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HLTH331 > Week 3: Carbohydrates > Flashcards

Week 3: Carbohydrates Flashcards

1
Q

What is a carbohydrate?

A

Organic molecules containing carbon, hydrogen, oxygen

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2
Q

What is a monosaccharide?

A

One sugar molecule

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3
Q

Monosaccharides

A

Glucose
Fructose
Galactose

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4
Q

What is a dissacharide?

A

Two sugar molecules

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5
Q

Disaccharides

A

Sucrose
Lactose
Maltose

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6
Q

Oligosaccharide

A

2-10 sugar molecules

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7
Q

Oligosaccharides

A

Raffinose
Stachyose

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8
Q

What is a polysaccharide?

A

10 or more sugar molecules

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9
Q

Metabolic fate of carbs

A
  1. Primary energy source for body
  2. Stored as glycogen in liver and muscle
  3. Converted to triglycerides in adipose tissue
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10
Q

Carbohydrate digestion

A

Digestion by salivary and pancreatic amylase
Digestion in small intestine where disaccharides are broken down into absorbable monosaccharides by their enzymes

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11
Q

What is lactose broken down in to?

A

Glucose and galactose by lactase

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12
Q

What is maltose broken down in to?

A

2 glucose molecules by maltase

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13
Q

What is sucrose broken down in to?

A

Glucose and fructose by sucrase

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14
Q

Carbohydrate absorption

A
  1. Broken down into simplest form (monosaccharides)
  2. Active transport of glucose by SGLT1 permits entry into enterocyte of small intestine
  3. Leave enterocyte by GLUT 2 to enter blood stream
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15
Q

Glycogenolysis

A

Formation of glucose from glycogen (when glucose is depleted such as during fasting or exercising)
**liver

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16
Q

Glycogenesis

A

Formation of glycogen from glucose (occurs after a meal)

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17
Q

Where is glycogen stored?

A

Liver (100-200g)
Skeletal muscle (350-750g)

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18
Q

Gluconeogenesis

A

Formation of glucose from non-carbohydrate sources such as glycerol, lactate, pyruvate, amino acids; provides glucose when dietary intake is insufficient

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19
Q

Factors to consider when choosing a carb source?

A
  1. Nutrient density
  2. Glycemic index
  3. Fructose content
  4. Fibre content
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20
Q

Nutrient density

A

Nutrients per reference amount of food, typically 100 kcal/100g serving

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21
Q

Example of nutrient density

A

Liver has very high nutrient density

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22
Q

Glycemic response

A

Change in blood glucose after eating a carbohydrate containing food

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23
Q

What is persistently high levels of blood glucose linked with?

A

Obesity and chronic disease

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24
Q

Glycemic index (GI)

A

Scale that ranks carbohydrate containing foods/drinks by how much it raises blood glucose

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25
Q

High GI

A

Quickly digested and absorbed, rapid rise in blood glucose and insulin

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26
Q

Low GI

A

Slow rise in blood glucose and insulin, slowly digested and absorbed

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27
Q

What is a limitation to the glycemic index?

A

Doesn’t consider amount of food you’re consuming

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28
Q

Glycemic load

A

Considers the amount of carbohydrate ingested
GL=GI/100 grams of carbs

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29
Q

What are low GI diets associated with?

A

Decreased risk of developing type 2 diabetes and CVD

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30
Q

What are high GI diets associated with?

A

Increased risk of developing type 2 diabetes and CVD

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31
Q

How does reactive hypoglycemia occur?

A

High GI meals produce an initial period of high blood glucose and a spike in insulin, leading to reactive hypoglycemia in which blood glucose levels drop below baseline causing a glucose crash

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32
Q

What does reactive hypoglycemia trigger and promote?

A

Promotes hunger and excessive food intake, beta cell dysfunction, dyslipidemia and endothelial dysfunction

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33
Q

Why is there discrepancy in research regarding GI?

A
  1. Changes in total carbohydrate and fibre intake (maybe low GI diets contain more fibre?)
  2. Weight loss (can impact insulin sensitivity)
  3. Presence of and use of treatment for diabetes
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34
Q

Glycemic index studies conclusions

A
  1. When calorie intake is controlled, low GI and high GI diets report similar outcomes
  2. Large variability btwn study findings for weight loss
  3. Fibre content is a large contributor
  4. Baseline characteristics matter
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35
Q

Glycemic index and baseline characteristics

A

A low GI diet does improve insulin sensitivity in those with high insulin to begin with (obesity)

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36
Q

Limitations of glycemic index

A
  1. Intra and inter variability
  2. Lifestyle factors
  3. Growing conditions and meal preparation alter GI
  4. GI is assessed on an empty stomach and without any other foods
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37
Q

Inter-variability

A

Variability within a single group or entity

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38
Q

Intra-variability

A

Variability or fluctuations within a single individual across diff measurements

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39
Q

Foods with lower GI

A

Protein, fibre, lipids

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40
Q

Degree of processing and GI

A

Increased processing leads to a higher GI

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41
Q

Cooking and GI

A

Increased cooking time leads to higher GI

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42
Q

Storage of foods and GI

A

If you cook a food, store it in fridge, then microwave it, it increases GI

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43
Q

Consumption order and GI

A

The order that you consume foods can impact your GI
ex. eating veggies and protein before carbs leads to a lower glycemic response than eating carbs first

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44
Q

CVD risk factors of fructose metabolism

A

Gut dysbiosis
De nova lipogenesis
Abdominal adiposity inflammation
Insulin suppression

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45
Q

Can individuals absorb fructose?

A

60% of individuals cannot completely absorb fructose when consumed in large amounts

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46
Q

What is different about fructose metabolism?

A

No negative feedback loop on fructolysis enzymes so the process keeps on happening

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47
Q

Where does fructose metabolism occur?

A

Liver

48
Q

Process of fructose metabolism

A
  1. Fructose is converted to fructose-1 phosphate by fructokinase
  2. Then its converted to triose-phosphates
  3. Converted to pyruvate which can enter Krebbs cycle
49
Q

What results from fructose metabolism?

A

Increased intracellular phosphate depletion (fatigue)
Uric acid

50
Q

What results from excess fructose intake?

A

Lipogenesis of fat in the liver
Can lead to to non-alcoholic fatty liver disease

51
Q

What can increased levels of uric acid lead to?

A
  1. Increased blood pressure
  2. T2D
  3. Obesity
52
Q

What are some common metabolic outcomes in animal models?

A

Visceral fat
Triglycerides
Insulin resistance
Uric acid
Non-alcoholic fatty liver disease

53
Q

Animal study limitations

A
  1. Unbalanced calorie intake btwn groups (is weight gain causing observed metabolic health issues?)
  2. Fructose intake is unrealistically elevated
54
Q

Average percentage of fructose in beverages

A

10-30%

55
Q

Typical % of administered fructose in animal studies

A

60-70%

56
Q

Fructose survival hypothesis

A
  1. Fructose is broken down by fruktokinase
  2. ATP converted to ADP, fructose metabolism depletes ATP reserves
  3. ADP is used to create uric acid which leads to mitochondrial damage and signals activation of the SURVIVAL SWITCH
57
Q

Fructose survival hypothesis - survival switch

A

Prepares our body for times of food insecurity such as in the winter

58
Q

Why is the survival switch triggered?

A

Fructose was previously most accessible in the fall, thereby preparing the body for the scarcity of food in the winter

59
Q

What does activation of the survival pathway lead to?

A

Increased foraging
Reduced REE
Insulin resistance
Systemic inflammation
Increased fat storage

60
Q

What does persistent activation of the survival switch lead to?

A

Obesity and noncommunicable diseases

61
Q

Fructose survival hypothesis -present day

A

Doesn’t hold true as fructose is regularly available

62
Q

Present day fructose health outcomes

A

Stroke, heart failure
Behavioural issues
Obesity, fatty liver
Diabetes
Heart disease

63
Q

What would studies that align with the fructose hypothesis show?

A

Differences btwn glucose and fructose regarding these adaptations

64
Q

Fructose and lipogenesis

A

Significant increase in FFA synthesis when consuming fructose diet bc of increased lipogenesis from fructose metabolism

65
Q

Fructose and metabolic health

A
  1. Fructose diet leads to increase in VAT
  2. Fasting ApoB increases in the fructose group
  3. Measures of insulin sensitivity decreased in fructose group
66
Q

Fructose and hepatic insulin resistance

A

Both isocaloric and hypercaloric fructose diets lead to hepatic insulin resistance

67
Q

Fructose and NAFLD

A

Risk of NAFLD increased with fructose in hypercaloric diet but not isocaloric group

68
Q

Limitations of long-term study research

A
  1. Small sample size
  2. Narrow demographic
  3. Short duration
  4. Poor study quality
69
Q

Limitations of human research

A

Duration of study is often less than a few weeks
Fructose intake is unrealistically elevated as a % of energy intake

70
Q

Dietary fibre

A

Non-digestible carbs and lignin that are naturally found in plants

71
Q

Dietary fibres

A

Cellulose
Pectins
Fructans
Resistant starches
Hemicellulose
Lignin
Gums
B-glucans

72
Q

Functional fibre

A

Isolated, extracted, manufactured non-digestible carbs that have positive physiological effects on humans

73
Q

Functional fibres

A

Fructans
Pectins
Psylium
Gums
B-glucans

74
Q

Total fibre

A

Dietary fibre present within the food plus functional fibre that has been added to the food

75
Q

Resistant starch

A

Starch that cannot be or are not easily enzymatically digested

76
Q

Types of resistant starch

A

RS1
RS2
RS3
RS4

77
Q

RS1 (dietary)

A

Physically inaccessible to digestion due to its location

78
Q

RS2 (dietary)

A

Resists digestion bc it it tightly packed inside of granules within food

79
Q

RS3 (functional)

A

Formed w moist-heat cooking and cooling of starches that has gelatinized

80
Q

RS4 (functional)

A

Results from chemical modification of starches

81
Q

Fibre requirements

A

25 g female
38 g males

82
Q

Properties of fibres

A
  1. Solubility in water
  2. Viscosity and gel formation
  3. Fermentibility
83
Q

Solubility in fibres

A

Water-insoluble fibres
Water-soluble fibres

84
Q

Water-insoluble fibres

A

Dont dissolve in water
Decrease intestinal time and increase fecal weight to positively impact laxation

85
Q

Types of water-insoluble fibre foods

A

Whole grains, bran, legumes, veggies

86
Q

Water-soluble fibers

A

Dissolves in hot water
Delay gastric emptying, increases intestinal time and decrease nutrient absorption to positively impact blood glucose and lipid concentration

87
Q

Types of water soluble fibres

A

Oats, barley, rye, chia, flaxseeds, fruits

88
Q

Do we still use solubility of fibers?

A

No, theres inconsistencies

89
Q

Viscosity and gel formation

A

Ability of fiber to both bind or hold water and form a gel
**most fibres can hold water but not all form a gel

90
Q

Viscous gel forming fibres

A

Pectin, B-glucans, mucilages, gum

91
Q

Positive effects of gel forming fibers

A
  1. Gastric distention, delayed gastric emptying, longer intestinal tract transit time
  2. Reduced nutrient digestion (glucose and lipids)
  3. Reduced micelle formation (gel traps bile)
  4. Decreased movement of nutrients within intestinal lumen
  5. Decreased nutrient effusion rates
92
Q

Fermentability

A

How quickly and efficiently gut microbiomes can degrade fiber through fermentation

93
Q

Positive effects of fermentation

A

Growth of bacterial pop. and short-chain fatty acid formation
Increases fecal bacteria mass which attracts water to enhance stool size
Promotes laxation and treats constipation

94
Q

Health benefits of fibre

A
  1. Diabetes
  2. Cardiovascular disease
  3. Appetite or satiety and weight control
  4. Gastrointestinal disorders
95
Q

Where does glycogenesis occur?

A

Liver and muscle
**requires energy

96
Q

What is liver glycogen important for?

A

Maintaining glucose homeostasis

97
Q

Why can’t glycogenolysis contribute to control of blood glucose levels?

A

Muscle doesn’t have the enzyme that converts phosphorylated glucose back to free glucose

98
Q

What does skeletal muscle glucose do once in cell?

A

Doesn’t exit cell once present

99
Q

Where does gluconeogenesis occur?

A

Liver

100
Q

What happens when total energy intake is used as a confounder?

A

When total energy intake is used as a confounder, the association btwn glycemic index and insulin sensitivity is removed

101
Q

Conclusion of study on energy intake and glycemic index

A

No association btwn GI and fasting insulin and insulin sensitivity

102
Q

Glycemic index and weight management studies

A

Low GI diets are generally no better than high GI diets for reducing body weight or fat

103
Q

Type 2 diabetes and fibre intake

A

Dose-response relationship
More fibre=greater reduction in risk of T2D

104
Q

Fibre and glycemic index

A

Increased fibre= low GI
Decreased fibre= high GI

105
Q

Effect of GI and fibre intake on RR for diabetes

A

High GI and low fibre diets doubled risk of diabetes

106
Q

Baseline characteristics and low GI diet

A

A low GI diet will improve insulin sensitivity in obese/overweight individuals who have high insulin to begin with
No effect on normal weight individuals

107
Q

What happens when you combine a high GI food with a low GI food?

A

Low GI

108
Q

Animal studies: paired feeding trials

A

Sucrose resulted in increased uric acid, triglycerides and insulin in the blood
**didnt differentiate btwn glucose and fructose

109
Q

Animal studies: increased energy intake

A

Fructose can accelerate metabolic syndrome, fatty liver and T2D in male breeder rats, independent of excess energy intake

110
Q

Animal studies : increased energy intake and leptin

A

In the fructose group, leptin didn’t suppress hunger like it was supposed to

111
Q

Fructose and health outcomes: hypercaloric vs isocaloric diets

A

Still see negative health outcomes regardless of weight gain

112
Q

Soft drink consumption and energy intake- Longitudinal and cross-sectional studies

A

Positive association btwn soft drink consumption and overall energy intake

113
Q

Soft drink consumption and energy intake- Long term experimental studies

A

Individuals did not compensate for the extra energy consumed

114
Q

Soft drink consumption and energy intake- Short term experimental studies

A

Mixed results

115
Q

Prebiotics

A

Substances that are not digested by the host but provides heath benefits by acting as a substrate for the growth and activity of healthy bacteria in the colon

HLTH331 (9 decks)

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