Nutrition 2 - edited

8/7/2019 Nutrition 2 - edited

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BIOCHEMISTRY: NUTRITION 2

DIABESITY

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Newly coined term for the relationship of DiabetesMellitus and Obesity.

DIABETES MELLITUS

Type 1 – formerly insulin-dependent DM (5-10%)

Type 2 – formerly non-insulin-dependent DM (90%)

Gestational – because of human placentallactogen that is present during the 6 th month of pregnancy. (So, this type is only present in

pregnant mothers)

Other types are those which cannot be classifiedunder the 3 types above:

o

Ex: Patients who survived the acutehemorrhagic pancreatitis (affects endocrineand exocrine pancreas)

Doc Uy said that she wanted to focus on the defect, frequency of ketosis,and the plasma insulin level.

Type 1 DM Type 2 DMAge of onset Usually during

childhood orpuberty symptoms

develop rapidly

Frequently after age35; symptomsdevelop gradually

Nutritional status attime disease onset

Frequentlyundernourished

Obesity usuallypresent

Prevalence 900,000 = 10% of diagnosed diabetics

10 million = 90% of diagnosed diabetics

Geneticpredisposition

Moderate Very strong

Defect ordeficiency

Beta-cells aredestroyed

,inability to produceinsulin, thereforerendering theperson insulin –dependent tosurvive

Insulin resistancecombined withinability of Beta-cells to produceappropriatequantities of insulin

Frequency ofketosis

Common(because of lowinsulin andincrease glucagon(decreased insulin:glucagon ratio) cannot take upglucose

Rare

Plasma insulin Low to absent -High early indisease(because of insulinresistance;muscles andadipose cells arenot responding);-Low in disease of long duration

Acute complications Ketoacidosis Hyperosmolar stateTreatment with oralhypoglycemic drugs

Unresponsive responsive

Treatment Insulin is alwaysnecessary

Diet, exercise, oralhypoglymic drugs;insulin may or may

not be necessary

Metabolic changes in TYPE 1 Diabetes (absent insulin):•

The metabolic abnormalities of DM result from adeficiency of INSULIN which profoundly affectsmetab in three tissues: liver, muscle, adiposetissue (Pancreas is not affected, although its beta-cell are the ones that secrete the insulin.)

•

Hyperglycemia and ketoacidosis

•

Hypertriacylglycerolemia - increase lipogenesisbecause of hyperglycemia (excess glucose isconverted to triacylgycerides)

•

Individual effects ( Refer to Figure 2 at back page ):

•

Intestines: increased glucose absorption(result to hyperglycemia)

•

Liver: increased hepatic glucose outputand increased gluconeogenesis (result tohyperglycemia)

•

Adipose & muscle: decreased glucoseuptake (by GluT-4 – insulin-dpt transporter

SUBJECT: BIOCHEMISTRY

TOPIC: NUTRITION 2

LECTURER: DR. UY

DATE: FEBRUARY, 2011

TYPE 1 DM:

It starts with a viralinfection. During thistime, there is still a100 % production of insulin (Honeymoonphase ). With thedecrease of normal

functioning B-cells, theamount of insulin alsodecreases. When B-cellsare destroyed (only about20% remaining), clinicalmanifestation of Type 1diabetes appears. One of the acute complicationsis Diabetic Ketoacidosis(DKA). Because there isno insulin available toabsorb the glucosepresent in the blood, fattyacids are oxidized by theliver leading to the

production of ketonebodies. These acidicketone bodies arenormally buffered in theblood but with thecontinuous release by theliver, the alkali reservesare depleted. Patientswith DKA (diabeticketoacidosis) needinsulin supplementationin order to survive.




that takes up glucose from thebloodstream)

•

Accumulation of VLDL thenhypertriacylglycerolemia, ketonebodies are formed because lipidsare the preferred fuel used.

•

In adipocytes, no glycerol kinase,that’s why glycerol is stilltransported to the liver to

produce pyruvate then glucose.Glycerol is used as a substrate forgluconeogenesis in the liver.

TYPE 2 DM:

Increase in insulin levels is for the control of blood glucose.(A) In the picture below, there is a repetitive increase anddecrease in insulin secretion due to the food intakethroughout the day. However, in obese individuals, there isa much higher increase in insulin after meals because of insulin resistance (the peripheral tissues cannot recognizethe insulin secretion in order to take up the glucose, that’swhy the beta-cells keep on secreting high insulin). (B) Theglucose level of both the insulin-resistant obese individualis kept in the same levels as that of the normal individualbecause of the action of the elevated insulin level.

(Refer to FIGURE 1 at the back of tranx)

Obese individuals develop insulin resistance which mayprecede with the development of diabetes in the later years.Obese patients have high blood glucose levels because of the amount of high carbohydrate diet that they have.Initially, there’s a normal blood glucose-insulin response bythe body. So when there is an increase in glucose levels,the pancreatic beta-cells in response would secrete insulin.

But with the initial insulin secreted, the GluT4 transportersin the muscles are not reacting; there is insulin-resistance !So, the normal response by the pancreas is to furtherincrease the level of insulin secreted. We have now whatwe call, “insulin resistance with compensatoryhyperinsulinemia”. Still, no response from the muscles willresult to a continuous increase in the blood glucose levels.The insulin secretion will decrease eventually due to theexhausted beta-cells, so there would be a decrease ininsulin secretion secondary to the dysfunctional beta-cells.

Hyperinsulinemia is not reversible that’s why insulinsupplementation is needed. The only thing that we can dois that we can delay the death of beta-cells. Beta-cells willget exhausted and then proceed with their apotosis.

To prevent confusion, Type 1 DM is caused by an externalfactor like a viral infection that destroys the functional beta-cells, therefore lowering insulin secretion and in effect,increasing glucose levels in the blood (HYPERGLYCEMIA).Type 2 DM , on the other hand, is caused primarily by theinsulin-resistance by the non-responsive GluT4 transportersin the muscle and adipose cells which leads to furtherincrease by the pancreatic beta-cells of insulin. Eventually,the beta-cells will tire and will also be non-responsive to theincrease in glucose levels (Parang napagod siya kasi dipinansin yung insulin na sinecrete nya kaya in turn, di na

din nya papansinin yung high blood glucose level at ititigilna nya pagrerelease ng insulin kasi hindi din naman siyapinapansin! ). These two reasons will lead tohyperglycemia in Type 2 DM.

Major factorscontributing tohyperglycemia observedin Type 2 DM:

1. Insulin resistance inperipheral tissues(muscles & adipose)

Increase productionof glucose by liverthroughgluconeogenesisand glycogenolysis.

Exercise isrecommended todecrease insulinresistance byincreasing thenumber of GluT-4recruited towardsthe membrane,therefore increasing the sensitivity of muscles.

2. Inadequate insulinsecretion from thepancreatic beta-cells.




Initially, Oral Anti-Diabetic (OADs) medicines can counterthe effects of low insulin but later on, there will be the needfor exogenous insulin especially when there is zero insulinsecretion already.

Beta cell dysfunction can be prevented if insulin resistanceis managed in the periphery by exercise and diet.

*Microvascular complications (retinopathy, nephropathy,neuropathy)

*Macrovascular complications (cardiovascular disease & stroke)

(Pls. refer to FIGURE 3 at the back of the tranx)Abnormal metabolism in Diabetes Mellitus (Type 1 and 2):

1.

Breakdown of tissue proteins

2.

Glycogenolysis

3.

Decrease in glucose uptake by tissues

4.

Increase in lipolysis

1-3: leads to hyperglycemia

Lipolysis in adipose cells leads to ketoacidosis. There is anincrease in free fatty acids in plasma which are brought tothe liver and their oxidation leads to an increase in hepaticoutput of ketone bodies.

OBESITY

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A disorder of body weight regulatory systemscharacterized by an accumulation of excess fat.

-

Prevalence has increased with age.

-

With increasing prevalence, the risk of developing diabetes, hypertension, and cardiovasculardisease has also increased.

-

Alarming because of the occurrence in children childhood obesity

Food intake = Energy Expenditure

**Hypothyroid – decrease metabolic rate – fatness

**Hyperthyroid – increased metabolic rate - thinness

Obesity is influenced by lifestyle (type of food eaten anddegree of physical activity)

Energy saved in calories is converted as fats. If you have noexercise, energy is saved and you’ll gain weight.

Genetics allow obesity, while the environment facilitatesobesity.

The Role of Satiey Signals in the Control of Food Intake:

Brain’s reaction to food:

by Normal Weight People

Hunger message to GIT (20 minutes) satietymessage to brain “stop eating” to GIT

By Obese People:

Overweight and Obese patients experience a delay inthe SATIETY message being transmitted and can takealmost twice as long to FEEL FULL. Therefore, patients

are unable to control their food intake.

Hypothalamus controls emotion and appetite. Afferentsignals that will influence the appetite and energyexpenditure are:

Serotonin & Dopamine: CNS Norepinephrine: PNS

CCK: Intestine Leptin: Adipose tissue




Insulin: Pancreas Ghrelin: Stomach

Appetite is controlled by the action of different tissuescombined. That’s why drugs made for appetite suppressiontarget different organs.

Leptin is a very good cytokine. Adipocytes secrete leptinwhich influence the hypothalamus in maintaining foodintake and energy expenditure at set point. During starvation, adipose tissues decrease leptin release and inturn increase food intake and decrease energy expenditure(evident in hibernating animals).

Obese individuals experience a delay in satiety becauseleptin secretion is reduced twice as low.

Apple-Shaped Pear-shapedUpper body obesity Lower body obesityVisceral Fat Subcutaneous FatHigh Free Fatty Acids(More oxidized fattyacids)

Low FFA

When a person isobese, the adipocytes willrecruit more adipocytesand itwill increase in size. Whenthis happens, it becomesmore difficult to lose.

Upper body obesity:

Insulin resistance leads to increased free fatty acids(easily oxidized) in plasma. This in turn causes,

Muscles: gain insulin resistance

Vasculature: increase constriction, decreaserelaxation, decrease in ENOS (endothelial NitricOxide Synthase)

Liver: increase glucose release

Pancreas: increase insulin secretion

Adiposopathy: Pathogenesis of Obesity-Related MetabolicDisease

Adipose tissues will keep on recruiting more adipose andeventually will be subjected to local hypoxia then cell death. Atthis point, the adipocytes will secrete inflammatory adipokines.

Adipose tissues are not simply for storage. It also functions

as an endocrine organ which secretes adipokines andcytokines .

TNF-α – Tumor Necrotic Factor-alpha

VEGF – Vascular Endothelial Growth Factor(recruits macrophages)

NFKB – stimulated in inflammatory pathway

Janus Kinase (JNK) – works with NFKB ininflammation and also helps in insulin resistance

Adiponection – more abundantly found in smalladipocytes and less in large adipocytes. So, largeadipose cells are more subjected to inflammation.




Adiponectin (cytokine found in small adipocytes)

Only known adipocyte secreting factor thatincreases tissue sensitivity to insulin.

Berg AH 2001 Nat Med 7:947-953.

Markedly decreased in Type 2DM and obesity.

Bajaj M 2002 JCEM 89:200-206 .

Potent anti-inflammatory agent that inhibits anumber of steps involved in the development of atherosclerosis.

Yang WS2002 Diab Care 25:376-380.

ASSESMENT OF OBESITY

Estimating the Desirable Body Weight (DBW)

INFANTS: 1 st 6 mos:

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DBW(gms)= Birth wt(gms)+(age in mos x 600)

7 – 12 mos:

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DBW(gms)= birth wt(gms)+(age in mosx500)

-

DBW (kg) = (age in mos) + 3

2

CHILDREN:

-

DBW (kg)= (no. of yrs x 2) + 8

ADULTS:

1. Body Mass Index-Based Formula

2. Derived Formula based on Body Mass Index

3. Tannhauser’s Method

4. “Adopted” Method

BODY MASS INDEX•

Calculated as weight /(height) 2 , in kg/m 2

•

Evaluates weight relative to height

•

Replaced percentage ideal body weight as criterionfor assessing obesity

•

Correlates significantly with body fat, morbidity,and mortality

Classification NIH A/PIOTF

It is from such information similar to ACS graph and lifeinsurance tables that criteria for defining overweight andobesity have been established by the NIH and WHO aslisted in this table. For Caucasians, BMI above 25 isconsidered overweight, and above 30 is considered obeseclass 1. For BMI above 35, then it is classified as obese

class 2 which portends much higher risk of morbidity andmortality esp diabetes.

However, similar plotting of morbidity and mortality risksagainst BMI in Asian populations such as HongKong, Korea,Singapore, Taiwan, and Malaysia all show that the oddsratio of developing illnesses goes up even at BMIs of 22 to23, and is doubled by the time BMI reaches 25 to 26.Hence the recommendation from the Asia PacificInternational Obesity Task Force is to modify the criteria fordefining obesity to reflect these observations. Lowercutoffs are used for Asians: overweight is defined as BMIabove 23, and obese class 1 as BMI above 25.

International basis WHO: NIH – Nat’l Institute for Health

In the Philippines A/PIOTF: Asia Pacific InternationalObesity Task Force

BMI Chart (There is no need to memorize this (Yeepee!), butknow how to derive BMI using this chart.




1.

Body Mass Index-based formula

In the absence of BMI chart:•

For men 5 feet(1.52m) tall = 112 lbs (51kg)•

For women 5 ft(1.52m) tall = 106 lbs(48kg)

•

For both sexes, add 4 lbs (1.8 kg) for every inchabove 5 feet.

Sample: Male,5’3” tall= 112+ (3x4)= 124 lbs(56kg)

2.

Derived Formula based on BMI:•

DBW (kg) = Desirable BMI x H (m) 2

•

Desirable BMI for men = 22

•

Desirable BMI for women = 21

Sample : Male 5’3” tall

DBW(kg) = 22 x 1.6m 2 = 22 x 2.56m

= 56.32 or 56

3.

Tannhauser’s Method •

Measure height in centimeters.

•

Deduct from this the factor 100 and the answer isthe DBW in kg.

•

The DBW obtained applies to Filipino stature bytaking off 10%.

•

Example: Height: 5’2” = 62”

62 x 2.54cm = 157.48cm -100= 57.48kg 57.48kg – 5.74(10% of 57.48) = 51.74 or

52 kg

4. “Adopted” method •

For 5 ft use 105 lbs.

•

For every inch above 5 ft, add 5 lbs

Example: Heigh t: 5’2”

5 feet = 105 lbs

2 inches = 5x2= + 10

115 lbs or 52 kg

Estimating the Total Energy Requirment (TER) per day•

ADULTS: Basal metabolic needs

(1cal/KDBW/hr x 24hrs) + Physical activity (%above basal)

NDAP Formula:

Activity level Male Female

In bed(mobile) 35 30

Light 40 35

Moderate 45 40

Heavy 50 -

PREGNANT WOMEN:o

TER/day = Normal requirement + 300Cals

LACTATING WOMEN:

o

TER/day = Normal requirement + 500 Cals

Filipino Food Pyramid

Fats, Oils & Sweetsuse sparingly

Milk, Yoghurt &

Cheese grp

2-3 servings

Meat, Poultry, fish, DryBeans, Eggs & Nuts grp

2-3 servings Vegetable grp

3-5 servings

Fruit grp

2-4 servings

Bread, Cereal, Rice & Pasta grp6-11 servings

A good diet is based on the right kind of food eaten onadequate amounts necessary to maintain our daily energyrequirements. An emphasis on the Filipino food pyramid guide on goodeating habits prepared by the Philippine Association for the

Study of Overweight and Obesity (PASOO). Less fats and proteins, more on complex carbohydrates,vegetables and fruits - The basis for this concept is thatcomplex carbohydrates and vegetables are more filling andeasily burn out compare to fats and proteins. A gram of carbo is equivalent to 4 calories compared to a gram of fatwhich contain 9 calories.

Carbohydrates:

American Diabetes Association (ADA)recommendations:

Monitoring carbohydrate, whether by carbohydratecounting, exchanges, or experienced-basedestimation, remains a key strategy in achieving glycemic control.




A dietary pattern that includes carbohydrate fromfruits, vegetables, whole grains, legumes, and low-fat milk is encouraged for good health.

The use of glycemic index and load may provide amodest additional benefit over that observed whentotal carbohydrate is considered alone.

Fiber:

ADA recommendation

Diabetes patients are encouraged to choose avariety of fiber-rich cereals, fruits, vegetables, andwhole-grain products

There are data suggesting that consuming a high-fiber diet (≈50 g fiber/day) reduces glycemia,hyperinsulinemia and lipidemia

Low GI foods that are rich in fiber and otherimportant nutrients are to be encouraged

Goals:

o

ADA/USDA (US Department of Agriculture)

As for general pop’n

Around 20-35 g/day (14g/1000kcal)

o

EASD (European Association for the Studyof Diabetes)

Ideally more than 40g/day (or 20g/1000 kcal)

About half should be soluble

Cereal-based foods should bewhole grain and high in fiber

Dietary fat and cholesterol:

ADA recommendation

To reduce risk for CVD

o

Limit saturated fat to 7% of total calories

o

Limit dietary cholesterol to <200 mg/day

o

Intake of trans fat should be minimized

In metabolic studies in which energy intake andweight are held constant, diets low in saturatedfatty acids and high in either carbohydrate or cis-

monounsaturated fatty acids lowered plasma LDLcholesterol equivalently. (Remember that cis- is thegood MUFA, because trans-MUFA acts like asaturated fatty acid which increases LDL.)

EASD recommendation

Saturated and trans-fatty acids <10% total dailyenergy; <8% if LDL is elevated

Oils rich in MUFA may provide 10%-20% totalenergy

PUFA should not exceed 10% total daily energy

Total fat intake should not exceed 35% total

energy

Protein:

ADA recommendations

For individuals with diabetes and normal renalfunction, there is insufficient evidence to suggestthat usual protein intake (15%-20% of energy)should be modified

RDA is 0.8 g good quality protein/kg body weight

Good-quality protein sources are defined as having high PDCAAS (Protein Digestibility – Corrected

Amino Acid Scoring pattern) scores

Examples: meat, poultry, fish, eggs, milk, cheese,and soy

Activity required to burn 250 kcal:

30 min jog

70 min walk

50 min biking

Nutrient Recommended IntakeCalories Approximately 500 to 1000

reduction from usual intakeTotal fat 30% or less of total caloriesSaturated Fatty acids 8-10% of total caloriesMonosaturated fatty acids Up to 15% of total caloriesPolyunsaturated fatty acids Up to 10% of total caloriesCholesterol <300 mg/dayProtein Approximately 15% of total

caloriesFiber 20-30 g/dayVitamins, minerals & traceelements

From natural sourcesaccording to recommendednational daily intake

Emphasis on a balanced low calorie diet ( 1000-1200calories for obese women and 1200-1600 calories for obesemen ) is elucidated in this slide. The components of a balancedlow calorie diet is shown here. The 500-1000 calories reductionwill reduce your weight to 0.5- 1 kg per week as recommendedby Naaso and Nhlbi.

Based on the computation of your daily energy requirementi.e. computing on your daily allowable calorie need based onyour activity. You can use here the manipulation of the BMIcomputation:

Ideal body weight in kg = ideal BMI range ( 20-21) x height in

meter 2 Then the ideal body weight is multiplied on the type of

energy expenditure (sedentary 26-28 calories, active- 30, moreactive 32. ) and the product will give you the total daily caloricrequirement where you will subtract your 500-1000 calories.

Example: a 1.6 m man with a sedentary lifestyle his totaldaily caloric requirement to maintain a normal BMI of 21 is1505 calories base on 21 x 1.6 m x 1.6 m x 28.

This is based on 55 percent carbohydrates more complexcarbohydrates and the rest of calories around 45 percentdivided to fats and proteins. emphasis also on polyunsaturatedfats (pufa) and monounsaturated fat( mufa) like the olive andsafflower oil; more fiber and vitamins.




FIGURE 3:

Nutrition 2 - edited

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