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FNN200
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Carb classifications
simple sugars
monosaccharides (Glucose, fructose, galactose, allulose, ribose)
Disaccharides (sucrose, lactose, maltose)
Oligosaccharides (3-10 monosaccharide units)
starchyose raffiones
Polysaccharides (10+ monosaccharide units)
starch and glycogen (amylose, amylopectin)
Fiber and resistant starch (cellulose, pectin, hemicellulose)
Glycosaminoglycans (chondroiti sulphate, hylauronic acid
Carbohydrates
hydrates of carbon
MONOSACCHARIDES ALL C6H1206
Isomers
identical molecular formulas but with different structures
Epimers
different configuration around only one C
D-glucose and D-galactose
Enantiomers
mirror images of eachother
Lglucose and D-glucose
Glycosidic bonds
can be alpha or beta depending on bond orientation
the body is unable to break down b-glycosidic bonds
EG. Maltose is 2 glucose units connected by a a1-4 bond
Most prevelant disaccharides
sucrose
maltose
lactose
Total sugars
natural sugars - naturally occuring in fruits
the other things in the food controls how the body digests them
Free sugars
added suggars are added to food in processing and preparation
sugars in honey, syrups, juices and juice concentrate also are free sugars
CFG and sugar
does nto have a specific number
just says that most sugars should come from naturally occuring sources
say to limit free sugars to less than 10% of daily calories
Front of package nutrition labels
containing amount of total sugars meeting or ex ceeding 15% of the daily value/serving
Complex carbohydrates (oligosaccharides)
Common in dried beans, peas, lentils, whole grains
cannot be digested
they are foods for gut microbiota
human digestive enzymes cant digest their glycosidic bonds - become prebiotics
Glucose polysaccharides
linear a1-4 = amylose which is a linear chain
branched a1-4 + a1-6 = amylopectin
several different connnections makign it more complex and therefore easier to break down
Glycogen is also branched a1-4 and a1-6 bonds
easily hydrolyzed for a quick release of glucose
allows it to be broken from many points
Branching of polysaccharides -
increases the surface area allowign a larger number of glucose molecules to be cleaved
Glycosidases
specific for a-glycosidic bonds
B1-4 bonds cannot be hydrolyzed by mammalian digestive enzymes
cellulose - not an energy source becomes it contains the beta bonds
Dietary fiber
things like cellulose which cannot be broken by our digestive enzymes because they contain B-bonds
eg. cellulose
Digestion and absorption of carbs
Mouth
starches → breakdown by salivary alpha amylase → makes alpha dextrins
Stomach
does not do digestion
Small intestine
Dextrins → pancreatic a-amylase breaks down → Maltose, dextrins and maltotriose
BBM Microvilli
maltose → broken down by a-glicosidase (maltase) → glucose
Limit dextrios → a-limitdextrikinase → glucose
Allergy vs intollerance
allergy = immune response to proteins in milk
attack proteins
Intolerance
digestive system cannot break down lactase sugar
Lactose intolerance
lactase contains a B1-4 linkage
this is the only one that humans are usually able to break down
Families of glucose transporters
Sodium glucose co-transporters (SGLT)
energy dependent - active transport
function coupled with sodium co-transport and ATP hydrolysis
SGLT1 → intestine
SGLT2 → Kidney
Glucose transporters (GLUT)
Facilitated diffusion
transport can be bidirectional → GLUT2
14 isoforms distributed througout the body
Monosaccharide absorption impacted by
concentration
affinidty and capacity of transporter
tissue localization
mode of transport
Small intestine absorption of glucose and galactose
SGLT1
uses sodium cotransport to bring from intestine to enerocyte
GLUT2
facillitated diffusion to the hepatic portal vein
sucrose transport
sucrose broken down into 1 fructose molecule and one glucose by sucrase
GLUT5 transports into enterocyte
GLUT2 transports into hepatic vein
GLUT2 at brush boarder membrane
when intestinal lumen glucose is really high
the GLUT2 will transport over to the brush boarder membrane
transient expression
the rate of transport is dependent on blood glucose contentration because it is facilitated diffusion
insulin causes GLUT2 to leave membrane and return to the intracellular storage vesicle
Renal reabsorption of glucose
kidney
SGLT2 enables body to retain glucose and prevents its loss through urine
has GLUT2 on the other side to brign into the blood
Enzyme kinetics
Km value (michaelis constant)
Km = the concentration of substrate when the reactin is at ½ it max velocity
Km
concentration of substrate when the reaction is at ½ its max velocity
Low Km = high affinity for substrate
High Km = low affinity for substrat3e
takes longer to reach the fullness
Affinity of GLUTS
GLUT1 = low Km cause we want it to be fast in
blood brain barrier, fetal placenta
GLUT2 = high kM low affinity
regulation of glucose concentrations
SGLT1
glucose and galactose
small intestine
uses active transport
SGLT2
glucose
kidney
active transporter
GLUT1
glucose
BBB, placenta, fetal tissue
low Km
GLUT2
glucose
liver, small intestine, basolateral side
can be translocated
Highest Km so that it can regulate blood glucose better
want to have more substrate to keep glucose in line
GLUT3
glucose
Brain, placenta, testes
low KM
brain needs to be cative
GLUT4
glucose
muscle and adipose tisue
moderate Km
Glut 5
Fructose transporter
small intestine
Low Km
GLUT4 Translocation
insulin sensitive transporter
Process - on muscle and adipose
insulin receptor binds insulin
activates a cascate which will translocate GLUT4 to teh outside fo the cell to bring in glucose from outside the cell
Muscle contraction also stimulates the translocation of GLUT4 independent fo insulin through a different signalling pathway
Monosaccharides post digestion
Glucose → oxidized for energy or put into storage as glycogen
30-40% will go to the liver and the remaiing will go to blood
Galactose → glycogen storage
Fructose → oxidized for energy and excess may be converted to triglycerides
Glycemic response
there is a spike after consuming glucose in plasma glucose
Glycemic index is the area under the curge in test food/reference food x 100
glycemic load = GI x g of digestible carb in a serving /100
Regular blood glucose levels
Fasted = 4.5-5.5 mmol/L
Fed = 7.8 mmol/L
Low GI and GL
GI = <55
GL = <10
Medium GI nd GL
GI = 56-69
GL = 11-19
High GI and GL
GI = >70
GL = >20
Low GI foods
Bran ceral
apple juice
apples
banannas
Low GL foods
all bran ceral
apples
beets
peanuts
Foods that have high GI but low GL
watermelon
while it has a high GI the actual amount in a serving is low and therefore it is not actually goign to have such a high spike
Food with low GI but a high GL
Macaroni
there is a GI of 47 which is considered low, but the GL is 23 which is high
Criticisms of GI and GL for food labeling
the reality depends on what else you eat
what activities you d
how much of the foods you eat etc
High gi would be a quick energt boost
Carbs and hormonal regulation
anabolic → insulin
triggers: blood glucose, hormones, incretins
Catabolic → glucagon
epinephrine/norepinephrine
triggers: hypoglycaemia
Monosaccharide darivitives
amino sugars, acetyl amino sugars, glyconic acids
almost all carb in cells is a derivitive
D and L monosaccharides
the position of the hydroxyl group on the asymmetric carbon is used to designate D andL isomers
OH on right is D on the Left is L
Allulose
found in some fruits but is rare
less sweet than sucrose but is still able ot be processed less making it less sweet
derivative of D fructose and is not efficiently metabolize for energy makign it low calorie
Sucrose
fructose and glucose
cane sugar, beet sugar, table sugar
Lactose
glucose and galactose
milk, aids in calcium absorption and supports beneficial bacteria growth
Maltose
two glucose units
found only briefly in a plant usually in the seets
an intermediate product of the digestion of complex starches in the guy and part of partial hydrolysis of starch in some foods like beers
Sweetness relative to sucrose
Fructose corn syrip is higher
also frucsose higher
All other sugars are less sweet
Sugar alcohols are all much sweeter than sugar
used in sugarless gums, dietetic candies, sugarless candies etc
High intensity sweetners
hundreds of times stronger than sucrose
Carb consumption
often a critical issue for those trying to loose weight or control blood sugar levels
most carb comes from cerial grains and refined sugar because of the increased production of sucrose
Cereal grains
large source of starch because of the endosperm
most of hte starch is attributed to amylose and amylopectin
AMDR for Carbs
45-65% of total energy consumption which allows people to plan their dietary carb levels on their lifestyle
encouraged to consume more whole grain and whole food products
DRI for carb is 130g/day for all individuals to prevent ketosis
Ketosis
state which ketone body production exceeds metabolism resulting in the accumulation of ketones in the blood and tissues
Dietart fiber AI
38g for men and 25 for women
goes down with age
Why does no digestioin occur in the stomach
because tha amylase can operate at 6.6-6.8pH so the low pH in the stomach causes the amylase to not function properly
starch breakdown
occurs in the brush boarder
uses an enzyme a-dextrinase or isomaltase
starch as a branched mixture of dextrines contianing a1-6 linkages
breaks down into a-dextrins, maltose and maltrioses
the remainder occurs in the intestinal surface
Enterocytes on the small intestine contain
maltase, lactase and sucrase to break down sucrose, maltose and a-dextrins
Fructose absorption
facilitative diffusion through GLUT5 transporter
fructose must be bound to a membrane protein carrier as well as move down the concentration gradient
euglycemia
the term relating to the maintenance of optimal fasting blood glucose levels despite changing nutrition and metabolic states
Glycemic Response
degree and duration to which blood glucose level is elevated after consuming a portion of food that would provide 50g of digestibel carb an dmeasured for the next 2 hours under the curve
Glycemic index
comparison of a foods glyfemic response to a food standard based on studies
glucose and white bread are the standards
blood glucose of 50% that of glucose would be a GI of 50
Glycemic load
GI normalized to a serving standards
multiply the GI by the amount of digestible carb in a serving then divide by 100
Impacts of high GI and GL on blood sugar
high GI food can worsen hyperglycemic state and glucose managemnet is essential to reduce health risks
Glucose transport into cells
uses GLUT
GLUT1 is the most widely expressed especiually in epithelial tissues and the BBB
GLUT 2 is in hepatocytes, pancreatic B-cells and basolateral membranes of intestinal and renal epithelial cels
GLUT3 goes grlucose in neurons and has a low Km to ensure that there is always a glucose supply
GLUT4 is in muscles and is regulated by insulin
GLUT5 is the small intestine and is the fructose transporter
GLUT7 acts to transport free glucose to cytosol after the action of glucose-6-phosphate important for glucose liberation and release into circulation
Monosaccharide activation
must be phosphorylated in order to be metabolized within a cell
this locks the monosaccharides within certain cells like in hepatoxytes
Hormones in carb metabolism
insulin
glucagon
epinephrine
cortisol
Insulin role in carb
increase uptake fo glucose in skeletal muscle and adipocites
increase the synthesis of glycogen in skeletal muscle and liver hepatocytes
increases fatty acid synthesis from excessive carbs
Glucagon
increases glycogen breakdown in liver
increases liver glycogen derived glucose release into blood
increases glucose manufacturing in liver
Epinephrine
increases glycogen breakdown in liver hepatocytes and skeletal muscle
increases liver glycogen-derived glucose release into blood
increases fat breakdown and mobilization from adipocytes
Cortisol
increased muscle protein breakdown into aminoa cds
increase gluconeogenesis and liver glucose release into blood
increase fat breakdown and mobilization from fat tissues
increase liver glycogen
Insulin
B-cells from pancrease
2 chains disulphide bonded
Produced in the pancreas
Golgi has proinsulin then it is converted to mature insulin through the stretching of amino acids
INsulin secretion
insulin release is energy dependend and stimulated by plasma glucose concentration
release is promoted by certain amino acids and epptides
Insulin mediated glucose uptake
insulin promotes the lowering of blood glucose through
adipose tissue and skeletal muscle taking in glucose through GLUT4 which is upregualted by the insulin
Metabolic roles of insulin
increases glycolysis and the pentose phosphate pathway
glycogen formation and fatty acid synthesis
Inhibits glucose formation via glycogen breakdown and a conversion from non carb molecules
also inhibits fat breakdown and fatty acid oxidation in adipocytes
Glucagon cells
from a-cells of pancreatic islets
circulates in the plasma
inactivated in the liver
Gluconeogenesis occurs because of amino acids whihc stimulate glucagon
protein containing meals are likely to stimulate glucagon release
mostly acts on the liver and adipose tissues
binding of glucagon to its receptors results in increase intracellular cAMP
promotes the conversion of glycogen to glucose and gluconeogenesis
breaking down of fats also occurs in adipose tissues
activation of adentl cyclase
skeletal muscle does not have glucagon receptors so does not influence glycogen breakdown
Non-nutritive sweetener guidelines
non sugar sweeteners should not be used as means of achieving weight control or reducing risk of diseases
people should consider reducing free sugars through consumption of naturally occuring sugars
Personalized microbiome effects of non-nutritive sweeteners study
Objective
determine the impact of NNS on glycemic responses
what did they do?
RCT on 120 adults
consumed NNS for 2 weeks (less than acceptable daily intake dose)
vehicle was glucose, the control was no subbplement
What did they find
saccharin and sucralose impared glucose tolerance compared to vehicle and control groups
there were distinct changes in microbiome
NNS effects on microbiome
responders
developed impared glucose response with NNS consumptuon (saccharin and sucralose)
Non-responders
no impared glucose response wiht NNS consumption
When microbes from responders where transplanted, the microbiome did result in a different impared response in mice
Key findings from NNS study
NNS can change gut microbiome and change hormonal regulation in glucose response
microbiome changed in responders
our microbiome diversity/balance can affect how we respond to NNS
personalized factors changin response
May change depending on metabolic conditions of individuals being tested