Week 3: Carbohydrates Flashcards
(115 cards)
1
Q
What is a carbohydrate?
A
Organic molecules containing carbon, hydrogen, oxygen
2
Q
What is a monosaccharide?
A
One sugar molecule
3
Q
Monosaccharides
A
Glucose
Fructose
Galactose
4
Q
What is a dissacharide?
A
Two sugar molecules
5
Q
Disaccharides
A
Sucrose
Lactose
Maltose
6
Q
Oligosaccharide
A
2-10 sugar molecules
7
Q
Oligosaccharides
A
Raffinose
Stachyose
8
Q
What is a polysaccharide?
A
10 or more sugar molecules
9
Q
Metabolic fate of carbs
A
- Primary energy source for body
- Stored as glycogen in liver and muscle
- Converted to triglycerides in adipose tissue
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
11
Q
What is lactose broken down in to?
A
Glucose and galactose by lactase
12
Q
What is maltose broken down in to?
A
2 glucose molecules by maltase
13
Q
What is sucrose broken down in to?
A
Glucose and fructose by sucrase
14
Q
Carbohydrate absorption
A
- Broken down into simplest form (monosaccharides)
- Active transport of glucose by SGLT1 permits entry into enterocyte of small intestine
- Leave enterocyte by GLUT 2 to enter blood stream
15
Q
Glycogenolysis
A
Formation of glucose from glycogen (when glucose is depleted such as during fasting or exercising)
**liver
16
Q
Glycogenesis
A
Formation of glycogen from glucose (occurs after a meal)
17
Q
Where is glycogen stored?
A
Liver (100-200g)
Skeletal muscle (350-750g)
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
19
Q
Factors to consider when choosing a carb source?
A
- Nutrient density
- Glycemic index
- Fructose content
- Fibre content
20
Q
Nutrient density
A
Nutrients per reference amount of food, typically 100 kcal/100g serving
21
Q
Example of nutrient density
A
Liver has very high nutrient density
22
Q
Glycemic response
A
Change in blood glucose after eating a carbohydrate containing food
23
Q
What is persistently high levels of blood glucose linked with?
A
Obesity and chronic disease
24
Q
Glycemic index (GI)
A
Scale that ranks carbohydrate containing foods/drinks by how much it raises blood glucose
25
High GI
Quickly digested and absorbed, rapid rise in blood glucose and insulin
26
Low GI
Slow rise in blood glucose and insulin, slowly digested and absorbed
27
What is a limitation to the glycemic index?
Doesn't consider amount of food you're consuming
28
Glycemic load
Considers the amount of carbohydrate ingested
GL=GI/100 grams of carbs
29
What are low GI diets associated with?
Decreased risk of developing type 2 diabetes and CVD
30
What are high GI diets associated with?
Increased risk of developing type 2 diabetes and CVD
31
How does reactive hypoglycemia occur?
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
32
What does reactive hypoglycemia trigger and promote?
Promotes hunger and excessive food intake, beta cell dysfunction, dyslipidemia and endothelial dysfunction
33
Why is there discrepancy in research regarding GI?
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
34
Glycemic index studies conclusions
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
35
Glycemic index and baseline characteristics
A low GI diet does improve insulin sensitivity in those with high insulin to begin with (obesity)
36
Limitations of glycemic index
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
37
Inter-variability
Variability within a single group or entity
38
Intra-variability
Variability or fluctuations within a single individual across diff measurements
39
Foods with lower GI
Protein, fibre, lipids
40
Degree of processing and GI
Increased processing leads to a higher GI
41
Cooking and GI
Increased cooking time leads to higher GI
42
Storage of foods and GI
If you cook a food, store it in fridge, then microwave it, it increases GI
43
Consumption order and GI
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
44
CVD risk factors of fructose metabolism
Gut dysbiosis
De nova lipogenesis
Abdominal adiposity inflammation
Insulin suppression
45
Can individuals absorb fructose?
60% of individuals cannot completely absorb fructose when consumed in large amounts
46
What is different about fructose metabolism?
No negative feedback loop on fructolysis enzymes so the process keeps on happening
47
Where does fructose metabolism occur?
Liver
48
Process of fructose metabolism
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
What results from fructose metabolism?
Increased intracellular phosphate depletion (fatigue)
Uric acid
50
What results from excess fructose intake?
Lipogenesis of fat in the liver
Can lead to to non-alcoholic fatty liver disease
51
What can increased levels of uric acid lead to?
1. Increased blood pressure
2. T2D
3. Obesity
52
What are some common metabolic outcomes in animal models?
Visceral fat
Triglycerides
Insulin resistance
Uric acid
Non-alcoholic fatty liver disease
53
Animal study limitations
1. Unbalanced calorie intake btwn groups (is weight gain causing observed metabolic health issues?)
2. Fructose intake is unrealistically elevated
54
Average percentage of fructose in beverages
10-30%
55
Typical % of administered fructose in animal studies
60-70%
56
Fructose survival hypothesis
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
Fructose survival hypothesis - survival switch
Prepares our body for times of food insecurity such as in the winter
58
Why is the survival switch triggered?
Fructose was previously most accessible in the fall, thereby preparing the body for the scarcity of food in the winter
59
What does activation of the survival pathway lead to?
Increased foraging
Reduced REE
Insulin resistance
Systemic inflammation
Increased fat storage
60
What does persistent activation of the survival switch lead to?
Obesity and noncommunicable diseases
61
Fructose survival hypothesis -present day
Doesn't hold true as fructose is regularly available
62
Present day fructose health outcomes
Stroke, heart failure
Behavioural issues
Obesity, fatty liver
Diabetes
Heart disease
63
What would studies that align with the fructose hypothesis show?
Differences btwn glucose and fructose regarding these adaptations
64
Fructose and lipogenesis
Significant increase in FFA synthesis when consuming fructose diet bc of increased lipogenesis from fructose metabolism
65
Fructose and metabolic health
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
Fructose and hepatic insulin resistance
Both isocaloric and hypercaloric fructose diets lead to hepatic insulin resistance
67
Fructose and NAFLD
Risk of NAFLD increased with fructose in hypercaloric diet but not isocaloric group
68
Limitations of long-term study research
1. Small sample size
2. Narrow demographic
3. Short duration
4. Poor study quality
69
Limitations of human research
Duration of study is often less than a few weeks
Fructose intake is unrealistically elevated as a % of energy intake
70
Dietary fibre
Non-digestible carbs and lignin that are naturally found in plants
71
Dietary fibres
Cellulose
Pectins
Fructans
Resistant starches
Hemicellulose
Lignin
Gums
B-glucans
72
Functional fibre
Isolated, extracted, manufactured non-digestible carbs that have positive physiological effects on humans
73
Functional fibres
Fructans
Pectins
Psylium
Gums
B-glucans
74
Total fibre
Dietary fibre present within the food plus functional fibre that has been added to the food
75
Resistant starch
Starch that cannot be or are not easily enzymatically digested
76
Types of resistant starch
RS1
RS2
RS3
RS4
77
RS1 (dietary)
Physically inaccessible to digestion due to its location
78
RS2 (dietary)
Resists digestion bc it it tightly packed inside of granules within food
79
RS3 (functional)
Formed w moist-heat cooking and cooling of starches that has gelatinized
80
RS4 (functional)
Results from chemical modification of starches
81
Fibre requirements
25 g female
38 g males
82
Properties of fibres
1. Solubility in water
2. Viscosity and gel formation
3. Fermentibility
83
Solubility in fibres
Water-insoluble fibres
Water-soluble fibres
84
Water-insoluble fibres
Dont dissolve in water
Decrease intestinal time and increase fecal weight to positively impact laxation
85
Types of water-insoluble fibre foods
Whole grains, bran, legumes, veggies
86
Water-soluble fibers
Dissolves in hot water
Delay gastric emptying, increases intestinal time and decrease nutrient absorption to positively impact blood glucose and lipid concentration
87
Types of water soluble fibres
Oats, barley, rye, chia, flaxseeds, fruits
88
Do we still use solubility of fibers?
No, theres inconsistencies
89
Viscosity and gel formation
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
Viscous gel forming fibres
Pectin, B-glucans, mucilages, gum
91
Positive effects of gel forming fibers
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
Fermentability
How quickly and efficiently gut microbiomes can degrade fiber through fermentation
93
Positive effects of fermentation
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
Health benefits of fibre
1. Diabetes
2. Cardiovascular disease
3. Appetite or satiety and weight control
4. Gastrointestinal disorders
95
Where does glycogenesis occur?
Liver and muscle
**requires energy
96
What is liver glycogen important for?
Maintaining glucose homeostasis
97
Why can't glycogenolysis contribute to control of blood glucose levels?
Muscle doesn't have the enzyme that converts phosphorylated glucose back to free glucose
98
What does skeletal muscle glucose do once in cell?
Doesn't exit cell once present
99
Where does gluconeogenesis occur?
Liver
100
What happens when total energy intake is used as a confounder?
When total energy intake is used as a confounder, the association btwn glycemic index and insulin sensitivity is removed
101
Conclusion of study on energy intake and glycemic index
No association btwn GI and fasting insulin and insulin sensitivity
102
Glycemic index and weight management studies
Low GI diets are generally no better than high GI diets for reducing body weight or fat
103
Type 2 diabetes and fibre intake
Dose-response relationship
More fibre=greater reduction in risk of T2D
104
Fibre and glycemic index
Increased fibre= low GI
Decreased fibre= high GI
105
Effect of GI and fibre intake on RR for diabetes
High GI and low fibre diets doubled risk of diabetes
106
Baseline characteristics and low GI diet
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
What happens when you combine a high GI food with a low GI food?
Low GI
108
Animal studies: paired feeding trials
Sucrose resulted in increased uric acid, triglycerides and insulin in the blood
**didnt differentiate btwn glucose and fructose
109
Animal studies: increased energy intake
Fructose can accelerate metabolic syndrome, fatty liver and T2D in male breeder rats, independent of excess energy intake
110
Animal studies : increased energy intake and leptin
In the fructose group, leptin didn't suppress hunger like it was supposed to
111
Fructose and health outcomes: hypercaloric vs isocaloric diets
Still see negative health outcomes regardless of weight gain
112
Soft drink consumption and energy intake- Longitudinal and cross-sectional studies
Positive association btwn soft drink consumption and overall energy intake
113
Soft drink consumption and energy intake- Long term experimental studies
Individuals did not compensate for the extra energy consumed
114
Soft drink consumption and energy intake- Short term experimental studies
Mixed results
115
Prebiotics
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
