Chapter 24B Nutrition, Metabolism, Body Temperature Slides by Barbara Heard and W. Rose. figures...

Chapter 24B

Nutrition, Metabolism,

Body Temperature

Slides by Barbara Heard and W. Rose.

figures from Marieb & Hoehn 9th ed.

Portions copyright Pearson Education

© 2013 Pearson Education, Inc.

Protein Metabolism

• Proteins deteriorate, so continually broken down and replaced

• Amino acids recycled new proteins or different compound

• Protein not stored in body– When dietary protein in excess, amino acids

• Oxidized for energy • Converted to fat for storage


Protein Synthesis

• Amino acids most important anabolic nutrients– Form all proteins; bulk of functional molecules

• Hormonally controlled

• Requires complete set of amino acids – Essential amino acids required in diet

• Synthesize 225 – 450 kg protein during lifetime


Catabolic-Anabolic Steady State

• Dynamic state in which– Organic molecules (except DNA) continuously

broken down and rebuilt– Organs have different fuel preferences– Uses nutrient pools

• Stores of amino acids, carbohydrates, fats


Nutrient Pools

• Three interconvertible pools– Amino acids– Carbohydrates – Fats

• Amount and direction of conversion directed by liver, adipose tissue, skeletal muscle


Amino Acid Pool

• Body's total supply of free amino acids

• Proteins lost in urine, hair, skin cells

• Source for – Resynthesizing body proteins – Forming amino acid derivatives– Gluconeogenesis


Carbohydrate and Fat Pools

• Easily interconverted through key intermediates

• Differ from amino acid pool – Fats and carbohydrates oxidized directly to

produce energy; amino acids first converted to carbohydrate

– Excess carbohydrate and fat can be stored; amino acids not stored as protein


Figure 24.17 Interconversion of carbohydrates, fats, and proteins.

Proteins

Proteins

Amino acids

Urea

Excreted in urine

Carbohydrates

Glycogen

Glucose

Glucose-6-phosphate

Glyceraldehyde 3-phosphate

Pyruvic acid

Acetyl CoA

Krebs cycle

Fats

Triglycerides (neutral fats)

Glycerol and fatty acids

Lactic acid

Ketonebodies

Keto acids


Catabolic-Anabolic Steady State of the Body

• Blood concentrations of energy sources equalized between absorptive state and postabsorptive state– Absorptive state during and 3-5 hours after

each meal; absorption of nutrients occurring– Postabsorptive state late morning, late

afternoon, all night; GI tract empty; energy sources supplied by breakdown of reserves


Absorptive State

• Anabolism exceeds catabolism

• Nutrients stored

• Carbohydrates– Glucose major cellular energy fuel – Glucose converted in liver to glycogen or fat

• Synthesized fat + protein released to blood for storage by adipose tissue as very low density lipoproteins (VLDLs)


Absorptive State

• Triglycerides– Lipoprotein lipase catalyzes lipids of

chylomicrons in muscle and fat tissues– Most glycerol and fatty acids converted to

triglycerides for storage– Triglycerides used by adipose tissue, liver,

and skeletal and cardiac muscle as primary energy source


Absorptive State

• Amino acids– Excess amino acids deaminated and used for

ATP synthesis or stored as fat in liver– Most amino acids used in protein synthesis


Figure 24.18a Major events and principal metabolic pathways of the absorptive state.

Major metabolic thrust:anabolism and energy storage

Amino acids

Proteins Glycogen

GlucoseGlycerol andfatty acids

Triglycerides

Major energy fuel:glucose (dietary)

Glucose

Liver metabolism:amino acids deaminated and

used for energy or stored as fat

Amino acids

Keto acids

Triglycerides

Major events of the absorptive state


Figure 24.18b Major events and principal metabolic pathways of the absorptive state.

Triglycerides

Glycogen

Protein

In liver:

Protein

Glucose

Amino acids

Glycogen

Fattyacids

Triglycerides

Gastrointestinaltract

Glucose

Keto acidsGlyceraldehyde

3-phosphate

Glycerol

Fattyacids

Glucose

Fattyacids

Glucose

In all tissues:

TriglyceridesIn adiposetissue:

Glycerol

In muscle:

Principal pathways of the absorptive state


Absorptive State: Hormonal Control

• Absorptive state primarily controlled by insulin

• Insulin secretion stimulated by– Elevated blood levels of glucose and amino

acids– Intestinal GIP and parasympathetic

stimulation


Insulin Effects on Metabolism

• Insulin, a hypoglycemic hormone, enhances– Facilitated diffusion of glucose into muscle and

adipose cells (brain and liver take up glucose without insulin)

– Glucose oxidation for energy– Glycogen and triglyceride formation– Active transport of amino acids into tissue cells– Protein synthesis– Inhibits glucose release from liver, and

gluconeogenesis


Homeostatic Imbalance

• Diabetes mellitus– Inadequate insulin production or abnormal

insulin receptors – Glucose unavailable to most body cells – Blood glucose levels high– Glucose lost in urine– Fats and proteins used for energy

metabolic acidosis, protein wasting, weight loss


Postabsorptive State

• Catabolism of fat, glycogen, and proteins exceeds anabolism– Net synthesis of fat, glycogen, proteins ends

• Goal - maintain blood glucose between meals– Makes glucose available to blood– Promotes use of fats for energy (glucose

sparing – save glucose for organs that need it most)


Sources of Blood Glucose

• Glycogenolysis in liver

• Glycogenolysis in skeletal muscle

• Lipolysis in adipose tissues and liver– Glycerol used for gluconeogenesis in liver

• Catabolism of cellular protein– Major source during prolonged fasting

• Amount of fat in body determines how long can survive without food


Figure 24.20a Major events and principal metabolic pathways of the postabsorptive state.

Proteins Glycogen Triglycerides

Amino acids Glucose

Glycerol and fatty acids

Glucose Fatty acidsand ketones

Amino acids

Keto acids

Glucose

Major metabolic thrust:catabolism and replacement of fuels in blood

Major energy fuels:glucose provided by glycogenolysis and

gluconeogenesis; fatty acids, and ketones

Liver metabolism:amino acids converted to glucose

Major events of the postabsorptive state


Figure 24.20b Major events and principal metabolic pathways of the postabsorptive state.

In muscle: Pyruvic andlactic acids

Protein

Amino acids

In liver:

Amino acids

Keto acids

Pyruvic andlactic acids

Storedglycogen

Glucose

In adipose tissue:

Triglycerides

Triglycerides

GlycerolFatty acids

Ketoacids

Blood glucose

In nervoustissue:

In most tissues:

Fattyacids +glycerol

Ketonebodies

Principal pathways of the postabsorptive state

4

2

42

4 2 3

1

3

3

Glycogen

(b)


Postabsorptive State: Hormonal and Neural Controls

• Glucagon - hyperglycemic hormone– Release stimulated by

• Declining blood glucose• Rising amino acid levels


Effects of Glucagon

• Glucagon promotes– Glycogenolysis and gluconeogenesis in the

liver– Lipolysis in adipose tissue fatty acids and

glycerol to blood


Postabsorptive State: Hormonal and Neural Controls

• Adipose tissue innervated by sympathetic nervous system– Quickly supplies glucose if blood levels low– Low plasma glucose, fight-or-flight response,

or exercise fat mobilization and glycogenolysis

• Initiated by sympathetic nervous system and epinephrine from adrenal medulla


Metabolic Role of the Liver

• Hepatocytes– ~500 metabolic functions– Process nearly every class of nutrient– Play major role in regulating plasma

cholesterol levels– Store vitamins and minerals– Metabolize alcohol, drugs, hormones, and

bilirubin


Cholesterol

• Structural basis of bile salts, steroid hormones, and vitamin D

• Major component of plasma membranes• 15% of blood cholesterol ingested; rest

made in body, primarily liver• Lost from body when catabolized or

secreted in bile salts• Part of hedgehog signaling molecule that

directs embryonic development


Cholesterol Transport

• Lipoproteins – Transport water-insoluble cholesterol and

triglycerides in blood– Regulate lipid entry/exit at target cells– Contain triglycerides, phospholipids,

cholesterol, and protein• Higher percentage of lipids lower density, hence

VLDLs, LDLs, HDLs


Lipoproteins

• Types of transport lipoproteins– HDLs (high-density lipoproteins)

• Highest protein content

– LDLs (low-density lipoproteins)• Cholesterol-rich

– VLDLs (very low-density lipoproteins)• Mostly triglycerides

– Chylomicrons• Lowest density


Figure 24.22 Approximate composition of lipoproteins that transport lipids in body fluids.

From intestine

80–95%

3–6%2–7%

1–2%Chylomicron

55–65%

Made by liver

10%

20%

45%

25%

LDL

Returned toliver

5%

30%

20%

45–50%

HDL

15–20%

10–15%

5–10%

Triglyceride

Phospholipid

Cholesterol

Proteinl

VLDL


Lipoproteins

• VLDLs– Transport triglycerides from liver to peripheral tissues

(mostly adipose)

• LDLs– Transport cholesterol to peripheral tissues for

membranes, storage, or hormone synthesis

• HDLs– Transport excess cholesterol from peripheral tissues

to liver to be broken down and secreted into bile– Also provide cholesterol to steroid-producing organs


Recommended Total Cholesterol, HDL, and LDL Levels

• Total cholesterol = 200 mg/dl or less– Levels > 200 mg/dl linked to atherosclerosis

• Form in which cholesterol transported in blood important to measure

• High HDL thought to protect against heart disease; >60 good; <40 not good

• High LDL cholesterol deposits in vessels; 100 or less good; 130 or above not good


Plasma Cholesterol Levels

• The liver produces cholesterol– At a basal level regardless of dietary

cholesterol intake– In response to saturated fatty acids



• Ratio of saturated/unsaturated fatty acids affects blood cholesterol levels

• Saturated fatty acids– Stimulate liver synthesis of cholesterol– Inhibit cholesterol excretion from body

• Unsaturated fatty acids– Enhance excretion of cholesterol– Enhance cholesterol catabolism to bile salts



• Trans fats– Healthy oils forced to be solids

• E.g., margarine

– Worse effect on cholesterol levels than saturated fats

– Increase LDLs and reduce HDLs



• Unsaturated omega-3 fatty acids (found in cold-water fish)– Lower proportions of saturated fats and

cholesterol– Make platelets less sticky help prevent

spontaneous clotting– Antiarrhythmic effects on heart– Lower blood pressure


Non-Dietary Factors Affecting Cholesterol

• Stress and cigarette smoking lower HDL levels

• Aerobic exercise and estrogen increase HDL levels and decrease LDL levels



• Statins– Cholesterol-lowering drugs– Estimated >10 million Americans take statins


Energy Balance

• Bond energy released from food must equal total energy output

• Energy intake = energy liberated during food oxidation

• Energy output– Immediately lost as heat (~60%)– Used to do work (driven by ATP)– Stored as fat or glycogen


Energy Balance

• Nearly all energy from food eventually converted to heat - cannot be used to do work

• Heat energy– Warms tissues and blood– Helps maintain homeostatic body temperature– Allows metabolic reactions to occur efficiently

• If energy intake = energy output – weight stable

• If not equal – gain or loss of weight


Obesity

• Body mass index (BMI) = W / H2

(W in kg, H in m)

• Considered overweight if BMI 25 to 30

• Considered obese if BMI greater than 30– Higher incidence of atherosclerosis, type 2

diabetes mellitus, hypertension, heart disease, and osteoarthritis

• More adults and children overweight than 20 years ago


Regulation of Food Intake

• Various nuclei of hypothalamus– Release peptides influence feeding behavior

• neuropeptide Y (NPY) enhances appetite • pro-opiomelanocortin (POMC) and

cocaine-/amphetamine-regulated transcript (CART) suppress appetite


Regulation of Food Intake

• Feeding behavior and hunger regulated by– Neural signals from digestive tract– Bloodborne signals related to body energy stores– Hormones– To lesser extent, body temperature and psychological

factors

• Operate through brain thermoreceptors, chemoreceptors, and others


Short-Term Regulation of Food Intake

• Neural signals from GI tract– High protein content of meal increases and

prolongs afferent vagal signals– Distension sends signals along vagus nerve

that suppress hunger center



• Nutrient signals related to energy stores– Increased nutrient levels in blood depress

eating• Rising blood glucose• Elevated blood amino acid levels • Blood levels of fatty acids



• Hormones– Gut hormones (e.g., insulin and CCK) depress

hunger– Glucagon and epinephrine stimulate hunger– Ghrelin (Ghr) from stomach stimulates

appetite; levels peak prior to mealtime


Long-Term Regulation of Food Intake

• Leptin– Hormone secreted by fat cells in response to

increased body fat mass– Indicator of total energy stores in fat tissue– Protects against weight loss in times of

nutritional deprivation


Long-Term Regulation of Food Intake

• Leptin– Acts on certain neurons in hypothalamus– Suppresses secretion of NPY which is a

potent appetite stimulant– Stimulates expression of appetite

suppressants (e.g., CART peptides)


Leptin

• Rising leptin some weight loss; not "magic bullet" for obese patients

• High leptin levels in obese patients; resistant to its action


Additional Factors in Regulation of Food Intake

• Temperature – cold activates hunger

• Stress – depends on individual

• Psychological factors

• Sleep deprivation

• Composition of gut bacteria


Metabolic Rate and Heat Production

• Metabolic rate– Total heat produced by chemical reactions

and mechanical work of body– Can be measured

• Directly – calorimeter measures heat liberated into water chamber

• Indirectly – respirometer measures oxygen consumption (directly proportional to heat production)


Basal Metabolic Rate

• Reflects energy body needs to perform its most essential activities

• Measured in postabsorptive state (npo 12 hours), reclining position, relaxed mentally and physically, room temperature 20-25C

• Recorded as kilocalories per square meter of body surface per hour (kcal/m2/h)– E.g., 70 kg adult BMR = 66 kcal/h

• Influenced by body surface area, age, gender, body temperature, stress, thyroxine


Factors that Influence BMR

• BMR increases as ratio of body surface area to volume increases

• Decreases with age

• Males have disproportionately higher BMR

• Increases with temperature or stress

• Thyroxine increases oxygen consumption, cellular respiration, and BMR

• Physical training has little effect on BMR


Metabolic Rate

• Total metabolic rate (TMR)– Rate of kilocalorie consumption to fuel all

ongoing activities– Increases with skeletal muscle activity and

food ingestion (food-induced thermogenesis)

• Greatest with protein and alcohol ingestion


Regulation of Body Temperature

• Body temperature reflects balance between heat production and heat loss

• At rest, liver, heart, brain, kidneys, endocrine organs generate most heat

• During exercise, heat production from skeletal muscles increases dramatically


Regulation of Body Temperature

• Normal body temperature = 37C 5C (98.6F)– Optimal enzyme activity at this temperature

• Increased temperature denatures proteins and depresses neurons– Children <5 convulsions at 41C(106F)– ~43C (109F) - limit for life

• Tissues tolerate low body temperatures


Core and Shell Temperature

• Core (organs within skull, thoracic & abdominal cavities) has highest temperature– Rectal temperature best clinical indicator

• Core temperature regulated; fairly constant– Blood - major agent of heat exchange

between core and shell

• Shell (skin) – lowest temperature– Fluctuates between 20C – 40C


Mechanisms of Heat Exchange

• Four mechanisms of heat transfer– Radiation - loss of heat by infrared rays– Conduction - transfer of heat by direct

contact– Convection - transfer of heat to surrounding

air– Evaporation - heat loss due to evaporation of

water from body surfaces• Heat absorbed by water during evaporation – heat

of vaporization


Mechanisms of Heat Exchange

• Insensible heat loss accompanies insensible water loss from lungs, oral mucosa, and skin– Loss ~ 10% of basal heat production

• Sensible heat loss – when body temperature rises and sweating increases water vaporization


Role of the Hypothalamus

• Hypothalamus receives afferent input from– Peripheral thermoreceptors in shell (skin) – Central thermoreceptors (some in

hypothalamus) in core

• Initiates appropriate heat-loss and heat-promoting activities


Heat-Promoting Mechanisms

• Constriction of cutaneous blood vessels– Sympathetic nervous system stimulates

• Shivering – heat from skeletal muscle activity

• Increased metabolic rate via epinephrine and norepinephrine– Chemical (nonshivering) thermogenesis -

infants– Brown adipose tissue in adults

• Enhanced thyroxine release - infants


Heat-Promoting Mechanisms

• Behavioral modifications (voluntary) measures include– Putting on more clothing– Drinking hot fluids– Changing posture (clasping arms across

chest)– Increasing physical activity (jumping up and

down)


Heat-Loss Mechanisms

• Heat-promoting center inhibited

• Dilation of cutaneous blood vessels

• Enhanced sweating

• Voluntary measures include– Reducing activity and seeking a cooler

environment– Wearing light-colored, loose-fitting clothing



• Hyperthermia– Elevated body temperature depresses

hypothalamus– Positive-feedback mechanism (heat stroke)

begins at core temperature of 41C increased temperatures

• Skin hot and dry; organs damaged

– Can be fatal if not corrected



• Heat exhaustion– Heat-associated collapse after vigorous

exercise– Due to dehydration and low blood pressure– Heat-loss mechanisms still functional– May progress to heat stroke if not cooled and

rehydrated promptly



• Hypothermia– Low body temperature from cold exposure

• Vital signs decrease

– Shivering stops at core temperature of 30 - 32C

– Can progress to coma and death by cardiac arrest at ~ 21C


Fever

• Controlled hyperthermia

• Due to infection (also cancer, allergies, or CNS injuries)

• Macrophages release cytokines (also called pyrogens)– Cause release of prostaglandins from

hypothalamus


Fever

• Prostaglandins reset hypothalamic thermostat higher heat-producing mechanisms – temperature

rises

• Natural body defenses or antibiotics reverse disease process– Cryogens (e.g., vasopressin) reset thermostat

to lower (normal) level heat-loss mechanisms temperature falls

Chapter 24B Nutrition, Metabolism, Body Temperature Slides by Barbara Heard and W. Rose. figures...

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