor wound healing; glossitis

Water-soluble vitamins are readily excreted in the urine and rarely reach toxic levels.

B. Thiamine (vitamin B₁)

1. Sources of thiamine include enriched and whole-grain cereals, brewer’s yeast, meats, legumes, and nuts.

C. Riboflavin (vitamin B₂)

1. Sources of riboflavin include milk, eggs, meats, poultry, fish, and green leafy vegetables.

2. Flavin adenine dinucleotide (FAD) and flavin mononucleotide (FMN) are the active forms of riboflavin.

a. FAD is a cofactor associated with succinate dehydrogenase, which converts succinate to fumarate in the citric acid cycle.

Tags: Rapid Review Biochemistry

Jun 18, 2016 | Posted by admin in BIOCHEMISTRY | Comments Off

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