SBM-BloodGlucose2001

8/8/2019 SBM-BloodGlucose2001

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1

Relationship of Nutrition toBlood Glucose Control

Arline McDonald, Ph.D.December 4, 2001


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2

Blood Glucose Responses to Diet

Short-term=Postprandial

response

Long-term=AdaptiveResponse to Diet/Exercise


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3

Blood Glucose Abnormalities

Abnormality Diet-Induced Underlying Associations

Hyperinsulinemia

Normoglycemia Yes Rapidly absorbed sugars

Hyperglycemia Yes Obesity, hypertension,hyperlipemia

Hypoglycemia

Fasting Yes Absence of food > 8 hrsPostprandial Yes Rapidly absorbed sugars,

alcohol

Idiopathicreactive

No High insulin sensitivity +reduced glucagon


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4

Conditions Requiring DietaryManagement for Blood Glucose Control

Diabetes mellitusType IType II

Hypertension Hyperlipidemia Liver disease Renal disease Cancer Obesity

Trauma

Sepsis Treatment with:HydrochlorothiazideChlorpropamidePropranololPrednisoneSulfonylureas


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5

Diabetes Prevention Program3-year Incidence of Type II Diabetes

0

5

10

15

20

2530

35

Placebo Metformin Diet + Exercise

New Engl J Med 2001; 344:1343


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6

Relationship of Source of Energyto Incidence of Type I Diabetes 1

-0.8

-0.6

-0.4

-0.2

0

0.2

0.40.6

0.8

TotalPlantCerealsAnimalDairyMeat

1 40 countries ecologic data

AJCN 2000;71:1525-9.

*

***

***

****

**

*p


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The Postprandial Plasma GlucoseResponse (Glucose Tolerance)

60

80

100

120

140

160

180

200

0 15 30 45 90 120 150 180

Plasma Glucosemg/dL

MinutesIngestio

n

Area Under Curve


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Plasma Glucose Response toDifferent Carbohydrate Sources

6080

100

120140160180

200220

0 15 30 45 90 120 150 180

Minutes

Standard

Simple Sugar Soluble Fiber + Sugar

Starch


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Fate of Dietary Carbohydrate

Glucose90 g

Glycogen20 g

Adipose Tissue

Triglyceride

2 g

CO 2

15-20 g

MuscleGlycogen25 g

ATP20 g20-45 g


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Proposed Etiology of Diet-InducedInsulin Resistance

GlucoseInsulin

Available glucosefrom soluble, rapidlydigested CHO with

high energy density

Rapid absorption& rise in glucose

to high peakconcentrationsInsulin secretion in

concentration torestore blood

glucose to fasting

levels

Downregulationof tissue insulin

receptors

High insulin peakRepeated highinsulin peaks


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Receptor Modification inInsulin Resistance Receptor number

Receptor activity

Post-receptor defect Enzyme activation Glucose transporters

Downregulation dietary glycemic index dietary fat body fat

Composition of dietary fat

Stress Response counterregulatoryhormones


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Metabolic Consequences of Insulin Resistance

Stimulation of SNS activity

Altered smooth muscle cellCa ++ transport

Increased renal sodiumreabsorption/retention

Mitogenic stimulation of vascular smooth musclecells

Increased plasminogenactivator inhibitor-type 1activity

Blood pressure

Fibrinolysis

Vascular tone

Plasma Volume

Atherogenesis


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Metabolic Consequences of Hyperglycemia

Microvascular Disease

Retinopathy

Nephropathy

Infection

NeuropathyMacrovascular Disease

Thickening of capillarybasement membrane

Retinal ischemia/vascularchanges & RBC aggregation

Glomerular injury fromprotein denaturation

Glycosylated Hgb/ O2 Microbial growth

?? Relationship toblood glucose


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Glycemic Index

Describes the incremental increase in bloodglucose from fasting levels over a definedtime interval following ingestion of CHO(AUC) relative to a standardProperty of food sources of digestible CHO

Function of efficiency of digestion andrate of absorption


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Glycemic Indexes of Foods

FoodAUC mg/L at

3 hours

100

866 100 811 94 652 75 954 110 () 424 49

583 67 () 638 74 263 30 263 30 258 30


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Primary Determinants

of Glycemic Index

Amount of Carbohydrate

Portion size Energy density

Availability of Carbohydrate Solubility Digestibility Extent of processing Type of processing


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Simple Sugars

highly solubleliquid formlow fiber contenthigh energy content

high Na + content

Starches

highly digestible amylopectin > amylose amylose > resistant starch refined starch > simple

sugars with fiber

High Glycemic Index Carbohydrates


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Effects of Soluble (Viscous) Dietary

Fiber on Blood Glucose Control

Direct Effects decreases rate of digestion

impedes access to digestive enzymes decreases rate of absorption

slows rate of diffusion across unstirred layer

Indirect Effects decreases absorption of dietary fat

inds bile acids regulates appetite

Ileal brake-second-meal effect


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Simple Sugar (SS) with andwithout Soluble Fiber (SDF )

60

80

100

120

140

160180

200

220

0 15 30 45 90 120 150 180

Minutes

StandardSS

SS & SDF


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Starch With and WithoutSoluble Dietary Fiber (SDF )

60

80

100

120

140

160

180

200

0 15 30 45 90 120 150 180

Minutes

StandardStarchStarch & SDF


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Noncarbohydrate Influences

On Glycemic Index

Dietary fat

Slows gastric emptying (short-term) Decreases insulin clearance (long-term)

Dietary sodium Facilitates glucose transport via

Na+-linked transporter Physical Activity Increases insulin sensitivity

improved skeletal muscle glucose transport kinetics


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Effects of Dietary Fat on

Blood Glucose Control

Total Amount

Determines gastricemptyingInhibits insulinclearance by

increased FFA inportal circulationContributes to bodyfat stores

Fatty Acid Composition

Saturated fatmembrane fluidity &receptor functionnumber of glucosetransporters

Monounsaturated fat promotes insulin secretion -6: 3 PUFA ratio membrane fluidity


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23

Relationship of Fasting Insulin to

Dietary Polyunsaturated Fat-C20-22

12 14 16 18 20 2224 26

25

20

15

10

5

r=-0.68; p< 0.001

C20-22 PUFA (% Total Fatty Acids)

F a s t

i n g

I n s u

l i n

( U / m L )

New Engl J Med 1993;328:238


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24

Relationship of Fasting Insulin to Ratioof C20:4 (arachidonic) to C20:3 (eicosapentanoic)

4 6 8 1012

25

20

15

10

5

r=-0.55; p= 0.003

Ratio of C20:4 to C20:3

F a s t

i n g

I n s u

l i n

( U / m L )

New Engl J Med 1993;328:2


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25

Glucose Response

to Monounsaturated Fatty Acids

0

2

4

6

810

12

Fasting Postprandial

StarchMUFA

Diabetes Care 1993; 14:1115.

CHO/Fat= 60:20 for starch and 40:40 for MUFA


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26

Insulin Response to

Monounsaturated Fatty Acids

0

2

4

6

810

12

Fasting Postprandial

StarchMUFA

CHO/Fat= 60:20 for starch and 40:40 for MUFA

Diabetes Care 1993; 14:1115.


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27

Effects of Energy Intake on


Relates to amount of carbohydrate and fat

Provides excess or deficiency of micronutrientsthat influence effectiveness of insulin Zinc, potassium, magnesium, chromium, vitamin E

Contributes to body fat If not balanced with expenditure Preferentially deposited in abdomen (age, gender)


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Relationship of Intake* to Storage

Capacity for Dietary CHO and Fat

100

1.67 0.570

20

40

60

80

100

120

CHO

Protein Fat

*Based on Intake of 40% CHO, 40% Fat, and 20% Protein

Bray, 1993


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29

Obesity and Insulin Resistance

Abdominal vs Glutealhigh portal free fatty acidconcentration inhibitshepatic insulin clearancehigher insulin levelrequired to facilitateglucose uptake

Pear-shape:Gluteal/Femoral

Fat DepositsGynoid Pattern

Apple-shape:Abdominal

Fat DepositsAndroidPattern


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Effects of Physical Activity

on Blood Glucose Control

prevents weight gain

increases muscle mass/fat mass ratioPromotes mobilization of free fatty acidsfrom abdominal adipocytesreduces km of skeletal muscle glucosetransportersenhances glycogenesis for up to 48 hourspost-activity


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Effects of Distribution of Energy

Intake on Blood Glucose Control

Variable Low GlycemicIndex

High GlycemicIndex

+ - + -Frequency of Eating

5-6 0 5-6 1-2

Energy Density/

Portion Size

High/Low

Small

High/

Large

Low/

Small

High/

Large

Timing Prior to orafter

activity

Noissues

Afteractivity

Beforeactivity


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32

Effects of Dietary Protein

on Blood Glucose Control

Minimal effect on postprandial blood glucoseresponse

AlanineGlycine Glucose Glucose


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Effects of Micronutrients on


Insulin Response

Chromium Zinc Vitamin E

CarbohydrateMetabolism Potassium Magnesium


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Summary of Dietary Effects on

Postprandial Glucose Response

Fat

Chemicalproperties

ViscousFiber

Physical form

Sources Available Carbohydrate

Interval to restoration of fasting glucose levels

Rate of glucose absorption

Rate of insulin release

Digestibility

SolubilityGastric Emptying Time

SodiumInsulin

resistance Obesity

Activity


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Summary

Short-term insulin response is dependent on

amount and digestibility of CHO, food matrix,and other components of the mealInsulin resistance can develop as anadaptive response to chronic intake of highglycemic loadsDietary modifications can facilitate insulineffectiveness


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Predicting the Postprandial

Plasma Glucose Response

60

80

100

120

140

160

180

200

0 15 30 45 90 120 150 180

Plasma Glucosem

g/dL

Minutes from Ingestion


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What has been ingested?

60

65

70

75

80

85

90

0 15 30 45 90 120 150 180

Plasma Glucosem

g/dL


High protein drink


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What has been ingested?

406080

100120140160180

200220

0 15 30 45 90 120 150 180

Plasma Glucosem

g/dL


High energy=refined sugar + starch


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Predicting the Postprandial

Plasma Glucose Response

60

70

80

90

100

110

120

130

0 15 30 45 90 120 150 180

Plasma Glucosem

g/dL


High Soluble Fiber + Starch

Documents

SBM-BloodGlucose2001